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Publication : POGZ promotes homology-directed DNA repair in an HP1-dependent manner.

First Author  Heath J Year  2022
Journal  EMBO Rep Volume  23
Issue  1 Pages  e51041
PubMed ID  34758190 Mgi Jnum  J:335406
Mgi Id  MGI:7435083 Doi  10.15252/embr.202051041
Citation  Heath J, et al. (2022) POGZ promotes homology-directed DNA repair in an HP1-dependent manner. EMBO Rep 23(1):e51041
abstractText  The heterochromatin protein HP1 plays a central role in the maintenance of genome stability but little is known about how HP1 is controlled. Here, we show that the zinc finger protein POGZ promotes the presence of HP1 at DNA double-strand breaks (DSBs) in human cells. POGZ depletion delays the resolution of DSBs and sensitizes cells to different DNA-damaging agents, including cisplatin and talazoparib. Mechanistically, POGZ promotes homology-directed DNA repair by retaining the BRCA1/BARD1 complex at DSBs in an HP1-dependent manner. In vivo CRISPR inactivation of Pogz is embryonically lethal. Pogz haploinsufficiency (Pogz(+) /delta) results in developmental delay, impaired intellectual abilities, hyperactive behaviour and a compromised humoral immune response in mice, recapitulating the main clinical features of the White Sutton syndrome (WHSUS). Pogz(+) /delta mice are further radiosensitive and accumulate DSBs in diverse tissues, including the spleen and brain. Altogether, our findings identify POGZ as an important player in homology-directed DNA repair both in vitro and in vivo.
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