#methylation

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Carl Linnaeus was the first to describe a naturally occurring mutant of toadflax (Linaria vulgaris) that converted the bilaterally symmetrical flower to a radially symmetrical form (Figure 20.31).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

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Methylation

Methylation risk variant results MTHFR, CBS, COMT, MTR and MTRR I had a DNA test done through ancestry. I sent the results to Life DNA and got some information. They had an offer on methylation genes so I had that analyzed. Out of 10 genes, 7 had risk variants. The variants are not unusual. Some of them lead to an increase in homocysteine which when increased can be a heart attack risk.  I …

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Life Support

Getting from fertilised egg to viable embryo is a labour-intensive process with endless logistics and huge energy demands. Oocytes, or egg cells, completely rely on a part of the cell called mitochondria for ATP – their source of energy. To keep up with energy demands, the number of mitochondria in an oocyte needs to boom from 1,000 to 300,000 through a process called mitochondrial fission – splitting into two. This splitting is driven by a protein called DRP1, but how DRP1 and fission affect embryo development was unclear. Deleting DRP1 from mouse oocytes meant that crucial genes that kickstart development couldn’t be switched on. The switches in the form of methylation marks (shown in green and magenta) are lost from the DNA without DRP1, and so the embryos cannot survive. Together, this shows how important the mitochondria are to the early stages of embryo development and survival.

Written by Sophie Arthur

Image from work by Deepak Adhikari and colleagues

Development and Stem Cell Program and Department of Anatomy and Developmental Biology, Monash Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Science Advances, June 2022

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How does the 2 m DNA fit into a nucleus of 10-15 μm diameter? The answer lies in DNA packaging.

To better understand the chromatin compaction levels, read our new infodump!

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https://sites.google.com/view/bobthebiotechquer/molecular-biology/dna-packaging

B&B - DNA Packaging

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Anyone else have a MTHFR mutation and joint pain?

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Abstract

Background

Age-associated epigenetic changes are implicated in aging. Notably, age-associated DNA methylation changes comprise a so-called aging “clock”, a robust biomarker of aging. However, while genetic, dietary and drug interventions can extend lifespan, their impact on the epigenome is uncharacterised. To fill this knowledge gap, we defined age-associated DNA methylation changes at the whole-genome, single-nucleotide level in mouse liver and tested the impact of longevity-promoting interventions, specifically the Ames dwarf Prop1 df/df mutation, calorie restriction and rapamycin.

Results

In wild-type mice fed an unsupplemented ad libitum diet, age-associated hypomethylation was enriched at super-enhancers in highly expressed genes critical for liver function. Genes harbouring hypomethylated enhancers were enriched for genes that change expression with age. Hypermethylation was enriched at CpG islands marked with bivalent activating and repressing histone modifications and resembled hypermethylation in liver cancer. Age-associated methylation changes are suppressed in Ames dwarf and calorie restricted mice and more selectively and less specifically in rapamycin treated mice.

Conclusions

Age-associated hypo- and hypermethylation events occur at distinct regulatory features of the genome. Distinct longevity-promoting interventions, specifically genetic, dietary and drug interventions, suppress some age-associated methylation changes, consistent with the idea that these interventions exert their beneficial effects, in part, by modulation of the epigenome. This study is a foundation to understand the epigenetic contribution to healthy aging and longevity and the molecular basis of the DNA methylation clock.

[didanawisgi]

Abstract

Lifestyle factors, such as food choices and exposure to chemicals, can alter DNA methylation and lead to changes in gene activity. Two such exposures with pharmacologically active components are coffee and tea consumption. Both coffee and tea has been suggested to play an important role in modulating disease-risk in humans by suppressing tumour progression, decreasing inflammation and influencing estrogen metabolism. These mechanisms may be mediated by changes in DNA methylation.

To investigate if DNA methylation in blood is associated with coffee and tea consumption we performed a genome-wide DNA methylation study for coffee and tea consumption in four European cohorts (N = 3,096). DNA methylation was measured from whole blood at 421,695 CpG sites distributed throughout the genome and analysed in men and women both separately and together in each cohort. Meta-analyses of the results and additional regional-level analyses were performed.

After adjusting for multiple testing, the meta-analysis revealed that two individual CpG-sites, mapping to DNAJC16 and TTC17, were differentially methylated in relation to tea consumption in women. No individual sites were associated in men or in the sex-combined analysis for tea or coffee. The regional analysis revealed that 28 regions were differentially methylated in relation to tea consumption in women. These regions contained genes known to interact with estradiol metabolism and cancer. No significant regions were found in the sex-combined and male-only analysis for either tea or coffee consumption.