Scientists describe genetic program behind primordial lung progenitors
In a project recently published by the review Nature Communications, researchers from the University of Seville and the Andalusian Centre of Molecular Biology and Regenerative Medicine (CABIMER) have identified new factors that are necessary for the repair of these breaks. These factors, in contrast with those already known, only affect the repair between sister chromatids of breaks that have arisen during chromosome duplication. Specifically, they are proteins that modify 'histones', which are the basic proteins that form the structure of the chromosomes.
The research group has shown that the inability to repair breaks in cells lacking these proteins derives from a deficient cohesin load. These are the proteins that keep the sister chromatids paired and together until their segregation in meiosis. With the lessening of cohesion between the chromatids, the repair is defective which leave many breaks unrepaired and increases the chromosomal reorganization.
The project carried out on the organism model Saccharomyces has identified new factors involved on the maintenance of genome integrity and a new mechanism with which the cohesin load in the chromosomes can be regulated, which could be of great value for deciphering the multiple mechanisms responsible for genome instability in the tumour cells and different neurodegenerative pathologies. Source:
University of Seville Journal reference:
Ortega, P., et al. (2020) Rpd3L and Hda1 histone deacetylases facilitate repair of broken forks by promoting sister chromatid cohesion. Nature Communications . doi.org/10.1038/s41467-019-13210-5 .
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