DNA2 suppresses recombination-restarted replication and checkpoint activation at stalled forks, and its loss triggers recombination-dependent synthesis, checkpoint signalling and cell-cycle exit, high...

YouTube video by Z Action Media (Zeruel)

DNA2 suppresses recombination-restarted replication and checkpoint activation at stalled forks, and its loss triggers recombination-dependent synthesis, checkpoint signalling and cell-cycle exit, high...

DNA2 suppresses recombination-restarted replication and checkpoint activation at stalled forks, and its loss triggers recombination-dependent synthesis, checkpoint signalling and cell-cycle exit, highlighting its essential role in proliferation and growth failure in primordial dwarfism.

YouTube video by JE END

DNA2 suppresses recombination-restarted replication and checkpoint activation at stalled forks, and its loss triggers recombination-dependent synthesis, checkpoint signalling and cell-cycle exit, high...

Nuclease–helicase DNA2 is a multifunctional genome caretaker that is essential for cell proliferation in a range of organisms, from yeast to human1–4. Bi-allelic DNA2 mutations that reduce DNA2 concentrations cause a spectrum of primordial dwarfism disorders, including Seckel and Rothmund–Thomson-related syndromes5–7. By contrast, cancer cells frequently express high concentrations of DNA2 (refs. 8–11). The mechanism that precludes cell proliferation in the absence of DNA2 and the molecular aetiology of DNA2-linked diseases remain elusive. Here we used yeast and human cells to demonstrate that DNA2 suppresses homologous recombination-restarted replication and checkpoint activation at stalled DNA replication forks. Loss of this control mechanism upon degradation of DNA2 in human cells causes recombination-dependent DNA synthesis and build-up of RPA-bound single-stranded DNA in the G2 phase of the cell cycle. Consequently, DNA2 deprivation triggers the DNA damage checkpoint and invariabl

Abstract. DNA replication faces challenges from DNA lesions originated from endogenous or exogenous sources of stress, leading to the accumulation of singl

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