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- W2910592488 abstract "Cell-fate maintenance is important to preserve the variety of cell types that are essential for the formation and function of tissues. We previously showed that the acetylated histone−binding protein BET-1 maintains cell fate by recruiting the histone variant H2A.z. Here, we report that Caenorhabditis elegans TLK-1 and the histone H3 chaperone CAF1 prevent the accumulation of histone variant H3.3. In addition, TLK-1 and CAF1 maintain cell fate by repressing ectopic expression of transcription factors that induce cell-fate specification. Genetic analyses suggested that TLK-1 and BET-1 act in parallel pathways. In tlk-1 mutants, the loss of SIN-3, which promotes histone acetylation, suppressed a defect in cell-fate maintenance in a manner dependent on MYST family histone acetyltransferase MYS-2 and BET-1. sin-3 mutation also suppressed abnormal H3.3 incorporation. Thus, we propose a hypothesis that the regulation and interaction of histone variants play crucial roles in cell-fate maintenance through the regulation of selector genes." @default.
- W2910592488 created "2019-01-25" @default.
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- W2910592488 date "2019-01-01" @default.
- W2910592488 modified "2023-10-16" @default.
- W2910592488 title "Maintenance of cell fates and regulation of the histone variant H3.3 by TLK kinase in<i>Caenorhabditis elegans</i>" @default.
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- W2910592488 doi "https://doi.org/10.1242/bio.038448" @default.
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