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The evolution of human diets led to preferences toward polyunsaturated fatty acid (PUFA) content with ‘Western’ diets enriched in ω-6 PUFAs. Mounting evidence points to ω-6 PUFA excess limiting metabolic and cognitive processes that define longevity in humans. When chosen during pregnancy, ω-6 PUFA-enriched ‘Western’ diets can reprogram maternal bodily metabolism with maternal nutrient supply precipitating the body-wide imprinting of molecular and cellular adaptations at the level of long-range intercellular signaling networks in the unborn fetus. Even though unfavorable neurological outcomes are amongst the most common complications of intrauterine ω-6 PUFA excess, cellular underpinnings of life-long modifications to brain architecture remain unknown. Here, we show that nutritional ω-6 PUFA-derived endocannabinoids desensitize CB1 cannabinoid receptors, thus inducing epigenetic repression of transcriptional regulatory networks controlling neuronal differentiation. We found that cortical neurons lose their positional identity and axonal selectivity when mouse fetuses are exposed to excess ω-6 PUFAs in utero. Conversion of ω-6 PUFAs into endocannabinoids disrupted the temporal precision of signaling at neuronal CB1 cannabinoid receptors, chiefly deregulating Stat3-dependent transcriptional cascades otherwise required to execute neuronal differentiation programs. Global proteomics identified the immunoglobulin family of cell adhesion molecules (IgCAMs) as direct substrates, with DNA methylation and chromatin accessibility profiling uncovering epigenetic reprogramming at 1400 sites in neurons after prolonged cannabinoid exposure. We found anxiety and depression-like behavioral traits to manifest in adult offspring, which is consistent with genetic models of reduced IgCAM expression, to suggest causality for cortical wiring defects. Overall, our data uncover a regulatory mechanism whose disruption by maternal food choices could limit an offspring’s brain function for life.


  • Immediate Communication
  • Published: 18 November 2019

SOME Geneticists scare the hell out of me??? AEWR.


Will we one day combine tardigrade DNA with our cells to go to Mars?

Chris Mason, a geneticist and associate professor of physiology and biophysics at Weill Cornell University in New York, has investigated the genetic effects of spaceflight and how humans might overcome these challenges to expand our species farther into the solar system. One of the (strangest) ways that we might protect future astronauts on missions to places like Mars, Mason said, might involve the DNA of tardigrades, tiny micro-animals that can survive the most extreme conditions, even the vacuum of space!

CRISPR, the revolutionary ability to snip out and alter genes with scissor-like precision, has exploded in popularity over the last few years and is generally seen as the standalone wizard of modern gene-editing. However, it’s not a perfect system, sometimes cutting at the wrong place, not working as intended and leaving scientists scratching their heads. Well, now there’s a new, more exacting upgrade to CRISPR called Prime, with the ability to, in theory, snip out more than 90% of all genetic diseases.

Just what is this new method and how does it work? We turned to IEEE fellow, biomedical researcher and dean of graduate education at Tuft University’s school of engineering Karen Panetta for an explanation.

When an undiagnosed rare genetic disease caused his young son’s kidneys to fail, Professor Chris Toumazou vowed to find a way of uncovering hidden health risks.

The professor of biomedical engineering realised that, although his son’s condition could not have been prevented, the family could have managed his lifestyle very differently had they known about his condition.

So, he embarked on a mission to help people change their lifestyles and avoid getting sick.

Researchers from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, Institute of Molecular and Clinical Ophthalmology Basel, and ETH Zurich, Switzerland, have presented new insights into the development of the human brain and differences in this process compared to other great apes. The study reveals features of brain development that are unique to humans, and outlines how these processes have diverged from those in other primates.

Since humans diverged from a common ancestor shared with chimpanzees and the other great apes, the has changed dramatically. However, the genetic and developmental processes responsible for this divergence are not understood. Cerebral organoids (brain-like tissues), grown from stem cells in a dish, offer the possibility to study the evolution of early brain development in the laboratory.

Sabina Kanton, Michael James Boyle and Zhisong He, co-first authors of the study, together with Gray Camp, Barbara Treutlein and colleagues analyzed human through their development from to explore the dynamics of gene expression and regulation using methods called single-cell RNA-seq and ATAC-seq. The authors also examined chimpanzee and macaque cerebral organoids to understand how organoid development differs in humans.