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ROT1  -  Rot1p

Saccharomyces cerevisiae S288c

Synonyms: Protein ROT1, Reversal of TOR2 lethality protein 1, YM8325.01, YMR200W
 
 
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High impact information on ROT1

  • ROT2 encodes glucosidase II, and ROT1 and BIG1 encode novel proteins [1].
  • Deletion of ROT1 caused cell aggregation and an abnormal morphology [2].
  • Although ROT1 is essential for growth of Saccharomyces cerevisiae strain BY4741, the growth of a rot1Delta haploid was partially restored by the addition of 0.6 M sorbitol to the growth medium [2].
  • ROT1 genetically interacted with several ER chaperone genes including KAR2, and the rot1-2 mutation triggered the unfolded protein response [3].
  • Mutation of the ROT1 gene caused defects in cell wall synthesis and lysis of autophagic bodies [4].
 

Biological context of ROT1

 

Anatomical context of ROT1

 

Regulatory relationships of ROT1

  • In fact, overexpression of CLB2 is toxic when ROT1 is partially inactivated, and reciprocally, deletion of CLB2 suppresses the lethality of the rot1 mutant, which indicates a functional antagonism between Clb2 and Rot1 [5].

References

  1. Cell wall integrity modulates RHO1 activity via the exchange factor ROM2. Bickle, M., Delley, P.A., Schmidt, A., Hall, M.N. EMBO J. (1998) [Pubmed]
  2. Rot1p of Saccharomyces cerevisiae is a putative membrane protein required for normal levels of the cell wall 1,6-beta-glucan. Machi, K., Azuma, M., Igarashi, K., Matsumoto, T., Fukuda, H., Kondo, A., Ooshima, H. Microbiology (Reading, Engl.) (2004) [Pubmed]
  3. Saccharomyces cerevisiae Rot1p Is an ER-Localized Membrane Protein That May Function with BiP/Kar2p in Protein Folding. Takeuchi, M., Kimata, Y., Hirata, A., Oka, M., Kohno, K. J. Biochem. (2006) [Pubmed]
  4. Causal links between protein folding in the ER and events along the secretory pathway. Takeuchi, M., Kimata, Y., Kohno, K. Autophagy. (2006) [Pubmed]
  5. Rot1 plays an antagonistic role to Clb2 in actin cytoskeleton dynamics throughout the cell cycle. Juanes, M.A., Queralt, E., Bañó, M.C., Igual, J.C. J. Cell. Sci. (2007) [Pubmed]
 
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