Many organisms can pause their growth cycle to enter a stationary phase (SP). The mechanisms governing SP entry in protozoans are not currently well known, with most studies carried out in yeast. However, a more complete understanding of the mechanisms behind SP entry could aid our understanding of protozoan infections, including malaria and cell cycle irregularities in cancer biology. Various kinases are known to play a role in SP entry in both bacteria and yeast. Protein kinase C (PKC) regulates cell proliferation in different contexts in both cancer cells and in yeast, but whether it has a role in instigating SP entry is unknown. In this study (Umachandran et al., 2022), the authors use the unicellular eukaryote Dictyostelium discoideum to investigate the role of the PKC ortholog pkcA in SP entry. The authors show that pkcA– cells have early-onset SP, which is reached at a lower cell density compared to wild-type Ax2 cells, under shaking conditions. By measuring polyphosphate (polyP) levels of Ax2 and pkcA– cells, the authors find that pkcA– cells produce excess polyP, leading to increased levels of extracellular polyP and contributing to their early entry into SP. Furthermore, rates of pinocytosis and exocytosis are lower and higher, respectively, in pkcA– cells compared to wild-type, resulting in starvation-like conditions normally associated with high cell density. Together, these findings suggest that reduced PkcA levels trigger SP because cells cannot acquire or retain nutrients efficiently, therefore mimicking the conditions of actual starvation.
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