A novel phosphate-starvation response in fission yeast requires the endocytic function of Myosin I (RNA-seq). Schizosaccharomyces pombe

S. pombe Myosin I (MyoI) plays a key role in cytoskeletal functions, in particular it is part of the endocytotic machinery. Here we show a novel role for MyoI in regulating the response to low phosphate stress. Deletion of MyoI led to an increased proliferation in low phosphate media when compared to a control strain; mutations in other proteins involved in the early steps of endocytosis, such as ARP2 and Sla2/END4, led to the same phenotype. We show that once cells are deprived of phosphate they undergo clear morphological changes, slow down growth but retain viability. This is reminiscent of a quiescence response, and it is completely abolished when MyoI is absent. Transcriptomic analysis revealed a wide perturbation of gene expression upon phosphate starvation, with rapid induction of stress-regulated genes. However, Æmyo1 cells displayed little or negligible effects at gene expression level when they were phosphate-starved. Using a combination of super resolution microscopy and genetic approaches we pinpointed the specific function of MyoI in endocytosis as critical for the response to low phosphate stress. Furthermore, introduction of point-mutated MyoI (with ablated endocytic function) into a ÆmyoI background failed to restore phosphate stress response. Taken together, our data indicate how endocytosis, and in particular MyoI, play a pivotal role in mediating cellular response to nutrients, bridging the external environment and internal molecular functions of the cells. Overall design: RNA-seq transcriptomic analysis in control and ∆myo1 S.pombe strains comparing gene expression profiles at 4 and 10 hours after phosphate depletion.