Matches in SemOpenAlex for { <https://semopenalex.org/work/W3104602535> ?p ?o ?g. }
- W3104602535 abstract "Mutations of SMC5/6 components cause developmental defects, including primary microcephaly. To model neurodevelopmental defects, we engineered a mouse wherein Smc5 is conditionally knocked out (cKO) in the developing neocortex. Smc5 cKO mice exhibited neurodevelopmental defects due to neural progenitor cell (NPC) apoptosis, which led to reduction in cortical layer neurons. Smc5 cKO NPCs formed DNA bridges during mitosis and underwent chromosome missegregation. SMC5/6 depletion triggers a CHEK2-p53 DNA damage response, as concomitant deletion of the Trp53 tumor suppressor or Chek2 DNA damage checkpoint kinase rescued Smc5 cKO neurodevelopmental defects. Further assessment using Smc5 cKO and auxin-inducible degron systems demonstrated that absence of SMC5/6 leads to DNA replication stress at late-replicating regions such as pericentromeric heterochromatin. In summary, SMC5/6 is important for completion of DNA replication prior to entering mitosis, which ensures accurate chromosome segregation. Thus, SMC5/6 functions are critical in highly proliferative stem cells during organism development." @default.
- W3104602535 created "2020-11-23" @default.
- W3104602535 creator A5000691809 @default.
- W3104602535 creator A5001893379 @default.
- W3104602535 creator A5033734741 @default.
- W3104602535 creator A5042422038 @default.
- W3104602535 creator A5046824782 @default.
- W3104602535 creator A5066046575 @default.
- W3104602535 date "2020-11-17" @default.
- W3104602535 modified "2023-10-16" @default.
- W3104602535 title "SMC5/6 is required for replication fork stability and faithful chromosome segregation during neurogenesis" @default.
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