Two New FASD Papers

The journal Epigenetics & Chromatin just put out two interesting new papers about the epigenetics of FASD. The first is by Veazey et al. They found significant alterations to histone mods (H3K9me2, H3K9ac, and H3K27me3) at days 7 and 17 that are dose dependent and correlate to severity of phenotype. They also found changes to homeobox and histone genes, two things we saw in our own earlier mouse model but had not pursued. They also noticed that in this model, the profiles were different after a 4 day recovery period, something we’ve also seen when examining the short and long term transcriptional changes across a wider window but have not examined at the epigenetic level. Another similarity was that the chromatin mods don’t usually line up with current transcription, which is also in line with our developmental footprint idea. This observation was also complemented by finding altered transcription in a number of epigenetic writers. I also imagine some of the differences between models here relate to stem cell models and ontogeny.

The second paper is by Zhang et al. and deals with the discovery of a glutamate transporter that shows age and sex dependent alterations to expression. The transcriptional increase appears to be driven by decreased DNA methylation and an increase in activating H3K4me3. Also of interest was that while the mRNA levels were increased the protein levels were decreased, which appears to be an increase in an imprinted miRNA, from a cluster we’ve previously identified, which was functionally confirmed to bind. Interestingly, there was also a correlation between this miRNA in the brain and levels of it in the serum. While it is a mouse specific cluster, it hints that the other clusters shared with humans may leave the same clues.

In terms of caveats, both papers have a bit of a bias in that they were not scanning the genome but rather pre-picked players, but that is also just my omic bias talking. Overall, these papers continue to provide evidence for the consensus idea that FASD is in part maintained by an initial alteration combined with recovery response that may one day be narrowed down to certain drivers of phenotype. The targets arising from these groups, and our own, would make excellent candidates for epigenome editing, which we just published a review on in the very same journal.


Transgenerational Memories

Transgenerational Memories

An interesting piece by the NPG

I wonder just what proportion of memory and experience ends up travelling through our genomes.

David Sweatt comments “The overwhelming response has been ‘Wow! But how the hell is it happening?'” 

You can find the articles and commentary on Pubmed

Coding and Regulatory reading frames in the same sequence?!

Coding and Regulatory reading frames in the same sequence?!

It turns out that some genes have regulatory and protein codon (genetic sequence) reading frames written in the same sequence, with mutations capable of affecting both protein regulation and function separately and yet together.

Human Adult Hippocampal Neurogenesis?!

Human Adult Hippocampal Neurogenesis?!


  • Nuclear-bomb-test-derived 14C in human hippocampal neurons reveals adult neurogenesis
  • One-third of hippocampal neurons are subject to exchange
  • The annual turnover rate is 1.75% within the renewing fraction in adult humans
  • The extent of adult neurogenesis is comparable in middle-aged humans and mice


Adult-born hippocampal neurons are important for cognitive plasticity in rodents. There is evidence for hippocampal neurogenesis in adult humans, although whether its extent is sufficient to have functional significance has been questioned. We have assessed the generation of hippocampal cells in humans by measuring the concentration of nuclear-bomb-test-derived 14C in genomic DNA, and we present an integrated model of the cell turnover dynamics. We found that a large subpopulation of hippocampal neurons constituting one-third of the neurons is subject to exchange. In adult humans, 700 new neurons are added in each hippocampus per day, corresponding to an annual turnover of 1.75% of the neurons within the renewing fraction, with a modest decline during aging. We conclude that neurons are generated throughout adulthood and that the rates are comparable in middle-aged humans and mice, suggesting that adult hippocampal neurogenesis may contribute to human brain function.”

US Supreme Court: Human Genetic Material Can’t Be Patented

Big news from the east side of Capitol Hill: It’s not okay to patent genetic material taken from the human body. Or at least, it’s not okay in the eyes of the nation’s highest court. SCOTUS took on the controversial and somewhat futuristic case earlier this year, and with all the torrid discussion about updating all patent laws, everyone knew that this decision would be a landmark one.

US Supreme Court: Human Genetic Material Can’t Be Patented