TOR signalling regulates mitotic commitment through stress-activated MAPK and Polo kinase in response to nutrient stress.
Cell growth and cell division are coupled to control cell size and this co-ordination is often modulated by the availability of nutrients. In many eukaryotes, TOR (target of rapamycin) signalling is involved in coupling nutrient sensing to cell growth and division controls. Nutrient stress inhibits TOR signalling to advance the timing of cell division and thus leads to continued cell division at reduced cell size. Most changes in the environment stimulate stress-activated MAPK (mitogen-activated protein kinase) signalling pathways. Several MAPKs also have a general role in the control of mitotic onset and cell division. In the present paper, I discuss the interplay between two major signalling pathways, the TOR and the stress MAPK signalling pathways, in controlling mitotic commitment, with the main focus being on fission yeast (Schizosaccharomyces pombe).
Petersen
Janni
J
University of Manchester, Michael Smith Building, Faculty of Life Sciences, Oxford Road, Manchester M13 9PT, UK. Janni.Petersen@manchester.ac.uk
D000818:Animals; D005502:Food; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008938:Mitosis; D011494:Protein Kinases / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D012568:Schizosaccharomyces / Q000166:cytology* / Q000201:enzymology*; D029702:Schizosaccharomyces pombe Proteins / Q000378:metabolism*
D029702:Schizosaccharomyces pombe Proteins; D011494:Protein Kinases; C523461:Tor1 protein, S pombe; C501407:Plo1 protein, S pombe; D017346:Protein Serine-Threonine Kinases; D048031:JNK Mitogen-Activated Protein Kinases