Mitotic fidelity is crucial in preventing aberrant cell divisions and associated consequences such as aneuploidy or catastrophic mitosis, which results in the death of at least one daughter cell. In the fission yeast Schizosaccharomyces pombe, perturbations in lipid metabolism, such as those due to mutations in lipid metabolic enzymes, are known to cause catastrophic mitosis; however, the incidence of this event is suppressed when cell cultures are supplemented with ammonium chloride, a source of nitrogen. Now, in this study (Zemlianski et al., 2024), Martin Převorovský and colleagues investigate this phenomenon further and show that mitotic fidelity can be partially rescued in yeast lipid metabolism mutants by multiple sources of nitrogen. Interestingly, however, this effect is not due to a rescue in lipid metabolism defects, suggesting an alternative, indirect mechanism, which the authors demonstrate may be attributed to target of rapamycin (TOR) signalling, a conserved signalling network that regulates nutrient sensing and utilisation. Here, inhibition of TOR signalling by rapamycin improves mitotic fidelity to levels comparable with those seen upon ammonium supplementation, but treating ammonium-supplemented cells with rapamycin does not have an additive effect, suggesting that these two compounds target the same pathway, likely TOR signalling. Thus, this paper demonstrates that nitrogen availability is important for mitotic fidelity in lipid metabolism mutants, and that this might be achieved indirectly through TOR.
