Classical quantitative genetics has long attributed phenotypic variation to individual effects and the interaction between heredity and environment:
V= G + E + GxE
V: phenotypic variance, phenotypic variance, g: genetic variance, genetic variance, e: environmental variance, environmental variables.
GxE here, that is, the interaction between heredity and environment, is a study of the effects of many external environments on methylation levels, and it has long been a part of classical genetics, not epigenetics.
Aside from environmental factors, genetic variables can be summed up in several parts:
G = A+D+epistasis
A: additive genetic variance, additive genetic effect, D: dominance,' dominant genetic effect'? Epistasis: gene-gene interaction, epistasis effect, or gene interaction.
The epistasis and gene interaction here, including the so-called transcription factors and the regulation between miRNA, lincRNA and non-coding RNA, are not epigenetics.
However, these non-epigenetic phenomena that jump out of Mendelian genetic model, such as D+ epistatic additive inheritance, can also be called non-Mendelian inheritance. Moreover, non-Mendelian genetic models are also of great research value, such as the various regulatory factors at the transcription level that are popular at present, so I won't go into details here.
Epigenetics in the true sense can only be considered as a breakthrough if it jumps out of the framework of the above classical genetics.
As far as the whole biological population is concerned, the influence of epigenetics on individuals is not significant compared with heredity, but its influence on a certain character of some organisms can still exceed genetic factors. Among them, there are still many breakthroughs in the study of hereditary epigenetic model. Comments can read this article:
Cross-representational inheritance: prevalence, mechanism and significance to genetic and evolutionary research.
Classical genetic experiment of mouse transmission: offspring inherit father's fear memory, natural neuroscience;
Terrible memories haunt mouse offspring: natural news and. comment
Because I am a large animal, in the category of large animals, typical epigenetic examples are: beautiful butted sheep, super polar advantage, polar advantage in sheep callipygelocus.
Sheep with this mutation will form a plump ass, and this mutation will only reflect this phenotype in the mutant heterozygote inherited from their father, and this phenotype will not be expressed until one year after the offspring are born, and it will only be expressed in the ass muscle group, and the muscles in the first half of the body, including shoulders and chest, have not changed. The formation mechanism is the interaction between imprinted genes and non-coding RNA, and the interaction between genes and the regional environment of DLK 1-DIO3 locus. There are many research papers on this example, and the latest progress can be seen here: a new view on the polar dominance of callipyge sheep.
Generally speaking, if you want to make great discoveries in the field of epigenetics, it is very important to find suitable traits for research, or luck is very important. . . . Because most normal or disease traits are derived from the interaction between classical heredity and environment, there are few truly pure epigenetic or epigenetic-dominated traits.
Author: Zhihu users.
Link:/question/26512948/answer/33398775
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You have talked a lot about the concept of epigenetics.
@Lucif X
The answer is particularly comprehensive. In fact, although the concept of epigenetics is very broad, scientists who do small RNA, DNA modification and post-translation modification are willing to put their research direction into the category of epigenetics, but there is no doubt that the most attractive aspect of epigenetics is acquired inheritance (Lamarckian inheritance), and its external manifestation is intergenerational inheritance.
Just in July this year, Cell magazine published an article, which is a classic combination of biological experiments and deep sequencing analysis. Taking Caenorhabditis elegans as a model organism, the intergenerational genetic mechanism caused by environmental change (hunger) was studied.
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As can be seen from this schematic diagram, in P0 generation, the experimental nematodes were divided into two groups, one group was fed with enough food continuously, the other group was fed with hunger stimulation in the larval stage, and its offspring were fed with enough food on average. As a result, the Theory of Three Represents of the nematodes fed by starvation was significantly longer than that of the other group.
So why is there such an experimental result?
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Source: transnational inheritance of hunger-induced small RNA in nematodes: cells.
By sequencing the transcriptome of P0 generation and F3 generation, the researchers found that starvation can induce the expression of some small RNAs, and the target genes of these small RNAs are generally related to nutritional metabolism. These small RNAs can be atavism (the author guessed that the changes of these small RNAs also occur in germ cells), and then F3 generation can still regulate the genes related to nutritional metabolism like nematodes stimulated by P0 generation.
At this point in the story, you will definitely think that dieting can prolong the life span of mammals. I don't know if the same mechanism exists in mice or primates. In a word, this study provides a new way for us to understand intergenerational inheritance.
Author: Zhihu users.
Link:/question/26512948/answer/33094137.
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The core of epigenetics research is to try to answer: the regulation method of genetic information transfer from genome to transcriptome in the central law.
The basis of modern genetics is the controllable expression of genes to realize the differentiation and proliferation of cells, and then realize the growth and development of organisms. As we all know, genome genes are written on 23 sets of chromosomes, and the genome genes of all cells in an organism are almost the same, so the question is: How can the same genome create different cell types?
At the level of molecular biology, gene expression is regulated by a class of protein called transcription factors. Each type of transcription factor has a specific set of regulatory genes in each cell; The combination of transcription factors and genomic DNA will activate/inhibit the transcription expression of this group of genes. However, one chemical phenomenon that affects the binding is methylation and acetylation.
Methylation and acetylation occur in several different regions: (1) transcription factor itself; (2) histone (chromatin) that helps to wrap chromosomes; (3) The region in the gene sequence for binding transcription factors is called a promoter. Methylation or acetylation of these sites will greatly affect the expression of each gene. It is the specificity of these modification sites that determines that different cell types have relatively different transcriptome, and then show relatively different cell functions.
Of course, since it is chemical modification, the modification process will naturally be affected by external factors. Some factors can activate/inhibit specific signal pathways in cells, thus reversibly/irreversibly changing the methylation and acetylation levels of some genes. If these changes are written into germ cells, some of them may be passed on to the next generation. These "external causes" are not only related to eating and drinking Lazarus, but also related to mental trauma and psychological stress. Of course, these studies are still in a relatively vague state.
The above is a basic science of epigenetics. I haven't read textbooks for many years. Please correct me if there are any mistakes.