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• W4366996323 startingPage "e0282277" @default.
• W4366996323 abstract "The MRE11A-RAD50-NBS1 complex activates the ataxia-telangiectasia mutated (ATM) pathway and plays a central role in genome homeostasis. The association of RAD50 mutations with disease remains unclear; hence, we adopted a medaka rad50 mutant to demonstrate the significance of RAD50 mutation in pathogenesis using the medaka as an experimental animal. A 2-base pair deletion in the rad50 gene was introduced into transparent STIII medaka using the CRISPR/Cas9 system. The mutant was analyzed histologically for tumorigenicity and hindbrain quality, as well as for swimming behavior, to compare with existing ATM -, MRE11A -, and NBS1 -mutation-related pathology. Our results revealed that the medaka rad50 mutation concurrently reproduced tumorigenesis (8 out of 10 rad50 Δ2/+ medaka), had a decrease in median survival time (65.7 ± 1.1 weeks in control vs. 54.2 ± 2.6 weeks in rad50 Δ2/+ medaka, p = 0.001, Welch’s t -test), exhibited semi-lethality in rad50 Δ2/Δ2 medaka and most of the major ataxia-telangiectasia phenotypes, including ataxia (rheotaxis ability was lower in rad50 Δ2/+ medaka than in the control, Mann–Whitney U test, p < 0.05), and telangiectasia (6 out of 10 rad50 Δ2/+ medaka). The fish model may aid in further understanding the tumorigenesis and phenotype of ataxia-telangiectasia-related RAD50 germline mutations and in developing novel therapeutic strategies against RAD50 molecular disorders." @default.
• W4366996323 created "2023-04-27" @default.
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• W4366996323 date "2023-04-25" @default.
• W4366996323 modified "2023-09-25" @default.
• W4366996323 title "A rad50 germline mutation induces tumorigenesis and ataxia-telangiectasia phenotype in a transparent medaka model" @default.
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• W4366996323 doi "https://doi.org/10.1371/journal.pone.0282277" @default.
• W4366996323 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37098078" @default.
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