Fassberg Seminar - Special Date: How cohesin folds the genome

Fassberg Seminar - Special Date

  • Date: Oct 17, 2018
  • Time: 11:00 - 12:00
  • Speaker: Dr. Jan-Michael Peters
  • IMP, Research Institute of Molecular Pathology / Vienna, Austria
  • Location: Max-Planck-Institut für biophysikalische Chemie (MPIBPC)
  • Room: Ludwig Prandtl Hall, Administration Building
  • Host: Dr. Melina Schuh
  • Contact: tommaso.cavazza@mpibpc.mpg.de
Fassberg Seminar - Special Date: How cohesin folds the genome
Mammalian genomes are large compared to the cells they are contained in, corresponding to 2 meters of DNA in humans and 20 meters in salamanders. At the various stages of the lifetime of a cell these genomes have to be transcribed, replicated, repaired, recombined, condensed and segregated with high speed and precision. For many of these processes it is crucial that the genome is folded correctly. I will present evidence that a key molecule mediating this genome organization is cohesin, a large ring-shaped ATPase complex initially discovered for its essential role in sister chromatid cohesion and chromosome segregation. Our work indicates that in addition to mediating cohesion in proliferating cells, cohesin has a universal role in all cells in forming chromatin loops. Several observations imply that cohesin forms these by a mysterious loop extrusion mechanism. This mechanism enables cohesin to connect distant genomic regions which are specified by the DNA binding protein CTCF. The size and lifetime of these loops are controlled by WAPL, a protein that can release cohesin from DNA and thereby destroy chromatin loops. I will discuss how cohesin might mediate loop extrusion, how this process could control gene expression, and how defects in this process could explain why cohesin subunits are among the most frequently mutated tumor suppressor genes in human cancers.
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