Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release
| Autor: | Keiji Miyata, Kouji Hirota, Ivan Psakhye, Dana Branzei, Takuya Abe, Ryotaro Kawasumi |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0303 health sciences
biology Cohesin Chromosomal Proteins Non-Histone Mutant Helicase Cell Cycle Proteins Chromatids Cell biology Proliferating cell nuclear antigen Establishment of sister chromatid cohesion 03 medical and health sciences 0302 clinical medicine DDX11 Vertebrates Centromere Genetics biology.protein Animals biological phenomena cell phenomena and immunity 030217 neurology & neurosurgery 030304 developmental biology Developmental Biology Anaphase |
| Zdroj: | Genes & Development. 35:1368-1382 |
| ISSN: | 1549-5477 0890-9369 |
| DOI: | 10.1101/gad.348581.121 |
| Popis: | The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the lethality and cohesion defects of ctf18 ddx11 mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels of ESCO1/2 acetyltransferases that acetylate cohesin to establish SCC do not rescue ctf18 ddx11 phenotypes. Notably, the tight proximity of sister centromeres and increased anaphase bridges characteristic of WAPL-depleted cells are abrogated by loss of both CTF18 and DDX11. The results reveal that vertebrate CTF18 and DDX11 collaborate to provide sufficient amounts of chromatin-loaded cohesin available for SCC generation in the presence of WAPL-mediated cohesin-unloading activity. This process modulates chromosome structure and is essential for cellular proliferation in vertebrates. |
| Databáze: | OpenAIRE |
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