Genome complexity: epigenetic marker patterns (Introduction)

by David Turell , Wednesday, October 20, 2021, 15:29 (920 days ago) @ David Turell

A new huge survey in mammals:

https://www.science.org/content/article/chemical-switches-genes-may-help-explain-why-la...

"When it comes to how long a mammal can live, a bigger body is usually better: The typical mouse life span is less than 4 years, whereas a bowhead whale may make it to 211. But within a species, this relationship can flip: Large dog breeds tend to have shorter life spans than smaller canines.

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"The analysis looked at a DNA modification called methylation, which can control whether genes are turned on or off. The patterns of methylation the team found add a new layer of information to better understood differences in the DNA sequences of genes themselves, the authors say. “It’s kind of a gold mine for people who either want to study what is unique about a certain species or conversely what is shared,” says aging researcher Steve Horvath of the University of California,

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"In DNA methylation, a molecule called a methyl group attaches to a base, usually cytosine. Horvath is known for showing that patterns of these methyl groups change as a person ages, and for creating an “epigenetic clock” that uses a DNA sample to estimate a person’s age within 3.6 years.

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"They used the data to devise an epigenetic clock that can be used to estimate the age of any living mammal from a DNA sample. This clock turned up some new genes that may govern aging, first author Ake Lu reports in a poster at the ASHG meeting this week and a January preprint.

"The consortium also wondered whether other individual or species-specific traits could be tied to DNA methylation. To explore this, computational biologist Amin Haghani, a postdoc in Horvath’s lab, first simply looked for methylation patterns. He found 55 clusters of methylated cytosines—between 33 and 1864 sites per cluster—many of which turned out to correlate with species-specific traits such as maximum life span, average adult weight, and age at sexual maturity. And others matched up with individual traits, such as age, sex, and tissue type.

"The team also showed, in work reported in a poster and a March preprint, that evolutionary trees constructed using cytosine methylation largely mirror phylogenies based on their gene sequences. “This is really interesting because it shows our DNA methylation is tracking evolution,” Haghani says.

"The genes switched on or off by the methylated bases near them may help control that trait—for example, the life span methylation cluster may govern stem cell genes important early in development, the team proposes. “Chances are, these cytosine sites are part of pathways or cell types that are important,” Horvath says.

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"Not all epigenetics researchers are surprised by the consortium’s findings. It’s logical that methylation patterns track with evolution because the process itself is controlled by genes with evolving sequences, says plant epigenomics researcher Frank Johannes of the Technical University of Munich. Horvath’s trees are “a molecular readout … of genetic diversity,” says Johannes, who notes that similar “phyloepigenetic” trees were constructed for plants 10 years ago. Still, he says, the new study offers “a large resource for comparative epigenomics.'”

Comment: makes lots of sense seeing this stronger view of epigenetics as mixed up in making evolution proceed. Lamarck is now reasonable. Perhaps methyl groups are God's controls?