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Biochem Soc Trans. 2009 Feb;37(Pt 1):273-7. doi: 10.1042/BST0370273.

TOR signalling regulates mitotic commitment through stress-activated MAPK and Polo kinase in response to nutrient stress.

Author information

1
University of Manchester, Michael Smith Building, Faculty of Life Sciences, Oxford Road, Manchester M13 9PT, UK. Janni.Petersen@manchester.ac.uk

Abstract

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).

PMID:
19143645
DOI:
10.1042/BST0370273
[Indexed for MEDLINE]

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