رکورد قبلیرکورد بعدی

" Rb and p130 control cell cycle gene silencing to maintain the postmitotic phenotype in cardiac myocytes. "


Document Type : AL
Record Number : 909641
Doc. No : LA0v4410n5
Title & Author : Rb and p130 control cell cycle gene silencing to maintain the postmitotic phenotype in cardiac myocytes. [Article]\ Sdek, Patima; Zhao, Peng; Wang, Yaping; Huang, Chang-Jiang; Ko, Christopher Y; Butler, Peter C; Weiss, James N; Maclellan, W Robb
Date : 2011
Title of Periodical : UCLA
Abstract : The mammalian heart loses its regenerative potential soon after birth. Adult cardiac myocytes (ACMs) permanently exit the cell cycle, and E2F-dependent genes are stably silenced, although the underlying mechanism is unclear. Heterochromatin, which silences genes in many biological contexts, accumulates with cardiac differentiation. H3K9me3, a histone methylation characteristic of heterochromatin, also increases in ACMs and at E2F-dependent promoters. We hypothesize that genes relevant for cardiac proliferation are targeted to heterochromatin by retinoblastoma (Rb) family members interacting with E2F transcription factors and recruiting heterochromatin protein 1 (HP1) proteins. To test this hypothesis, we created cardiac-specific Rb and p130 inducible double knockout (IDKO) mice. IDKO ACMs showed a decrease in total heterochromatin, and cell cycle genes were derepressed, leading to proliferation of ACMs. Although Rb/p130 deficiency had no effect on total H3K9me3 levels, recruitment of HP1-γ to promoters was lost. Depleting HP1-γ up-regulated proliferation-promoting genes in ACMs. Thus, Rb and p130 have overlapping roles in maintaining the postmitotic state of ACMs through their interaction with HP1-γ to direct heterochromatin formation and silencing of proliferation-promoting genes.
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0v4410n5_7726.pdf
0v4410n5.pdf
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