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Gene Review

RIM15  -  Rim15p

Saccharomyces cerevisiae S288c

Synonyms: Serine/threonine-protein kinase RIM15, TAK1, YFL033C
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High impact information on RIM15

  • Accordingly, deletion of RIM15 suppresses the growth defect of a temperature-sensitive adenylate-cyclase mutant and, most importantly, renders cells independent of cAPK activity [1].
  • Conversely, overexpression of RIM15 suppresses phenotypes associated with a mutation in the regulatory subunit of cAPK, exacerbates the growth defect of strains compromised for cAPK activity, and partially induces a starvation response in logarithmically growing wild-type cells [1].
  • The Saccharomyces cerevisiae protein kinase Rim15p was identified previously as a stimulator of meiotic gene expression [1].
  • Biochemical analyses reveal that cAPK-mediated in vitro phosphorylation of Rim15p strongly inhibits its kinase activity [1].
  • Taken together, these results place Rim15p immediately downstream and under negative control of cAPK and define a positive regulatory role of Rim15p for entry into both meiosis and stationary phase [1].

Biological context of RIM15

  • The Saccharomyces cerevisiae RIM15 gene was identified previously through a mutation that caused reduced ability to undergo meiosis [2].
  • Stimulation of yeast meiotic gene expression by the glucose-repressible protein kinase Rim15p [2].
  • The Rim15 regulon comprises several gene clusters implicated in the adaptation to respiratory growth, including classical oxidative stress genes such as SOD1 and SOD2, suggesting that the reduced life span of rim15delta cells may be due to their deficiency in oxidative damage prevention [3].
  • In this review, we focus on Rim15, a protein kinase required in yeast for the proper entry into stationary phase (G0) [4].

Anatomical context of RIM15

  • Thus, Rim15 integrates signals from at least three nutrient-sensory kinases (TOR, PKA, and Sch9) to properly control entry into G(0), a key developmental process in eukaryotic cells [5].

Associations of RIM15 with chemical compounds

  • We report here an analysis of the cloned RIM15 gene, which specifies a 1,770-residue polypeptide with homology to serine/threonine protein kinases [2].
  • Thus, glucose repression of Rim15p may be responsible for glucose inhibition of Ime1p-Ume6p interaction [2].
  • In Saccharomyces cerevisiae, the conserved protein kinase A (PKA) and rapamycin-sensitive TOR (TORC1) pathways antagonize G0 entry in response to carbon and/or nitrogen availability primarily by inhibiting the PAS kinase Rim15 function [6].

Regulatory relationships of RIM15

  • Unlike PKA, which negatively regulates stress-responsive element (STRE)- and post-diauxic shift (PDS)-driven gene expression, Sch9 appears to exert additional positive control on the Rim15-effector Gis1 to regulate PDS-driven gene expression [7].

Other interactions of RIM15

  • Two-hybrid interaction assays suggest that Ime1p-Ume6p interaction is diminished in a rim15 mutant [2].
  • However, the triple deletion of stress-resistance genes MSN2/MSN4 and RIM15, which causes a major decrease in chronological life span, extends replicative life span [8].
  • The role of superoxide dismutases and of other stress-resistance proteins in extending the chronological life span of yeast, worms, and flies indicates that the negative effect of Sod2, Msn2/Msn4/Rim15 on the replicative life span of S. cerevisiae is independent of aging [8].
  • Tests of epistasis as well as transcriptional analyses of Gis1-dependent expression indicate that Gis1 acts in this pathway downstream of Rim15 to mediate transcription from the previously identified post-diauxic shift (PDS) element [9].
  • Thus, Rim15 plays a key role in G0 entry through its ability to integrate signaling from the PKA, TORC1, and Pho80-Pho85 pathways [6].


  1. Saccharomyces cerevisiae cAMP-dependent protein kinase controls entry into stationary phase through the Rim15p protein kinase. Reinders, A., Bürckert, N., Boller, T., Wiemken, A., De Virgilio, C. Genes Dev. (1998) [Pubmed]
  2. Stimulation of yeast meiotic gene expression by the glucose-repressible protein kinase Rim15p. Vidan, S., Mitchell, A.P. Mol. Cell. Biol. (1997) [Pubmed]
  3. The novel yeast PAS kinase Rim 15 orchestrates G0-associated antioxidant defense mechanisms. Cameroni, E., Hulo, N., Roosen, J., Winderickx, J., De Virgilio, C. Cell Cycle (2004) [Pubmed]
  4. Rim15 and the crossroads of nutrient signalling pathways in Saccharomyces cerevisiae. Swinnen, E., Wanke, V., Roosen, J., Smets, B., Dubouloz, F., Pedruzzi, I., Cameroni, E., De Virgilio, C., Winderickx, J. Cell division [electronic resource]. (2006) [Pubmed]
  5. TOR and PKA signaling pathways converge on the protein kinase Rim15 to control entry into G0. Pedruzzi, I., Dubouloz, F., Cameroni, E., Wanke, V., Roosen, J., Winderickx, J., De Virgilio, C. Mol. Cell (2003) [Pubmed]
  6. Regulation of G0 entry by the Pho80-Pho85 cyclin-CDK complex. Wanke, V., Pedruzzi, I., Cameroni, E., Dubouloz, F., De Virgilio, C. EMBO J. (2005) [Pubmed]
  7. PKA and Sch9 control a molecular switch important for the proper adaptation to nutrient availability. Roosen, J., Engelen, K., Marchal, K., Mathys, J., Griffioen, G., Cameroni, E., Thevelein, J.M., De Virgilio, C., De Moor, B., Winderickx, J. Mol. Microbiol. (2005) [Pubmed]
  8. Chronological aging-independent replicative life span regulation by Msn2/Msn4 and Sod2 in Saccharomyces cerevisiae. Fabrizio, P., Pletcher, S.D., Minois, N., Vaupel, J.W., Longo, V.D. FEBS Lett. (2004) [Pubmed]
  9. Saccharomyces cerevisiae Ras/cAMP pathway controls post-diauxic shift element-dependent transcription through the zinc finger protein Gis1. Pedruzzi, I., Bürckert, N., Egger, P., De Virgilio, C. EMBO J. (2000) [Pubmed]
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