Abstract
Hippo signaling controls cellular processes that ultimately impact organogenesis and homeostasis. Consequently, disease states including cancer can emerge when signaling is deregulated. The major pathway transducers Yap and Taz require cofactors to impart transcriptional control over target genes. Research into Yap/Taz-mediated epigenetic modifications has revealed their association with chromatin-remodeling complex proteins as a means of altering chromatin structure, therefore affecting accessibility and activity of target genes. Specifically, Yap/Taz have been found to associate with factors of the GAGA, Ncoa6, Mediator, Switch/sucrose nonfermentable (SWI/SNF), and Nucleosome Remodeling and Deacetylase (NuRD) chromatin-remodeling complexes to alter the accessibility of target genes. This review highlights the different mechanisms by which Yap/Taz collaborate with other factors to modify DNA packing at specific loci to either activate or repress target gene transcription.
Highlights
Recruitment and/or activation of transcription factors and proteins capable of altering target gene transcriptional activity is a hallmark of many signaling pathways
Mechanistic studies into how Hippo signaling effectors Yes-associated protein (Yap) and Taz influence target gene transcriptional activity has revealed the significance of imparting chromatin alterations at target loci
Yki/Yap/Taz recruitment of and interaction with chromatin remodelers of the Switch/sucrose nonfermentable (SWI/SNF) complex, GAGA factor, Mediator complex, nuclear receptor coactivator 6 (Ncoa6), and Nucleosome Remodeling and Deacetylase (NuRD) complexes have all been documented as means for Yki/Yap/Taz mediated alterations of target gene transcriptional activity [23,24,25,26,27,28,29,30,31,32,33] and are reviewed (Table 1)
Summary
Recruitment and/or activation of transcription factors and proteins capable of altering target gene transcriptional activity is a hallmark of many signaling pathways. Overall activity of the Hippo signaling kinase cascade serves to prevent the transcriptional activity of downstream effectors Yap and Taz. When signaling is not active, Yap/Taz can enter the nucleus and bind to DNA through interaction with cofactors to impart effects on transcription. Mechanistic studies into how Hippo signaling effectors Yap and Taz influence target gene transcriptional activity has revealed the significance of imparting chromatin alterations at target loci. Yki/Yap/Taz recruitment of and interaction with chromatin remodelers of the SWI/SNF complex, GAGA factor, Mediator complex, Ncoa, and NuRD complexes have all been documented as means for Yki/Yap/Taz mediated alterations of target gene transcriptional activity [23,24,25,26,27,28,29,30,31,32,33] and are reviewed (Table 1)
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