Epigenetics: Episode. 3
Information about the inactivity of X chromosomes is mainly found in living and cells. In January, arrangements are made for the restoration of structural chromosomes. Many parts of the X chromosome are missing in many such investigations. Depending on which part was missing, the chromosome was either inactive or had no air at all. In other investigations, no part of the X chromosome was isolated but another was linked to the autosome. What part of an X chromosome was transferred to it, this autosome has inactive documents.
These experiments showed that there is a special part on the X chromosome that is important for inactivity. This section was named X-In Activation Center. In 1991, a group from the Hunt World Lab at Stanford University in California discovered that the X-in activation center contained a gene called Xist. This gene is expressed only by the inactive X chromosome instead of the active X chromosome. Because the gene showed only one X chromosome, it made him the best candidate to control the inactivity of the X chromosome, when two identical chromosomes were behaving differently.
Attempts were made to identify the V protein made from this gene. But in 1992 something strange happened. Transcripts of the Xist gene were used to make RNA copies. The processing of this RNA was similar to that of other RNAs. Supplying means that some genes were cut and different structures were attached to each part of the transcript to increase its strength. So far, so good. But before the RNA can encode the protein, it has to go into the cytoplasm outside the nucleus A. This is because ribosomes called protein factories and amino acids that bind to the chain of proteins are only present in the cytoplasm. But Xist RNA never went beyond the nucleus. This means it will never make protein.
This explains at least one thing that has puzzled scientists since the discovery of the Xist gene. Xist RNA is a long molecule consisting of 1720 pairs. The codon of three twenty pairs is an amino acid code as we have seen before. Therefore, in theory, seventeen hundred and twenty pairs of Xist RNA are capable of coding about five thousand seven hundred amino acids. But when scientists examined this RNA, they did not understand any reason why this RNA could encode such a long chain. Xist had stop codons (signaling the elimination of proteins) in places and the longest part without any stop codons. It consisted of 894 base pairs, or 298 amino acids. How can there be a gene that makes a transcript of 17kb but uses only 5% of it to encode protein? This would be a huge misuse of energy.
But because Xist did not go beyond the nucleus, its low protein coding capacity is irrelevant. This RNA does not act as a messenger RNA that carries the code for the protein. This is a type of RNA called non-coding RNA ncRNA. Xist doesn’t code for proteins, but that doesn’t mean it doesn’t work. Rather, the Xist itself is a functional molecule and plays a key role in the inactivation of the X chromosome.
Non-coding RNA was a new discovery in 1992 and only one more type existed. Even today, there is something extraordinary about Xist. Not because it does not go beyond the nucleus, but because it does not go beyond the chromosome that makes it. When ES cells begin to become specific, only one chromosome, Xist, forms RNA. This is the chromosome that is inactive. Xist does not separate from this chromosome but begins to spread on it.
Let’s go back to our example of DNA code as a script. This time we will assume that the script is written on the wall. This could be a poem or a speech written in the classroom. At the beginning of the summer holidays, the school is converted into residential apartments.
People come and paint over the script. There are no poems or speeches for the residents to read, but the script is still there, but only hidden from our view.
When Xist attaches to the chromosome that made it, it takes the form of an embedded epigenetic paralysis. It is embedded in more and more genes and turns them off. Initially, it acts as a barrier between the genes and the enzymes that convert them into messenger RNA. But as the inactivity of the X chromosome stabilizes, this chromosome changes every single one of these genetic modifications. The histone modifications that normally turn on genes are removed. They are replaced by a reproductive histone modification that turns off the genes.
Some normal histone proteins are taken down altogether. Houston H2A is replaced by a slightly different macro H2A. DNA methylation is used on gene promoters, which is an effective way to turn off genes.
All of these changes result from the binding of repressor molecules to the chromosomes and the DNA is covered in such a way that the enzymes that transcribe the genes do not have access to it. The DNA twists strongly as the two ends of a wet towel are twisted. As a result, the entire chromosome reaches the edge of the nucleus. By this stage, all X chromosomes have become inactive, except for Xist, which is like a small oasis of activity in the middle of the transcription desert.
Whenever a cell divides, the X chromosome copies every existing modification to the new cell, thus remaining inactive in all X cell cells.
Although the effects of Xist are amazing, some of the questions in the description above are still unanswered. Who controls the expression of Xist? Why does it turn on when ES cells become specific? Is Xist only functional in the cells of the substance or can it also be active in men ?.
(to be continued)