The molecular mechanism by which life responds to unseeded mutations in genes has been cracked

has evolved many ways to deal with genetic mutations, one of which is the "genetic compensation effect". However, little has long been known in the scientific community about the molecular mechanisms by which the effects of genetic compensation work.
April 4, Nature reported online on important research advances in the molecular mechanism of genetic compensation effects by Professors Chen Jun and Peng Jinrong of Zhejiang University. For the first time, the team revealed that the gene compensation effect was triggered by messenger RNA (mRNA) carrying an early termination cryptic device, involving the upstream transfer protein 3a (Upf3a) in the senseless mutation mRNA degradation pathway (NMD). At the same time, it is revealed that phosgenic sequence nucleic acid is a necessary condition to raise the compensation effect gene, and further research proves that the increase of the transvestitive level of the compensatory effect gene is caused by the exogenous genetic modification of the compensatory gene promoter region histogenesis. This study provides new ideas for the treatment of diseases.
In 2015, Peng Jinrong's lab found that Capn3a, a calcium-adjusted protease (Capn3a) that affects the liver development of zebrafish, had a small liver ideopaedic when the gene was lowered in different ways, while the liver, a genetic mutation, developed normally. "Knocking out mutants to grow a normal liver suggests that the genetic compensation effect may be at work." Ma Zhipeng, the first author of the paper, speculated.
Since then, Chen Jun's team has continued to conduct a large number of comparative experiments on zebrafish, and by constructing different mutants of the calcitonin protease gene, it has been found that only unyielding mutations can activate the genetic compensation effect, and by improving the expression of family genes of the same origin as the mutated gene sequence.
It is interesting that by importing exogenetic DNA into zebrafish, they can also activate the genetic compensation effect in the body, i.e., the genetically modified imported genetically modified organisms with senseless mutations and idroid sequences can improve gene expression with ogenosces in the body. These experiments prove that unsymic mutations and esothogeneic sequences are two prerequisites for genetic compensation effects.
Based on the existing NMD pathway, Chen Jun's team took a different approach, knocking out Upf3a, capn3a mutant liver bes smaller, compensating for the same gene expression also decreased, the genetic compensation effect disappeared. Therefore, it is concluded that the body should deal with the unsymicated mutation, in which Upf3a is an important "intermediary" to induce the effect of genetic compensation.
genetic compensation effect is not unique to zebrafish, but also in mice, athropomorthic mustard and other model organisms. This is an extraordinary story with potentially wide-ranging significance, according to experts reviewing the journal Nature. As the authors point out, the introduction of unsympathetic mutations may be a clinical way to treat genetic diseases that exist that compensate for the existence of genes. (Source: Cui Xueqin Xinyu, China Science Daily)
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