Since more than hundred years heritance of the genetic information was thought to be autonomously controlled by the germ cells. Therefore, acquired traits cannot be genetically inherited. Instead, mutations occurring only in germ cells are responsible for any heritable genetic changes, be it during evolution or as cause of genetic disorders. The team of Björn Schumacher at the Institute for Genome Stability in Aging and Disease at the CECAD Excellence Cluster of the University of Cologne now challenges that assertion.
The scientists investigated how the genome integrity in primordial germ cells (PGCs) is controlled. PGCs need to survey their genomes particularly rigorously because they give rise to all sperms or eggs of an organism. Studying PGCs in mammals is a complicated endeavor so Schumacher’s team used the nematode Caenorhabditis elegans as a simple animal model for shedding new light onto how PGCs control the integrity of the genomes they will pass on to their offspring.
Strikingly, they uncovered that somatic niche cells that surround the PGCs control their response to DNA damage. PGCs need to arrest their division when their genomes are damaged until the DNA is repaired. However, whether or not they stop generating germ cells depended on signals from the somatic niche cells. These niche cells are in intimate contact with the PGCs and instruct them whether to divide and generated germ cells or whether to stay inactive. When the niche cells fail to signal to the PGCs that they need to first repair before generating germ cells, they might pass on dangerous mutations to the next generation. The somatic control of the integrity of the PGC’s genomes gives the parental body a direct role in controlling the quality of the heritable genetic information. These new insights open new perspectives for understanding inheritance and causes of infertility.
Somatic niche cells regulate the CEP-1/p53-mediated DNA damage response in primordial germ cells.
Ou HL, Kim CS, Uszkoreit S, Wickström SA, Schumacher B
Developmental Cell 50, 1–17, July 22, 2019. doi.org/10.1016/j.devcel.2019.06.012
Prof. Björn Schumacher
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