Journal
JOURNAL OF CELL SCIENCE
Volume 124, Issue 1, Pages 25-34Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.070987
Keywords
G1 arrest; Cell cycle control; Nutritional stress; Sexual differentiation
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Funding
- Ministerio de Ciencia e Innovacion, MICINN [BFU2007-62670/BMC, BFU2008-00408/BMC]
- Programa Nacional de Formacion de Profesorado Universitario (FPU)
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Yeast Reb1 and its mammalian ortholog TTF1 are conserved Myb-type DNA-binding proteins that bind to specific sites near the 3'-end of rRNA genes (rDNA). Here, they participate in the termination of transcription driven by RNA polymerase I and block DNA replication forks approaching in the opposite direction. We found that Schizosaccharomyces pombe Reb1 also upregulates transcription of the ste9(+) gene that is required for nitrogen-starvation-induced growth arrest with a G1 DNA content and sexual differentiation. Ste9 activates the anaphase-promoting complex or cyclosome ('APC/C') in G1, targeting B-cyclin for proteasomal degradation in response to nutritional stress. Reb1 binds in vivo and in vitro to a specific DNA sequence at the promoter of ste9(+), similar to the sequence recognized in the rDNA, and this binding is required for ste9(+) transcriptional activation and G1 arrest. This suggests that Reb1 acts as a link between rDNA metabolism and cell cycle control in response to nutritional stress. In agreement with this new role for Reb1 in the regulation of the G1-S transition, reb1 Delta and wee1(ts) mutations are synthetically lethal owing to the inability of these cells to lengthen G1 before entering S phase. Similarly, reb1 Delta cdc10(ts) cells are unable to arrest in G1 and die at the semi-permissive temperature.
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