Abstract:
:RETINOBLASTOMA (RB) is a tumour suppressor gene originally discovered in patients that develop eye tumours. The pRb protein is now well established as a key cell-cycle regulator which suppresses G1-S transition via interaction with E2F-DP complexes. pRb function is also required for a wide range of biological processes, including the regulation of stem-cell maintenance, cell differentiation, permanent cell-cycle exit, DNA repair, and genome stability. Such multifunctionality of pRb is thought to be facilitated through interactions with various binding partners in a context-dependent manner. Although the molecular network in which RB controls various biological processes is not fully understood, it has been found that pRb interacts with transcription factors and chromatin modifiers to either suppress or promote the expression of key genes during the switch from cell proliferation to differentiation. RETINOBLASTOMA-RELATED (RBR) is the plant orthologue of RB and is also known to negatively control the G1-S transition. Similar to its animal counterpart, plant RBR has various roles throughout plant development; however, much of its molecular functions outside of the G1-S transition are still unknown. One of the better-characterized molecular mechanisms is the cooperation of RBR with the Polycomb repressive complex 2 (PRC2) during plant-specific developmental events. This review summarizes the current understanding of this cooperation and focuses on the processes in Arabidopsis in which the RBR-PRC2 cooperation facilitates cell differentiation and developmental transitions.
journal_name
J Exp Botjournal_title
Journal of experimental botanyauthors
Kuwabara A,Gruissem Wdoi
10.1093/jxb/eru069subject
Has Abstractpub_date
2014-06-01 00:00:00pages
2667-76issue
10eissn
0022-0957issn
1460-2431pii
eru069journal_volume
65pub_type
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更新日期:2007-01-01 00:00:00
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journal_title:Journal of experimental botany
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journal_title:Journal of experimental botany
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journal_title:Journal of experimental botany
pub_type: 杂志文章
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更新日期:2004-03-01 00:00:00
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