Usually when I think of cherries, I think of them as pairs. I think most of us imagine them that way, but recently, I stumbled on a picture of a triple cherry:
Which I found interesting, but I couldn't find any more info on this, so I hoped to find some answers here. Why do they sometimes grow like that and how often does it happen compared to their regular twin counterparts?
Why do they (cherries from a cherry tree) sometimes grow like that (in triplets) and how often does it happen compared to their regular twin counterparts?
After doing a considerable amount of research, I also wasn't able to find much of any literature that addresses your question, aside from this. From that article it says:
When you think of cherries you imagine them in pairs, don't you? It's also common to find cherries grouped in quadruplets on a single bunch of stems. This happens because of the way cherry flowers bloom -- several pink blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too. It's smart to keep cherries attached to their stems whenever possible, as they will stay fresh for much longer. And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.
The bolded section seemed to be most revealing, and so, I was able to find a time-lapse video that depicts the various stages of the flowering & fruiting process for a cherry tree. The video is only 4 minutes long, and I highly suggest watching it.
From watching the video, it can be confirmed that the statements made by the previously quoted passage are true -- "several (pink) blossoms grow from a single focal point, and when those flowers wilt and become fruit, the resultant cherries are connected, too".
Consider the following series of images, which are screenshots from the time-lapse video. You should view these images in an alternating left to right, right to left fashion, going from top to bottom (so, snake-shaped).
As can be seen, each flower does grow from a shared focal point, and, the cherry fruit does originate out of the exact same location as where the flower was.
What's most interesting to note, and which begins to answer your question, is:
When viewing the third row (left to right), for the first two images, there are multiple cases of three cherries growing from the same stem. However, in each case, one of the three cherries are actually extremely underdeveloped. But then, if you compare the second and third image (still in the 3nd row, left to right), those underdeveloped cherries completely disappear!
It would then seem to me that, since one of the three cherries are severely underdeveloped (most likely due to limited nutrition & resources), the farmer who is tending to the tree will prune these (underdeveloped) cherries, thus leaving only pairs of two. In extreme cases, perhaps, the third (or even fourth) cherry achieves enough development for the farmer to not consider pruning it, but, this appears to be the exception.
Further supporting this idea, consider the next series of screenshots (from the same video).
When harvesting, the farmer deliberitely picks the cherries by pairs of two. There's even a time when he almost pulls off three, but then makes sure to leave the third. This process of pruning underdeveloped cherries, as well as harvesting in pairs or two, is most likely common practice amongst cherry growers.
And when you're harvesting the fruits, harvest the cherries at the stem (no higher!) or you risk next year's buds snapping off along with them.
Given that quote, it could be that picking in pairs of two is the most efficient method of harvesting that also best ensures the safety of next year's buds. So, to restate the reason, it would appear that cherries are rarely seen in groups of three (or more) due to nutritional constraints, and the pruning & harvesting methods of the farmer, or tree owner.
In ancient times, on the zone Mercia, the vampire species was being exterminated due to how massive the population had become. While powerful, the vampires were not able to win in this battle. Using extreme levels of magic sacrificing the lives of many in the process, the vampires stole one minute from the zone and created a copy world separate from Mercia.
This world was frozen in time, but the vampires found that they did not require feeding while in the copy world. Their stamina was unending for a near hundred years for their time, but slowly the energy of the spell used was fading out. They started to need to feed again. The world remained frozen and they ate the entire population, but the world was slowly being erased entirely as well.
The vampires had to return to Mercia, but they were still in small numbers. They needed to find an opportunity by which they could come back and conquer. They could see into the real world of Mercia and waited until they saw a potential set of beings whom they could use to strengthen their numbers.
A small team of vampires travelled to Mercia through the magical properties of Lake Mercia. They attempted to kidnap multiple individuals, but only succeeded with one. They converted their captive, and eventually had an army strong enough to at least lead an invasion to the Mercian country for the time being.
Unfortunately for the vampires, they were thwarted. With their paradox lives on the line, all it took was the speeding up of their world being destroyed for their extinction to occur. The vampire bride who they took—Rynk Hellborn—and the two who set off to save her in different realities—Blood Prowler, and Kyle Waktini—caused everything to collapse. All that was left in the end was a young male lynx who saved himself by remaining in the waters of Lake Mercia. His name, was Astral.
Astral was a perfect fusion of three race types: the vampire gene, the Banshee Mobian species, and the Nighless Species. He used his experience to seek permanent power sources. He used magic to channel the Chronos Force and mixed it with the magic of Lake Mercia. He salvaged the last remains of the vampire world and created a stable pocket-dimension location which he called “Gino Pla’Tem” (Temporary world).
Astral needed a population. He kidnapped Daricha Banshee females, and used them to start a genetic lineage. He genetically impregnated each one with specific amounts of his own ancestral genes using a combination of advanced technology and magic to ensure the designed species coming forward would be to his desires.
Once Astral had a sufficient amount of the children developed, he stopped production on impregnating the Daricha females, and transferred to artificial wombs on a production line. He planned to return every Daricha banshee to the original location they came from individually, but realized that some came from less than pleasant circumstances.
Thus, Astral allowed those who wished to, to remain, while returning those who wished to their previous location, and any who wished to leave but not return to their original worlds were sent to Mercia.
Now Astral had his species, and he began training them, educating them. They were his “Trinities”.
It was some short years into his ruling of Gino Pla’Tem when Astral realized he required successors in case he was killed. At the very least, he needed someone who could be his second-in-command. So, he found the birthed children with the highest intelligence probabilities in development and increased the concentration on production with them.
To Astral’s surprise, the developing child turned out to be three: triplets in an artificial womb. They certainly varied in potential, but each was above all current or past produced Trinities. Instead of choosing simply the smartest of the three, Astral decided it would be best to have all three act in the same role.
They were given the highest levels of education, with personal sessions by Astral and educating Trinities on matters abroad. Six months after development had been completed, they were to be named. The first was called “Simble”. He was the technical oldest, and the most intelligent by probability of the three. The second and third were to be named, but they declined, and instead wished to name themselves. The second settled on “Glyph” and the third on “Triven”.
They were made well aware of their pre-ordained destiny as heirs to the Hellervein throne, and given far less restrictions than that of other Trinities. They were allowed free roam of travelling the multiverse. They could make demands of other Trinities if they wished. They could even take and store items from other worlds, and bring people to Gino Pla’Tem.
The three did not take too far an advantage of these possibilities at first. They were more conservative in their usage of their privileges. They travelled often to different worlds, but almost never interacted with other people: instead choosing to stay in nature-based environments, but also playing pranks on the public by leaving various markings or destructive landscapes to spook people. They had their fun, but they were very cautious of their actions as vampires. They knew the moment they fed off of someone, there would be more danger to their lives, so they abstained.
The triplets cared very little really about Gino Pla’Tem, especially after going about the multiverse. They had curfews, however, and being at home often resulted in little else other than education, which they found themselves pursuing on their own time regardless.
It wasn’t long before both Kyle Waktini and Blood Prowler tracked what Astral was doing to Gino Pla’Tem. Astral was planning to use his Trinity armies to invade Mercia and conquer: convert everyone to vampires. In fact, he had already begun sending waves in, and they were winning.
Becoming aware of their two grandfathers’ presence, the triplets argued amongst each other if they should intervene. Triven noted that he was feeling guilty by what was being done, the invasion. Glyph was conflicted but did not wish to get into the debate. It was left for Simble to decide, and he had a very interesting idea.
They were in agreement. The three aided Blood and Kyle secretly in their efforts to stop Astral, and left the final result to decide what should happen. In truth, Triven aided more than what was agreed upon and in the end, Blood and Kyle managed to at least delay the waves of armies long enough to force a bargain.
The triplets released a monster that was captured by Astral: kept in the chronos volcano so that it could not disrupt the plans. At the worst possible moment for Astral, the creature charged in and attacked. The Vlasek was free to destroy.
Astral’s world was held hostage now. With Kyle, Blood, and Vlasek all working against him, he was forced to recall his forces. He did not beg them to spare him, but he did tell them to leave. Vlasek said he would just destroy them all either way, but Blood and Kyle were sympathetic at the least.
The triplets watched to see what the final decision would be. In the end, Astral’s world was left alone as the three “heroes” left. Astral made a demand before they departed, however. They would remain impartial and uninvolved with further matters with his young kingdom. He would wait to confront the rulers of Mercia for terms of a peace and freedom to travel back.
Astral was quick to discover what the triplets had done. He was expectedly bitter but despite the rest of the Trinities calling for it, none of the triplets were punished. He did ask why they did what they did, however, with Simble stating that they were “acting upon the ruling authority they would practice upon their succession of the throne”.
In actuality, the tallest triplet was really just making a coy statement. It was their own form of rebellion. Astral was silent to this, so Glyph spoke second. She answered that they came to the conclusion that acting as conquerors would only lead to unwanted attention from other members of the multiverse who would wish to do them harm. She claimed that they would be destroyed if the three of them had not acted to help end the conflict.
In actuality, she had no idea how strong the Trinity forces were in compared to any other force, and Astral knew that she was not accurate, but what mattered is that they successfully convinced him that was what they thought. He dismissed them, which gave the three a vast amount of confusion. They expected some form of punishment: death even. They received none.
The three discussed amongst themselves why they did intervene. Triven was blatantly of the opinion that it was simply what should have been done, but both he and Glyph had to ask Simble why he went along with it. The leading member of the triplets replied simply that he wanted to see if Astral would impress him, and he was disappointed.
Word spread to the other Trinities. Prior, the others were already holding growing resentment toward the royal triplets for being considered superior, but now that they all knew the triplets were responsible for their defeat, most began to hate them.
Encounter With The Known Riskers
Astral began sending out teams of Trinities throughout the multiverse to find more suitable worlds for them, and to research what they could use for Gino Pla’Tem. The royal triplets remained in Gino Pla’Tem after being threatened by one of the groups that they would kill them if the three ventured outside of the pocket dimension.
Triven was boastful that they would destroy any who came after them, but Simble dismissed this, stating that regardless of their superior skills, fighting against ten of their own kind would end badly for them if they were to make only a few mistakes.
Glyph approached her brothers, informing them that they had been given an offer by one of the Trinity scouting parties to act as protection when they travelled through the multiverse. Triven was not pleased at this idea, but Simble asked who this was.
The three went to the city-like area of Gino Pla’Tem where they met the group known as “The Known Riskers”, given such a title for how often they went into far more dangerous places, and acted dangerously as well. Their leader was a tall and built Trinity named “Carmet”.
The three asked what Carmet wanted in return for their protection. Carmet answered that he would train them to be more capable physically, but all that they would need to provide him and his group was free roam to populated lands of the multiverse.
The three were aware of how shady such an idea was, and immediately came to the conclusion that the Known Riskers would use this to cause attacks on cities. They demanded that Carmet promise no harm to the public they went across. Carmet agreed on the caveat that they would retaliate in self-defense. Glyph spoke up to this, stating that she and her brothers would be the judges of what was considered self-defense.
Regardless of the tension, it was agreed upon. The Known Riskers brought the triplets with them on their travels. At first, they stayed mostly in nature and ventured with one member to populated sections to find information, but then the Known Riskers began to grow more cocky.
They walked blatantly to various cities. Their appearance intimidated most of the areas, but they made sure to promise no intent of harm. Their actions seemed to match these words. They were all quite friendly with the public: constantly showing off their powers and magical knowledge.
As long as the triplets were with them, the Known Riskers were free to do most of what they desired. The Riskers began spreading out. Sometimes not all of them would be there when they all visited a location.
Triven spoke first, stating that the agreement was to end, that they could not allow the Known Riskers to “chaperone” them anymore. The others agreed, and so they spoke with Carmet to end the partnership. Carmet stated that he expected the joy to last shorter than it did, but showed no resistance to their wishes.
The three were alone again as they went throughout the multiverse. It wasn’t long before one of the scout groups found them, surrounding them. The Known Riskers appeared, and killed the opposing scout group. Simble reminded Carmet that their partnership was over. Carmet replied that they were simply defending the royal bloodline, but that they wouldn’t be there forever to save them, at least not any more.
Carmet’s underlying threat was not lost on the three, but they tried to continue on regardless. Another attack came a few days later. Carmet’s group was not there to aid them, but the three survived: defeating their opponents together. One died while the others fled. Another attack came just the day after that, but this time, one of the attackers was identified as a Known Risker.
Simble refused to go and speak to Astral, while Triven was too furious and wanting to kill Carmet and his group to care what was done, so Glyph went to speak to their father, but when she came to the throne room, there was Carmet.
The massive Trinity was discussing to Astral about various ventures to populated areas, wording it almost as if to blame the triplets, and offering his aid to them as a possible protector. Astral asked what Glyph needed, but the sister triplet was disheartened by Astral’s talk with Carmet, and lost her resolve to confront him on the matter.
Carmet approached Glyph outside of the throne room. Glyph asked what Carmet wanted, if he was just wanting their presence so he could cause destruction to places randomly as his “Vikings” raided and pillaged. Carmet informed her that such activity would be a bonus if anything, but that his scouting group need scapegoats when searching for powers they may use to grow stronger against the non-vampire world.
The massive Trinity said that they were to be the conquering species, and that she should want to push those under her feet as he did, that it was their right to claim vengeance on the multiverse worlds. Glyph replied that she had no desire to subjugate or influence the multiverse, especially through rule. She warned Carmet that he would not last long once discovered what he was really planning.
In response to this, Carmet took hold of Glyph and warped out of the castle to a remote forest. He pinned her to the ground, squeezing at her arms as he growled out “Tell me what I cannot do”. Glyph, using her advanced knowledge of magic, was able to propel Carmet into the air, releasing herself as Triven and Simble arrived to her aid.
Carmet landed with a blast: prepared to battle them there if needed. Simble made a challenge to the large Trintity. He informed Carmet that they could incriminate him if needed, bringing up specific actions the Known Riskers took part in that were against the scout group rules. Carmet replied that they would all be incriminated if Simble released the information. Simble replied that they were willing to risk that. Carmet asked what Simble’s challenge was.
The tallest of the triplets stated that Triven would battle Carmet at the Arena. The stakes would be that if Triven won the battle, Carmet would dissolve his scout party and put himself at Astral’s mercy. If he won, the triplets would dissolve their evidence against the Known Riskers, and pardon the actions entirely.
Carmet agreed to the challenge, with Glyph fuming at Simble for making such a challenge. Simble replied that they were at an impasse with Carmet and his group, and that their relationship with the other Trinities was on the edge of exile. Carmet could use his own information to harm them if they did not make him believe they could ruin him.
Glyph asked what they would do if Triven lost the fight. Triven simply growled, stating that he wouldn’t lose. The two Trinities met at the Arena. Carmet attempted to use his words to intimidate the shorter opponent, but Triven remained focused on an aggressive front. They battled for two minutes before Carmet had Triven pinned to the ground. The triplet struggled, roaring at his enemy, but Carmet kept him down until the limit was up. Triven had lost the battle.
Glyph confronted Simble, stating that he knew Triven would lose, and asked why he had him fight. Simble answered that he tricked Carmet into thinking he would be getting what he wanted, that if Triven had won, no-doubt it would have resulted in Carmet not honoring the agreement, but if he won, they would not incriminate him, but he would not be bothering them further. Glyph asked why Simble thought Carmet would leave them alone, with Simble replying that Carmet wouldn’t want to risk any more trouble.
Simble was partially correct. The Known Riskers did not interfere with the triplets from that point onward, but Triven’s loss earned them further mockery. Despite this, Simble appeared content. He travelled to the world the Known Riskers now had permission to. As expected, the area was being overrun. The Known Riskers were celebrating.
When they saw Simble, they tried to attack him, but he vanished from their sight, reappearing further inside the city, and taking a special artifact inside—a strange glowing staff—before departing secretly to a different zone.
Soon after, Simble returned to Gino Pla’Tem to meet with his siblings again.
DURATION OF MULTIPLE PREGNANCIES
The duration of a normal singleton pregnancy ranges from 37 weeks to 42 weeks from the time of the last menstrual period. Twin pregnancies occasionally progress to 40 weeks but almost always deliver early. As the number of fetuses increases, the expected duration of the pregnancy decreases. The average duration is 35 weeks for twins, 33 weeks for triplets, and 30 weeks for quadruplets.
The production of a RNA copy from a DNA strand is called transcription, and is performed by RNA polymerases, which add one ribonucleotide at a time to a growing RNA strand as per the complementarity law of the nucleotide bases. This RNA is complementary to the template 3′ → 5′ DNA strand,  with the exception that thymines (T) are replaced with uracils (U) in the RNA.
In prokaryotes, transcription is carried out by a single type of RNA polymerase, which needs to bind a DNA sequence called a Pribnow box with the help of the sigma factor protein (σ factor) to start transcription. In eukaryotes, transcription is performed in the nucleus by three types of RNA polymerases, each of which needs a special DNA sequence called the promoter and a set of DNA-binding proteins—transcription factors—to initiate the process (see regulation of transcription below). RNA polymerase I is responsible for transcription of ribosomal RNA (rRNA) genes. RNA polymerase II (Pol II) transcribes all protein-coding genes but also some non-coding RNAs (e.g., snRNAs, snoRNAs or long non-coding RNAs). RNA polymerase III transcribes 5S rRNA, transfer RNA (tRNA) genes, and some small non-coding RNAs (e.g., 7SK). Transcription ends when the polymerase encounters a sequence called the terminator.
MRNA processing Edit
While transcription of prokaryotic protein-coding genes creates messenger RNA (mRNA) that is ready for translation into protein, transcription of eukaryotic genes leaves a primary transcript of RNA (pre-RNA), which first has to undergo a series of modifications to become a mature RNA. Types and steps involved in the maturation processes vary between coding and non-coding preRNAs i.e. even though preRNA molecules for both mRNA and tRNA undergo splicing, the steps and machinery involved are different.  The processing of non-coding RNA is described below (non-coring RNA maturation).
The processing of premRNA include 5′ capping, which is set of enzymatic reactions that add 7-methylguanosine (m 7 G) to the 5′ end of pre-mRNA and thus protect the RNA from degradation by exonucleases. The m 7 G cap is then bound by cap binding complex heterodimer (CBC20/CBC80), which aids in mRNA export to cytoplasm and also protect the RNA from decapping.
Another modification is 3′ cleavage and polyadenylation. They occur if polyadenylation signal sequence (5′- AAUAAA-3′) is present in pre-mRNA, which is usually between protein-coding sequence and terminator. The pre-mRNA is first cleaved and then a series of
200 adenines (A) are added to form poly(A) tail, which protects the RNA from degradation. The poly(A) tail is bound by multiple poly(A)-binding proteins (PABPs) necessary for mRNA export and translation re-initiation. In the inverse process of deadenylation, poly(A) tails are shortened by the CCR4-Not 3′-5′ exonuclease, which often leads to full transcript decay.
A very important modification of eukaryotic pre-mRNA is RNA splicing. The majority of eukaryotic pre-mRNAs consist of alternating segments called exons and introns. During the process of splicing, an RNA-protein catalytical complex known as spliceosome catalyzes two transesterification reactions, which remove an intron and release it in form of lariat structure, and then splice neighbouring exons together. In certain cases, some introns or exons can be either removed or retained in mature mRNA. This so-called alternative splicing creates series of different transcripts originating from a single gene. Because these transcripts can be potentially translated into different proteins, splicing extends the complexity of eukaryotic gene expression and the size of a species proteome.
Extensive RNA processing may be an evolutionary advantage made possible by the nucleus of eukaryotes. In prokaryotes, transcription and translation happen together, whilst in eukaryotes, the nuclear membrane separates the two processes, giving time for RNA processing to occur.
Non-coding RNA maturation Edit
In most organisms non-coding genes (ncRNA) are transcribed as precursors that undergo further processing. In the case of ribosomal RNAs (rRNA), they are often transcribed as a pre-rRNA that contains one or more rRNAs. The pre-rRNA is cleaved and modified (2′-O-methylation and pseudouridine formation) at specific sites by approximately 150 different small nucleolus-restricted RNA species, called snoRNAs. SnoRNAs associate with proteins, forming snoRNPs. While snoRNA part basepair with the target RNA and thus position the modification at a precise site, the protein part performs the catalytical reaction. In eukaryotes, in particular a snoRNP called RNase, MRP cleaves the 45S pre-rRNA into the 28S, 5.8S, and 18S rRNAs. The rRNA and RNA processing factors form large aggregates called the nucleolus. 
In the case of transfer RNA (tRNA), for example, the 5′ sequence is removed by RNase P,  whereas the 3′ end is removed by the tRNase Z enzyme  and the non-templated 3′ CCA tail is added by a nucleotidyl transferase.  In the case of micro RNA (miRNA), miRNAs are first transcribed as primary transcripts or pri-miRNA with a cap and poly-A tail and processed to short, 70-nucleotide stem-loop structures known as pre-miRNA in the cell nucleus by the enzymes Drosha and Pasha. After being exported, it is then processed to mature miRNAs in the cytoplasm by interaction with the endonuclease Dicer, which also initiates the formation of the RNA-induced silencing complex (RISC), composed of the Argonaute protein.
Even snRNAs and snoRNAs themselves undergo series of modification before they become part of functional RNP complex. This is done either in the nucleoplasm or in the specialized compartments called Cajal bodies. Their bases are methylated or pseudouridinilated by a group of small Cajal body-specific RNAs (scaRNAs), which are structurally similar to snoRNAs.
RNA export Edit
In eukaryotes most mature RNA must be exported to the cytoplasm from the nucleus. While some RNAs function in the nucleus, many RNAs are transported through the nuclear pores and into the cytosol.  Export of RNAs requires association with specific proteins known as exportins. Specific exportin molecules are responsible for the export of a given RNA type. mRNA transport also requires the correct association with Exon Junction Complex (EJC), which ensures that correct processing of the mRNA is completed before export. In some cases RNAs are additionally transported to a specific part of the cytoplasm, such as a synapse they are then towed by motor proteins that bind through linker proteins to specific sequences (called "zipcodes") on the RNA. 
For some RNA (non-coding RNA) the mature RNA is the final gene product.  In the case of messenger RNA (mRNA) the RNA is an information carrier coding for the synthesis of one or more proteins. mRNA carrying a single protein sequence (common in eukaryotes) is monocistronic whilst mRNA carrying multiple protein sequences (common in prokaryotes) is known as polycistronic.
Every mRNA consists of three parts: a 5′ untranslated region (5′UTR), a protein-coding region or open reading frame (ORF), and a 3′ untranslated region (3′UTR). The coding region carries information for protein synthesis encoded by the genetic code to form triplets. Each triplet of nucleotides of the coding region is called a codon and corresponds to a binding site complementary to an anticodon triplet in transfer RNA. Transfer RNAs with the same anticodon sequence always carry an identical type of amino acid. Amino acids are then chained together by the ribosome according to the order of triplets in the coding region. The ribosome helps transfer RNA to bind to messenger RNA and takes the amino acid from each transfer RNA and makes a structure-less protein out of it.   Each mRNA molecule is translated into many protein molecules, on average
In prokaryotes translation generally occurs at the point of transcription (co-transcriptionally), often using a messenger RNA that is still in the process of being created. In eukaryotes translation can occur in a variety of regions of the cell depending on where the protein being written is supposed to be. Major locations are the cytoplasm for soluble cytoplasmic proteins and the membrane of the endoplasmic reticulum for proteins that are for export from the cell or insertion into a cell membrane. Proteins that are supposed to be expressed at the endoplasmic reticulum are recognised part-way through the translation process. This is governed by the signal recognition particle—a protein that binds to the ribosome and directs it to the endoplasmic reticulum when it finds a signal peptide on the growing (nascent) amino acid chain. 
Each protein exists as an unfolded polypeptide or random coil when translated from a sequence of mRNA into a linear chain of amino acids. This polypeptide lacks any developed three-dimensional structure (the left hand side of the neighboring figure). The polypeptide then folds into its characteristic and functional three-dimensional structure from a random coil.  Amino acids interact with each other to produce a well-defined three-dimensional structure, the folded protein (the right hand side of the figure) known as the native state. The resulting three-dimensional structure is determined by the amino acid sequence (Anfinsen's dogma). 
The correct three-dimensional structure is essential to function, although some parts of functional proteins may remain unfolded.  Failure to fold into the intended shape usually produces inactive proteins with different properties including toxic prions. Several neurodegenerative and other diseases are believed to result from the accumulation of misfolded proteins.  Many allergies are caused by the folding of the proteins, for the immune system does not produce antibodies for certain protein structures. 
Enzymes called chaperones assist the newly formed protein to attain (fold into) the 3-dimensional structure it needs to function.  Similarly, RNA chaperones help RNAs attain their functional shapes.  Assisting protein folding is one of the main roles of the endoplasmic reticulum in eukaryotes.
Secretory proteins of eukaryotes or prokaryotes must be translocated to enter the secretory pathway. Newly synthesized proteins are directed to the eukaryotic Sec61 or prokaryotic SecYEG translocation channel by signal peptides. The efficiency of protein secretion in eukaryotes is very dependent on the signal peptide which has been used. 
Protein transport Edit
Many proteins are destined for other parts of the cell than the cytosol and a wide range of signalling sequences or (signal peptides) are used to direct proteins to where they are supposed to be. In prokaryotes this is normally a simple process due to limited compartmentalisation of the cell. However, in eukaryotes there is a great variety of different targeting processes to ensure the protein arrives at the correct organelle.
Not all proteins remain within the cell and many are exported, for example, digestive enzymes, hormones and extracellular matrix proteins. In eukaryotes the export pathway is well developed and the main mechanism for the export of these proteins is translocation to the endoplasmic reticulum, followed by transport via the Golgi apparatus.  
Regulation of gene expression refers to the control of the amount and timing of appearance of the functional product of a gene. Control of expression is vital to allow a cell to produce the gene products it needs when it needs them in turn, this gives cells the flexibility to adapt to a variable environment, external signals, damage to the cell, and other stimuli. More generally, gene regulation gives the cell control over all structure and function, and is the basis for cellular differentiation, morphogenesis and the versatility and adaptability of any organism.
Numerous terms are used to describe types of genes depending on how they are regulated these include:
- A constitutive gene is a gene that is transcribed continually as opposed to a facultative gene, which is only transcribed when needed.
- A housekeeping gene is a gene that is required to maintain basic cellular function and so is typically expressed in all cell types of an organism. Examples include actin, GAPDH and ubiquitin. Some housekeeping genes are transcribed at a relatively constant rate and these genes can be used as a reference point in experiments to measure the expression rates of other genes.
- A facultative gene is a gene only transcribed when needed as opposed to a constitutive gene.
- An inducible gene is a gene whose expression is either responsive to environmental change or dependent on the position in the cell cycle.
Any step of gene expression may be modulated, from the DNA-RNA transcription step to post-translational modification of a protein. The stability of the final gene product, whether it is RNA or protein, also contributes to the expression level of the gene—an unstable product results in a low expression level. In general gene expression is regulated through changes  in the number and type of interactions between molecules  that collectively influence transcription of DNA  and translation of RNA. 
Some simple examples of where gene expression is important are:
- Control of insulin expression so it gives a signal for blood glucose regulation. in female mammals to prevent an "overdose" of the genes it contains. expression levels control progression through the eukaryotic cell cycle.
Transcriptional regulation Edit
Regulation of transcription can be broken down into three main routes of influence genetic (direct interaction of a control factor with the gene), modulation interaction of a control factor with the transcription machinery and epigenetic (non-sequence changes in DNA structure that influence transcription).
Direct interaction with DNA is the simplest and the most direct method by which a protein changes transcription levels. Genes often have several protein binding sites around the coding region with the specific function of regulating transcription. There are many classes of regulatory DNA binding sites known as enhancers, insulators and silencers. The mechanisms for regulating transcription are very varied, from blocking key binding sites on the DNA for RNA polymerase to acting as an activator and promoting transcription by assisting RNA polymerase binding.
The activity of transcription factors is further modulated by intracellular signals causing protein post-translational modification including phosphorylated, acetylated, or glycosylated. These changes influence a transcription factor's ability to bind, directly or indirectly, to promoter DNA, to recruit RNA polymerase, or to favor elongation of a newly synthesized RNA molecule.
The nuclear membrane in eukaryotes allows further regulation of transcription factors by the duration of their presence in the nucleus, which is regulated by reversible changes in their structure and by binding of other proteins.  Environmental stimuli or endocrine signals  may cause modification of regulatory proteins  eliciting cascades of intracellular signals,  which result in regulation of gene expression.
More recently it has become apparent that there is a significant influence of non-DNA-sequence specific effects on transcription. These effects are referred to as epigenetic and involve the higher order structure of DNA, non-sequence specific DNA binding proteins and chemical modification of DNA. In general epigenetic effects alter the accessibility of DNA to proteins and so modulate transcription.
In eukaryotes the structure of chromatin, controlled by the histone code, regulates access to DNA with significant impacts on the expression of genes in euchromatin and heterochromatin areas.
Enhancers, transcription factors, Mediator complex and DNA loops in mammalian transcription Edit
Gene expression in mammals is regulated by many cis-regulatory elements, including core promoters and promoter-proximal elements that are located near the transcription start sites of genes, upstream on the DNA (towards the 5' region of the sense strand). Other important cis-regulatory modules are localized in DNA regions that are distant from the transcription start sites. These include enhancers, silencers, insulators and tethering elements.  Among this constellation of elements, enhancers and their associated transcription factors have a leading role in the regulation of gene expression. 
Enhancers are regions of the genome that are major gene-regulatory elements. Enhancers control cell-type-specific gene expression programs, most often by looping through long distances to come in physical proximity with the promoters of their target genes.  Multiple enhancers, each often at tens or hundred of thousands of nucleotides distant from their target genes, loop to their target gene promoters and coordinate with each other to control expression of their common target gene. 
The schematic illustration at the left shows an enhancer looping around to come into close physical proximity with the promoter of a target gene. The loop is stabilized by a dimer of a connector protein (e.g. dimer of CTCF or YY1), with one member of the dimer anchored to its binding motif on the enhancer and the other member anchored to its binding motif on the promoter (represented by the red zigzags in the illustration).  Several cell function specific transcription factors (there are about 1,600 transcription factors in a human cell  ) generally bind to specific motifs on an enhancer  and a small combination of these enhancer-bound transcription factors, when brought close to a promoter by a DNA loop, govern level of transcription of the target gene. Mediator (a complex usually consisting of about 26 proteins in an interacting structure) communicates regulatory signals from enhancer DNA-bound transcription factors directly to the RNA polymerase II (pol II) enzyme bound to the promoter. 
Enhancers, when active, are generally transcribed from both strands of DNA with RNA polymerases acting in two different directions, producing two eRNAs as illustrated in the Figure.  An inactive enhancer may be bound by an inactive transcription factor. Phosphorylation of the transcription factor may activate it and that activated transcription factor may then activate the enhancer to which it is bound (see small red star representing phosphorylation of transcription factor bound to enhancer in the illustration).  An activated enhancer begins transcription of its RNA before activating transcription of messenger RNA from its target gene. 
DNA methylation and demethylation in transcriptional regulation Edit
DNA methylation is a widespread mechanism for epigenetic influence on gene expression and is seen in bacteria and eukaryotes and has roles in heritable transcription silencing and transcription regulation. Methylation most often occurs on a cytosine (see Figure). Methylation of cytosine primarily occurs in dinucleotide sequences where a cytosine is followed by a guanine, a CpG site. The number of CpG sites in the human genome is about 28 million.  Depending on the type of cell, about 70% of the CpG sites have a methylated cytosine. 
Methylation of cytosine in DNA has a major role in regulating gene expression. Methylation of CpGs in a promoter region of a gene usually represses gene transcription  while methylation of CpGs in the body of a gene increases expression.  TET enzymes play a central role in demethylation of methylated cytosines. Demethylation of CpGs in a gene promoter by TET enzyme activity increases transcription of the gene. 
Transcriptional regulation in learning and memory Edit
In a rat, contextual fear conditioning (CFC) is a painful learning experience. Just one episode of CFC can result in a life-long fearful memory.  After an episode of CFC, cytosine methylation is altered in the promoter regions of about 9.17% of all genes in the hippocampus neuron DNA of a rat.  The hippocampus is where new memories are initially stored. After CFC about 500 genes have increased transcription (often due to demethylation of CpG sites in a promoter region) and about 1,000 genes have decreased transcription (often due to newly formed 5-methylcytosine at CpG sites in a promoter region). The pattern of induced and repressed genes within neurons appears to provide a molecular basis for forming the first transient memory of this training event in the hippocampus of the rat brain. 
In particular, the brain-derived neurotrophic factor gene (BDNF) is known as a "learning gene."  After CFC there was upregulation of BDNF gene expression, related to decreased CpG methylation of certain internal promoters of the gene, and this was correlated with learning. 
Transcriptional regulation in cancer Edit
The majority of gene promoters contain a CpG island with numerous CpG sites.  When many of a gene's promoter CpG sites are methylated the gene becomes silenced.  Colorectal cancers typically have 3 to 6 driver mutations and 33 to 66 hitchhiker or passenger mutations.  However, transcriptional silencing may be of more importance than mutation in causing progression to cancer. For example, in colorectal cancers about 600 to 800 genes are transcriptionally silenced by CpG island methylation (see regulation of transcription in cancer). Transcriptional repression in cancer can also occur by other epigenetic mechanisms, such as altered expression of microRNAs.  In breast cancer, transcriptional repression of BRCA1 may occur more frequently by over-expressed microRNA-182 than by hypermethylation of the BRCA1 promoter (see Low expression of BRCA1 in breast and ovarian cancers).
Post-transcriptional regulation Edit
In eukaryotes, where export of RNA is required before translation is possible, nuclear export is thought to provide additional control over gene expression. All transport in and out of the nucleus is via the nuclear pore and transport is controlled by a wide range of importin and exportin proteins.
Expression of a gene coding for a protein is only possible if the messenger RNA carrying the code survives long enough to be translated. In a typical cell, an RNA molecule is only stable if specifically protected from degradation. RNA degradation has particular importance in regulation of expression in eukaryotic cells where mRNA has to travel significant distances before being translated. In eukaryotes, RNA is stabilised by certain post-transcriptional modifications, particularly the 5′ cap and poly-adenylated tail.
Intentional degradation of mRNA is used not just as a defence mechanism from foreign RNA (normally from viruses) but also as a route of mRNA destabilisation. If an mRNA molecule has a complementary sequence to a small interfering RNA then it is targeted for destruction via the RNA interference pathway.
Three prime untranslated regions and microRNAs Edit
Three prime untranslated regions (3′UTRs) of messenger RNAs (mRNAs) often contain regulatory sequences that post-transcriptionally influence gene expression. Such 3′-UTRs often contain both binding sites for microRNAs (miRNAs) as well as for regulatory proteins. By binding to specific sites within the 3′-UTR, miRNAs can decrease gene expression of various mRNAs by either inhibiting translation or directly causing degradation of the transcript. The 3′-UTR also may have silencer regions that bind repressor proteins that inhibit the expression of a mRNA.
The 3′-UTR often contains microRNA response elements (MREs). MREs are sequences to which miRNAs bind. These are prevalent motifs within 3′-UTRs. Among all regulatory motifs within the 3′-UTRs (e.g. including silencer regions), MREs make up about half of the motifs.
As of 2014, the miRBase web site,  an archive of miRNA sequences and annotations, listed 28,645 entries in 233 biologic species. Of these, 1,881 miRNAs were in annotated human miRNA loci. miRNAs were predicted to have an average of about four hundred target mRNAs (affecting expression of several hundred genes).  Friedman et al.  estimate that >45,000 miRNA target sites within human mRNA 3′UTRs are conserved above background levels, and >60% of human protein-coding genes have been under selective pressure to maintain pairing to miRNAs.
Direct experiments show that a single miRNA can reduce the stability of hundreds of unique mRNAs.  Other experiments show that a single miRNA may repress the production of hundreds of proteins, but that this repression often is relatively mild (less than 2-fold).  
The effects of miRNA dysregulation of gene expression seem to be important in cancer.  For instance, in gastrointestinal cancers, nine miRNAs have been identified as epigenetically altered and effective in down regulating DNA repair enzymes. 
The effects of miRNA dysregulation of gene expression also seem to be important in neuropsychiatric disorders, such as schizophrenia, bipolar disorder, major depression, Parkinson's disease, Alzheimer's disease and autism spectrum disorders.  
Translational regulation Edit
Direct regulation of translation is less prevalent than control of transcription or mRNA stability but is occasionally used. Inhibition of protein translation is a major target for toxins and antibiotics, so they can kill a cell by overriding its normal gene expression control. Protein synthesis inhibitors include the antibiotic neomycin and the toxin ricin.
Post-translational modifications Edit
Post-translational modifications (PTMs) are covalent modifications to proteins. Like RNA splicing, they help to significantly diversify the proteome. These modifications are usually catalyzed by enzymes. Additionally, processes like covalent additions to amino acid side chain residues can often be reversed by other enzymes. However, some, like the proteolytic cleavage of the protein backbone, are irreversible. 
PTMs play many important roles in the cell.  For example, phosphorylation is primarily involved in activating and deactivating proteins and in signaling pathways.  PTMs are involved in transcriptional regulation: an important function of acetylation and methylation is histone tail modification, which alters how accessible DNA is for transcription.  They can also be seen in the immune system, where glycosylation plays a key role.  One type of PTM can initiate another type of PTM, as can be seen in how ubiquitination tags proteins for degradation through proteolysis.  Proteolysis, other than being involved in breaking down proteins, is also important in activating and deactivating them, and in regulating biological processes such as DNA transcription and cell death. 
Measuring gene expression is an important part of many life sciences, as the ability to quantify the level at which a particular gene is expressed within a cell, tissue or organism can provide a lot of valuable information. For example, measuring gene expression can:
- Identify viral infection of a cell (viral protein expression).
- Determine an individual's susceptibility to cancer (oncogene expression).
- Find if a bacterium is resistant to penicillin (beta-lactamase expression).
Similarly, the analysis of the location of protein expression is a powerful tool, and this can be done on an organismal or cellular scale. Investigation of localization is particularly important for the study of development in multicellular organisms and as an indicator of protein function in single cells. Ideally, measurement of expression is done by detecting the final gene product (for many genes, this is the protein) however, it is often easier to detect one of the precursors, typically mRNA and to infer gene-expression levels from these measurements.
MRNA quantification Edit
Levels of mRNA can be quantitatively measured by northern blotting, which provides size and sequence information about the mRNA molecules. A sample of RNA is separated on an agarose gel and hybridized to a radioactively labeled RNA probe that is complementary to the target sequence. The radiolabeled RNA is then detected by an autoradiograph. Because the use of radioactive reagents makes the procedure time consuming and potentially dangerous, alternative labeling and detection methods, such as digoxigenin and biotin chemistries, have been developed. Perceived disadvantages of Northern blotting are that large quantities of RNA are required and that quantification may not be completely accurate, as it involves measuring band strength in an image of a gel. On the other hand, the additional mRNA size information from the Northern blot allows the discrimination of alternately spliced transcripts.
Another approach for measuring mRNA abundance is RT-qPCR. In this technique, reverse transcription is followed by quantitative PCR. Reverse transcription first generates a DNA template from the mRNA this single-stranded template is called cDNA. The cDNA template is then amplified in the quantitative step, during which the fluorescence emitted by labeled hybridization probes or intercalating dyes changes as the DNA amplification process progresses. With a carefully constructed standard curve, qPCR can produce an absolute measurement of the number of copies of original mRNA, typically in units of copies per nanolitre of homogenized tissue or copies per cell. qPCR is very sensitive (detection of a single mRNA molecule is theoretically possible), but can be expensive depending on the type of reporter used fluorescently labeled oligonucleotide probes are more expensive than non-specific intercalating fluorescent dyes.
For expression profiling, or high-throughput analysis of many genes within a sample, quantitative PCR may be performed for hundreds of genes simultaneously in the case of low-density arrays. A second approach is the hybridization microarray. A single array or "chip" may contain probes to determine transcript levels for every known gene in the genome of one or more organisms. Alternatively, "tag based" technologies like Serial analysis of gene expression (SAGE) and RNA-Seq, which can provide a relative measure of the cellular concentration of different mRNAs, can be used. An advantage of tag-based methods is the "open architecture", allowing for the exact measurement of any transcript, with a known or unknown sequence. Next-generation sequencing (NGS) such as RNA-Seq is another approach, producing vast quantities of sequence data that can be matched to a reference genome. Although NGS is comparatively time-consuming, expensive, and resource-intensive, it can identify single-nucleotide polymorphisms, splice-variants, and novel genes, and can also be used to profile expression in organisms for which little or no sequence information is available.
RNA profiles in Wikipedia Edit
Profiles like these are found for almost all proteins listed in Wikipedia. They are generated by organizations such as the Genomics Institute of the Novartis Research Foundation and the European Bioinformatics Institute. Additional information can be found by searching their databases (for an example of the GLUT4 transporter pictured here, see citation).  These profiles indicate the level of DNA expression (and hence RNA produced) of a certain protein in a certain tissue, and are color-coded accordingly in the images located in the Protein Box on the right side of each Wikipedia page.
Protein quantification Edit
For genes encoding proteins, the expression level can be directly assessed by a number of methods with some clear analogies to the techniques for mRNA quantification.
One of the most commonly used methods is to perform a Western blot against the protein of interest.  This gives information on the size of the protein in addition to its identity. A sample (often cellular lysate) is separated on a polyacrylamide gel, transferred to a membrane and then probed with an antibody to the protein of interest. The antibody can either be conjugated to a fluorophore or to horseradish peroxidase for imaging and/or quantification. The gel-based nature of this assay makes quantification less accurate, but it has the advantage of being able to identify later modifications to the protein, for example proteolysis or ubiquitination, from changes in size.
MRNA-protein correlation Edit
Quantification of protein and mRNA permits a correlation of the two levels. The question of how well protein levels correlate with their corresponding transcript levels is highly debated and depends on multiple factors. Regulation on each step of gene expression can impact the correlation, as shown for regulation of translation  or protein stability.  Post-translational factors, such as protein transport in highly polar cells,  can influence the measured mRNA-protein correlation as well.
Analysis of expression is not limited to quantification localisation can also be determined. mRNA can be detected with a suitably labelled complementary mRNA strand and protein can be detected via labelled antibodies. The probed sample is then observed by microscopy to identify where the mRNA or protein is.
By replacing the gene with a new version fused to a green fluorescent protein (or similar) marker, expression may be directly quantified in live cells. This is done by imaging using a fluorescence microscope. It is very difficult to clone a GFP-fused protein into its native location in the genome without affecting expression levels so this method often cannot be used to measure endogenous gene expression. It is, however, widely used to measure the expression of a gene artificially introduced into the cell, for example via an expression vector. It is important to note that by fusing a target protein to a fluorescent reporter the protein's behavior, including its cellular localization and expression level, can be significantly changed.
The enzyme-linked immunosorbent assay works by using antibodies immobilised on a microtiter plate to capture proteins of interest from samples added to the well. Using a detection antibody conjugated to an enzyme or fluorophore the quantity of bound protein can be accurately measured by fluorometric or colourimetric detection. The detection process is very similar to that of a Western blot, but by avoiding the gel steps more accurate quantification can be achieved.
An expression system is a system specifically designed for the production of a gene product of choice. This is normally a protein although may also be RNA, such as tRNA or a ribozyme. An expression system consists of a gene, normally encoded by DNA, and the molecular machinery required to transcribe the DNA into mRNA and translate the mRNA into protein using the reagents provided. In the broadest sense this includes every living cell but the term is more normally used to refer to expression as a laboratory tool. An expression system is therefore often artificial in some manner. Expression systems are, however, a fundamentally natural process. Viruses are an excellent example where they replicate by using the host cell as an expression system for the viral proteins and genome.
Inducible expression Edit
In nature Edit
In addition to these biological tools, certain naturally observed configurations of DNA (genes, promoters, enhancers, repressors) and the associated machinery itself are referred to as an expression system. This term is normally used in the case where a gene or set of genes is switched on under well defined conditions, for example, the simple repressor switch expression system in Lambda phage and the lac operator system in bacteria. Several natural expression systems are directly used or modified and used for artificial expression systems such as the Tet-on and Tet-off expression system.
Genes have sometimes been regarded as nodes in a network, with inputs being proteins such as transcription factors, and outputs being the level of gene expression. The node itself performs a function, and the operation of these functions have been interpreted as performing a kind of information processing within cells and determines cellular behavior.
Gene networks can also be constructed without formulating an explicit causal model. This is often the case when assembling networks from large expression data sets.  Covariation and correlation of expression is computed across a large sample of cases and measurements (often transcriptome or proteome data). The source of variation can be either experimental or natural (observational). There are several ways to construct gene expression networks, but one common approach is to compute a matrix of all pair-wise correlations of expression across conditions, time points, or individuals and convert the matrix (after thresholding at some cut-off value) into a graphical representation in which nodes represent genes, transcripts, or proteins and edges connecting these nodes represent the strength of association (see ). 
The following experimental techniques are used to measure gene expression and are listed in roughly chronological order, starting with the older, more established technologies. They are divided into two groups based on their degree of multiplexity.
Polyploid Plant Info
Extra chromosomes in people is bad. It causes genetic disorders, such Down syndrome. In plants, however, polyploidy is very common. Many types of plants, such as strawberries, have multiple copies of chromosomes. Polyploidy does create one little glitch when it comes to plant reproduction.
If two plants which crossbreed have differing numbers of chromosomes, it’s possible that the resulting offspring will have an uneven number of chromosomes. Instead of one or more pairs of the same chromosome, the offspring can end up with three, five, or seven copies of the chromosome.
Meiosis doesn’t work very well with odd numbers of the same chromosome, so these plants are often sterile.
Fruit Ripening: Meaning, Factors and Controls | Plant Physiology
There are several developmental phases through which the fruit passes and fruit ripening is one of them. In fact, ripening begins moment the growth of the fruit is completed. Fruit maturity is a stage of fruit harvesting while fruit ripening is a stage of fruit consumption.
The fruit ripening is associated with many visible changes in the colour, the flavour and the aroma. Thus, the fruit is ready for eating purposes. Fruit ripening is a type of ageing and many people prefer to call it “fruit ageing” than fruit ripening. In many fruits the ripening occurs after picking or the process is hastened after picking. Ripening processes are of degradative nature.
Studies in recent years have shown that several biochemical processes must occur sequentially. However, these processes may not be linked with each other.
Factors Affecting Fruit Ripening:
In the following some of the important factors affecting fruit ripening are described:
The visible changes in the fruit leading to ripening are accompanied by a rapid increase in respiration. This process is called climacteric and is distinctly visible in many fleshy fruits like apple, banana, apricots, papaya, tomato etc. However, fruits like figs or cherries do not show climacteric.
This does not mean that the non-climacteric fruits always have low rate of respiration. Some of the compound fruits in fact have high activity of respiration. In general climacteric fruits are rich in carotenoids whereas non-climacteric fruits contain anthocyanins. In apple once the climateric begins the free fructose disappears from the cytoplasm due to phosphorylation.
Simultaneously there is a change in tonoplast permeability which presumably permits movement of fructose from the vacuole to the cytoplasm. Thus, there is an increased respiration. The alternative explanation is that the rate of respiration is regulated by ADP. Thus respiration rate in low if ATP/ADP ratio is high.
The climacteric rise in respiration results from a high energy requirement in the initial stages of fruit ripening. The respiration is enhanced when ATP is split and level of ADP rises. Tomato fruits when sprayed with 2, 4- DNP are prevented from ripening.
One of the factors inducing increased respiration is natural un-couplers of oxidative phosphorylation. Climacteric fruit extracts did act as un-couplers of oxidative phosphorylation. The present thinking is that increased respiration may be attributed to high energy requirements in ripening.
Tracer studies have shown that in several fruits increased RNA synthesis accompanies fruit ripening. Most of the evidence is based on assays of the rate of incorporation of RNA precursors and indicates that RNA synthesis includes mRNA and is enhances during early part of climacteric rise.
In picked up apples about 50% RNA increased at the initiation of the climacteric increase. When the climacteric is high the increase in its synthesis does not occur.
In general, new synthesis of RNA seems to be essential for the ripening process. Pears sprayed with Act.D did not ripe. The rise in the RNA concentration is followed by an increase in the protein content because of new synthesis. Indeed the synthesis of new proteins is essential for the ripening of many fruits.
When the mature, unripe banana and pears were sprayed with cycloheximide, ripening was inhibited. This was especially so when it was administered during early stages. It is assumed that enzymes involved in ripening were synthesized during the early stages.
Changes in the pattern and activities of several enzymes are reported during fruit ripening. In general, several hydrolytic enzymes increase. These include polygalacturonase, cellulase, pectin methyl esterase, etc. Some of the enzymes soften the fruits and bring about changes in taste as well. The sweetness in several fruits is caused by breakdown of starch into sugar. Sometimes fruits abound in free fatty acids.
However, the importance of several enzymes in ripening of fruit is not clear. This category includes lipidase and peroxidase. It is believed that these enzymes may be involved in the biosynthesis of ethylene. Sometimes different isozymes are associated with fruit ripening.
Increase in chlorophyllase, lipase causes breakdown of chlorophyll and free fatty acids, respectively. Similarly increased lipoxidase is also reported. Large increase in acid phosphatase activity parallels the climacteric in mangoes. In several fruits enzymes of glycolysis, oxidative processes—HMP shunt and citric acid cycle also increase.
Fruit ripening is also accompanied by dramatic changes in its colour e.g., in tomato following sequence of colour changes are observed:
The red colour is due to lycopene. Carotenoid formation occurs when chloroplast is converted into chromoplast. However, not in all the cases the change in fruit colour is associated with the formation of carotenoids.
On the contrary in many fruits anthocyanin is synthesized during ripening as in apple. The present thinking is that synthesis of carotenoids and anthocyanin in ripening fruits is regulated by phytochrome system.
v. Effect of Potassium Nutrition on Fruit Ripening:
In tomato fruit increased potassium (K + ) nutrition causes an increase in the concentration of organic acids, in particular citric and malic acids. It may be recalled that tomato is a climacteric fruit so that the pre-climacteric respiration minimum is followed by a peak during which the rate rises by 110—250%.
When the plants are supplied with high concentrations of K they have reduced rate of respiration especially during the climacteric phase. There is great accumulation of oxaloacetic acid (OAA) which is also increased by K application.
This increase is due to the oxidation of malate by malate dehydrogenase and can be inhibited by malate and succinate oxidation by tomato fruit mitochondria. The rate of endogenous concentration of OAA could be controlled by the rate of transamination with L-glutamate through the action of GOT.
Fruit ripening is also retarded by osmotic water intake and by washing out of some unidentified substances. Besides the climacteric respiration, other characteristic metabolic pathways can be seen. For instance, in ripening mango fruits aspartate and glutamate decrease, while α-aminobutyrate increases.
Together with changes in enzyme activities, the following metabolism of aspartate and glutamate must occur:
This metabolism indicates that the most significant amino acids are decomposed. This may partly explain why protein synthesis ceases during ripening.
Hormonal Regulation of Fruit Ripening:
As many as five types of plant hormones are known to regulate fruit ripening. In recent years occurrence of IAA in fruits has been demonstrated beyond doubt. While young seeds are the main site of IAA synthesis, in the mature fruit it is synthesised in the fruit flesh. In fact auxins slow down fruit ripening except in some cases where they may quicken.
Perhaps auxins prevent ethylene formation in fruits. Obviously auxins must be degraded endogenously through series of enzymes like IAA—oxidase, etc. to control fruit ripening. Moment the auxins are degraded the fruit tissue becomes sensitive to ethylene.
Very little is known about the endogenous cytokinin content and its metabolism in fruits. On the basis of their function in the leaves, they possibly contribute in keeping the protein and chlorophyll content constant.
The effect of gibberellins in a way is comparable to auxins and cytokinins. Most studies have been done on oranges where GA inhibits degradation of chlorophyll/and delay carotenoids accumulation. Thus pigment formation is delayed. Similarly banana fruits sprayed with GA do not undergo yellowing even though other processes occur normally.
In large number of fruits, before the ripening is ultimately achieved there is accumulation of ABA (Fig. 25-2). Perhaps this phytohormone regulates fruit ripening. In apples after a week of harvesting ABA content increases many times. ABA concentration is very high in the inner part of the green fruit flesh of tomatoes.
It may be mentioned that tomatoes ripen in a centrifugal direction and as the process progresses the relationship is reversed. Thus in ripened part ABA level falls down. In the following diagram (Fig. 25-3) a relationship between phytochrome, ABA and lycopene content of ripening tomatoes is given.
It will be observed that with the red light illumination of tomatoes, ABA content rises several-fold in first few days and then declines. The present thinking is that ABA triggers lycopene synthesis.
Ethylene is an important hormone concerned with ripening. Fruits fail to ripen in the absence of ethylene. It is shown that ethylene probably brings about the climacteric. Similarly, non-climacteric fruits once treated with ethylene also show increased respiration. Perhaps difference between climacteric and non-climacteric fruits may be due to ethylene production. Ripening can be induced only when auxin is degraded by IAA oxidase, etc.
In view of the reported effect of ethylene in altering the proportion of individual tRNA species, ethylene may be regulating translation of mRNA and thus initiate ripening. In tomatoes, exogenous application by ABA enhances ethylene production.
Whether ABA induces ethylene synthesis in vivo is not clear. Light is also shown to induce ethylene formation. For instance, red light induces ethylene formation while FR slows it. Obviously the phenomena of fruit ripening appear to by a set of highly complex physiological events.
It may be stated that ethylene formation in plants is not exclusively induced by light. It is also produced when a tissue is injured, or diseased or due to physical and chemical stresses. Even action of some metal ions e.g. Cu ++ and Ca ++ causes ethylene formation. Most studies are available in tomato.
In the following scheme a possible relationship between phytochrome and some hormones in fruit ripening has been elucidated:
The above scheme provides tentative relationships between various components though precise relationships between various components though precise relationship of ABA and ethylene is not well understood. There are reports that ethylene causes increase in ABA level and the latter hormone might initiate fruit ripening by stimulating ethylene production.
During ripening there is breakdown of insoluble protopectin into soluble pectic compounds. The process is enzymes mediated. No detailed mechanism of softening is known. During ripening there is shortening of the polymer chain length, demethylation of carboxyl groups and deacetylation of hydroxyl groups.
All these affect cell wall consistency through change in the bonding with associated cell wall constituents e.g., cellulose, hemicellulose.
Most climacteric fruits possess starch as a storage reserve. This is broken down into soluble sugars due to enzymes. Thus fruit attains sweetness.
Loss of Astringency:
In some fruits which are unripe, there is abundance of tannins of low molecular weight (polyphenols) which react with proteins e.g. banana or sapota. When eaten they give astringent taste. With ripening, tannins polymerise into large molecules and lose their capacity to react with protein. Instead they get trapped in the cell.
Sourness of fruits is due to organic acids. The taste is determined by the ratio of sugars and acids. With increased ripening, the total activity decreases. However, in banana, the acids increase on ripening.
Aroma and Flavour:
Ripe fruits have intense aroma and flavour. Aroma is due to the volatile chemical compounds which are enzymatically synthesised and emitted. These volatile compounds are esters and lactones, alcohols, acids, aldehydes, ketones, acetals, phenols, ethers, etc.
Harvesting does not indicate the end of a fruit life. Several of the fruits can be successfully stored up to several weeks by controlling mechanical injury, transpiration, respiration, decay and physiological breakdown. Several physiological and chemical agents are employed to slow down metabolic rates in fruits.
By refrigeration of fruits, storage period is enhanced. It helps in two ways: slowing down respiration due to low temperature and checking microorganisms development. Temperature also influences endogenous ethylene production.
Recently controlled atmosphere (CA) storage is used in collaboration with refrigeration. These processes maintain high quality of fruits. The technique is affectively used in storing apples, citrus, etc. The CA is affected by increasing CO2 in the atmosphere or reducing O2 levels.
Similarly, some fruits are stored under low pressure. It is a new approach in the long-term storage of fruits. In this method, ethylene evolved is removed, and the partial presence of oxygen is lowered. This slows down the ripening.
Studies at the Bhabha Atomic Research Centre, Mumbai have demonstrated the potential of low- dose gamma irradiation for retarding ripening in mango, papaya and banana. Irradiation also increases pigmentation.
Sometimes fruits are dipped in wax emulsions or plastic films. Even treatment with GA retards ripening.
Artificial Fruit Ripening:
Ethylene is currently used commercially to induce ripening in mangoes, tomatoes, banana, and even degreasing citrus fruits. Temperature affects the process of artificial ripening with ethylene. This gas merely removes chlorophyll and unmasks yellow and orange pigments.
In some fruits, there is synthesis of these pigments also. In fruits with pronounced climacteric, 0.1-100 ppm ethylene is effective when applied in the pre-climacteric stage. There are several sources of ethylene (ethrel, CPTA). Sometimes acetylene and carbon monoxide are also used for artificial ripening of bananas and mangoes.
Hot water dip treatment of mangoes enhances ripening and colour development. This also lessens microbial growth. The ripening is independent of maturity of fruit. In order to have characteristic taste, only optimal mature fruits should be artificially ripened.
What are the risks to a mother in carrying identical triplets?
Overall, the metabolic stress to her body of carrying triplets is considerable and as the pregnancy advances, the stress and risks increase.
There is an increased risk of every pregnancy complication including:
- Hypertension and Preeclampsia.
- Placenta Praevia.
- Premature Labour and delivery.
- Ante Partum Haemorrhage.
- Post Partum Haemorrhage.
- Gestational Diabetes.
- Caesarean section delivery is most likely. Because of this there are the associated risks of any abdominal surgery including bleeding, infection, delayed healing and pain.
Average Pregnancy Weight Gain with Triplets
|First Trimester||Second Trimester||Third Trimester||Average Total Weight Gain|
|1.8-2.3 kilos||13+ kilos||5-6.9 kilos||20+ kilos|
NB Any rapid gain or loss of weight is concerning, especially in the third trimester of pregnancy. Monitoring weight is just one way of assessing maternal/foetal well being and should not be considered in isolation of other observations.
Funny Cherry Puns
Need a funny fruit pun or cherry joke to make your family chuckle as you tuck into a cherry-fic slice of cherry pie?
1. What did the cherry say to the cherry pie? I really crust you.
2. Is it bad to swallow a cherry whole? No don't worry, it's just one of the pitfalls of life.
3. What do fruit bowls say when they dress up as a ghost on Halloween? Be cherry afraid!
4. How do berries start off the fruity olympics? They cherry the Olympic torch around the globe.
5. What do fruits look for at a talent show? A berry that can really cherry a tune.
6. What do fruits do when they are really really afraid? They run away as fast as their legs can cherry them.
7. Berries are the most fashionista of the fruits, they can really cherry off the wildest outfits.
8. What do you call a very little cherry? Pit-iful.
9. Why did the cherry go to the good drinks factory? It was cordially invited.
10. What do you call lots of cherries getting together to practice music? A jam session.
11. What happens to a cherry tree when it grows up? It blossoms.
12. What do fruits do when they are avoiding a problem? They cherry their heads in the sand.
13. Why did the cherry blossom tree seem scared when it was trying to make a cherry pie? Because it was baking like a leaf.
14. My friend mashed up some cherries on halloween and said they were blood. I was cherry-fied!
15. What do red berries say during the season they love best? Cherry Christmas and a Happy New Year!
16. Why shouldn't you be too inquisitive with a cherry? Ask no questions tell no pies.
17. Why are cherries unassuming? Because they often get made into humble pie.
18. What did the cherry say when it won its third Olympic gold medal? That's just the cherry on top of a successful career.
19. What do you do when you try to bake a cherry pie for the first time and it doesn't turn out so well? Just wait for the second bite of the cherry.
20. What did one cherry say to the other cherry? If you weren't so tasty we wouldn't be in this jam.
21. Why did I start making a cherry pie? Bake-cause I love it.
22. What do you call a very tall cherry blossom tree in Italy? The leaning flower of Pisa.
23. What does a hippy cherry wear to a festival? A pie dye T-shirt.
24. Why is cherry pie so legendary? Because it is history in the baking.
25. What do you call a cherry that is hard as nails? Tough as old fruits.
26. Why does a little cherry always look up to its parents? It tries to follow in their fruitsteps.
27. What does a cherry say when it delivers bad news? Don't fruit the messenger.
16 This Is Us Quotes to Make you Cherish Family Moments
Every family has a story, a collection of little moments together — heartwarming or heartbreaking — that make that story great. This Is Us is an American television drama series that will make you laugh and cry with its characters and their family’s story.
The storyline follows the life of Kevin, Kate, Randall and their parents. This Is Us juxtaposes moments from the present with events that took place in the past to form a compelling and emotional narrative. The dynamic of the series highlights the fact that the things we learn growing up and the experiences we have affect the way we think, and ultimately define who we become later.
Even though the series shows a lot of daily struggle, family drama and downfalls, it also focuses on themes of tackling problems, love, forgiveness, and building meaningful relationships. This Is Us beautifully shows that life is complicated yet so beautiful at the same time.
That’s the truth. I don’t know what I think we are. I just know that I like the fact that there’s a ‘we’ for us to talk about.
The hardest part about seeing someone you love in pain is not being able to do anything about it, except try not to make it worse.
You deserve it. You deserve the beautiful life you made. You deserve everything.
You got to own your choices, boys. Choose them fully and don’t look back.
Sometimes, in marriage, someone has to be the one to push to make the big moves.
If at some point in your life, you find a way to show somebody else the same kindness that your parents showed you, that’s all the present I’ll need.
— Dr. Nathan Katowski
Now I want you to picture the love of your life. Imagine that you have 30 seconds to win her back. One shot, three sentences. What are those sentences, and who are you saying them to?
When you’re a mom, you get a front row seat to the best show in town: watching your kids grow up.
You find your soul mate, you get married, you stay together until you die. Period.
Sometimes you just got to do the right thing. You got to do the right thing, even if it’s not what you want.
How you present yourself on the outside reflects how you feel on the inside.
Life feels like Pac-Man sometimes. It’s the same game over and over again. Same board. Same ghosts. Sometimes, you get a bunch of cherries but eventually and inevitably, those ghosts catch up with you.
I am thankful for my family. I’m thankful that we’re all safe and there’s no one in the world that I’d rather be too hot or too cold with.
We’re their parents. We do the best we can. But at the end of the day what happens to them, how they turn out, that’s bigger than us.
It’s a helluva lot easier to accept who you are, in all your damaged glory, than to try to be someone you’re not. It’s sure a hell of a lot more fun, too.
And when I make my son laugh, I try to catch the sound of him laughing. How it rolls up from his chest.
Where We Are