Stress-activated MAP kinase (MAPK) pathways are important for integrating cellular responses – including mitotic commitment – with changes in nutrient availability. Although the MAPKs that are expressed in different eukaryotic cell types vary, the control of mitotic commitment via these signalling pathways is conserved. On page 1737, Sonya Hartmuth and Janni Petersen provide new mechanistic data that help to explain how nutritional availability influences mitotic entry in a study of the fission yeast Schizosaccharomyces pombe. They show that nutrient stress (generated by moving cells from a rich to a poor nitrogen source) and nutrient starvation (an acute withdrawal of nitrogen) induce different activation levels of Spc1, the main MAPK in S. pombe; this differential Spc1 activation translates to mitotic progression or blockade, respectively. They also investigate how the S. pombe target of rapamycin (TOR) kinases Tor1 and Tor2 – and the two complexes in which they are known to function – control mitotic entry in response to changes in nutrient availability. They show that TOR complex 1 (TORC1) but not TORC2 is required to induce mitotic entry in response to nutrient stress, and that Tor1 is the kinase involved in mediating this effect. Finally, they propose that there are two TORC1 subcomplexes in S. pombe, one containing Tor1 and the other containing Tor2.