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- W4200455488 abstract "Werner syndrome (WS) is a rare recessive genetic disease characterized by premature aging. Individuals with this disorder develop normally during childhood, but their physiological conditions exacerbate the aging process in late adolescence. WS is caused by mutation of the human WS gene (WRN), which encodes two main domains, a 3'-5' exonuclease and a 3'-5' helicase. Caenorhabditis elegans expresses human WRN orthologs as two different proteins: MUT-7, which has a 3'-5' exonuclease domain, and C. elegans WRN-1 (CeWRN-1), which has only helicase domains. These unique proteins dynamically regulate olfactory memory in C. elegans, providing insight into the molecular roles of WRN domains in humans. In this review, we specifically focus on characterizing the function of MUT-7 in small interfering RNA (siRNA) synthesis in the cytoplasm and the roles of siRNA in directing nuclear CeWRN-1 loading onto a heterochromatin complex to induce negative feedback regulation. Further studies on the different contributions of the 3'-5' exonuclease and helicase domains in the molecular mechanism will provide clues to the accelerated aging processes in WS." @default.
- W4200455488 created "2021-12-31" @default.
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- W4200455488 date "2021-12-08" @default.
- W4200455488 modified "2023-10-16" @default.
- W4200455488 title "MUT-7 Provides Molecular Insight into the Werner Syndrome Exonuclease" @default.
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- W4200455488 doi "https://doi.org/10.3390/cells10123457" @default.
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- W4200455488 hasPublicationYear "2021" @default.
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