BIONEWS
A Nature Genetics study finds the chromatin marks that turn genes on have barely changed since the last common ancestor of complex life, while the marks that silence genes have been rewritten again and again.
Every cell in your body carries the same DNA. A liver cell reads liver genes; a neuron reads neuron genes. The mechanism that decides which genes a cell actually uses predates the split between animals, plants, and fungi, and a new Nature Genetics study shows it has barely changed in roughly two billion years. The mechanism that tells a cell to ignore a gene has been reinvented in nearly every major branch of complex life.
DNA does not float loose inside a cell. It wraps around spool-like proteins called histones, and small chemical tags on those histones tell the cell which stretches of DNA to read out as genes and which to leave alone. The whole packaging-and-tagging system is called chromatin, and the tags are histone post-translational modifications, or hPTMs. Different hPTMs correspond to different instructions: some mark a gene as "on," others mark it as "off," and cells maintain those marks through cell division so a liver cell stays a liver cell.
A team led by Arnau Sebé-Pedrós at the Centre for Genomic Regulation in Barcelona asked which of those marks are ancient and which are recent inventions. To answer it, they had to look at branches of life that almost no chromatin study has profiled before.
The last common ancestor of all complex cellular life, LECA, lived roughly two billion years ago. After LECA, life split into the ancestors of animals, plants, and fungi and into a series of deeply branching single-celled relatives that have been largely invisible to genome-regulation studies. Sebé-Pedrós's group profiled chromatin in four of those branches: discobans and rhizarians, which include amoebae and other free-living single cells; ichthyosporeans, close cousins of animals; and cryptomonads, a group of single-celled algae.
Phys.org and News-Medical summarize the same finding. Gene-activation marks, the chemical tags that tell a cell to read a gene, are conserved across all of these branches. The marks that tell a cell to ignore a gene are not. Each lineage has built its own silencing machinery, often more than once.
That asymmetry has practical consequences. Faults in chromatin regulation show up across a wide range of human diseases, including cancers, where the silencing machinery often fails to keep transposons, or jumping pieces of DNA that can damage the genome if left active, quiet, or where tumor-suppressor genes get locked into the "off" state. If silencing is the moving target, that helps explain why "chromatin dysregulation" shows up across so many different diseases.
The CRG team built a new ChIP-seq pipeline to make this kind of cross-species comparison tractable, and the underlying data is now public in NCBI GEO under accessions GSE329959 and GSE329952. The Sebé-Pedrós Lab describes the work as part of a broader effort to characterize eukaryotic life at the molecular level, the same kind of inventory that projects like the Earth BioGenome Project aim to build for genomes as a whole. The next step is to push the same map deeper into under-sampled branches of the tree of life, so other groups can run the same comparison on species that have not yet been profiled.