@AdamMarblestone @s_r_constantin All these clocks are looking at CpG methylation. But.. non-CpG methylation is also a thing, and seems to matter in the brainhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3785061/ …
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Original clocks weren't looking for anything but correlation with age, presumably used CpG because more abundant so easier to measure. I'm about a year out of date but I don't think we are (yet) saying much about the biological effects of these methylation changes.
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The papers I've been looking at are largely correlational; newer clocks are looking at more than age (hazard ratios for mortality is the new thing in GrimAge and PhenoAge). What would be a good way to measure causality here?
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And does methylation editing stay in place? If you take a methyl away, wait a /some week(s) and measure again, will that site look like that of a control mice?
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Cells will override it given stimuli (we don't understand), but w persistent expression of your CRISPR stuff I'd guess you'd have persistent demethylation. NB if you wanted to do this
#InVivo you'd prob want to use a mouse with the Cas9 engineered in, to avoid immune response.1 reply 0 retweets 0 likes -
Cool. And can CRISPR activate or inactivate other genes while you’re at it if you think there is more that needs to happen than methylation changes, to drive the system. A few orthogonal Cas9’s engineered in but many mice getting many different cocktails of gRNAs at embryo stage!
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Replying to @AdamMarblestone @MartinBJensen and
p.s., of course in addition to methylation there are lots of other epigenetic assays like HiC, transcriptome itself, and so on... which could maybe make clocks... maybe an exosome RNA clock...
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Add persistent maintenance of the DNA encoding your gRNAs but make it all drug inducible and you have a hell of a platform for combinatorial i/o for aging
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