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- W2054599502 startingPage "e1004471" @default.
- W2054599502 abstract "Genome maintenance in germ cells is critical for fertility and the stable propagation of species. While mechanisms of meiotic DNA repair and chromosome behavior are well-characterized, the same is not true for primordial germ cells (PGCs), which arise and propagate during very early stages of mammalian development. Fanconi anemia (FA), a genomic instability syndrome that includes hypogonadism and testicular failure phenotypes, is caused by mutations in genes encoding a complex of proteins involved in repair of DNA lesions associated with DNA replication. The signaling mechanisms underlying hypogonadism and testicular failure in FA patients or mouse models are unknown. We conducted genetic studies to show that hypogonadism of Fancm mutant mice is a result of reduced proliferation, but not apoptosis, of PGCs, resulting in reduced germ cells in neonates of both sexes. Progressive loss of germ cells in adult males also occurs, overlaid with an elevated level of meiotic DNA damage. Genetic studies indicated that ATM-p53-p21 signaling is partially responsible for the germ cell deficiency." @default.
- W2054599502 created "2016-06-24" @default.
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- W2054599502 date "2014-07-10" @default.
- W2054599502 modified "2023-10-18" @default.
- W2054599502 title "Hypersensitivity of Primordial Germ Cells to Compromised Replication-Associated DNA Repair Involves ATM-p53-p21 Signaling" @default.
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- W2054599502 doi "https://doi.org/10.1371/journal.pgen.1004471" @default.
- W2054599502 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4091704" @default.
- W2054599502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25010009" @default.
- W2054599502 hasPublicationYear "2014" @default.
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