Metabolic control of cytokinesis by glucose cAMP–PKA signaling in fission yeast

Cytokinesis, the final step of cell division, must be precisely coordinated with the cellular metabolic status, yet the underlying regulatory mechanisms remain poorly understood. Here we show that in Schizosaccharomyces pombe, glucose signaling promotes cytokinesis via the evolutionarily conserved cAMP–PKA signaling pathway. Loss of the Pka1 catalytic subunit delays assembly and constriction of the contractile actomyosin ring (CAR), whereas constitutive PKA activation enhances CAR integrity and accelerates cytokinesis. Mechanistically, Pka1 downregulates the basal activity of the stress-activated MAPK Sty1 under glucose-rich conditions, thereby stabilizing the formin For3 and its nucleated actin cables, which collaborate to regulate CAR dynamics. Remarkably, cAMP–PKA signaling also facilitates cytokinesis through a parallel, actin cable–independent mechanism. Additionally, mitochondrial respiration contributes to cytokinesis in the presence of glucose through a PKA-independent pathway. These findings reveal a multilayered network that links carbon source metabolism to cytoskeletal organization and underscore the importance of tight PKA activity control for robust cell division.