Fission yeast cells use distinct cell size control mechanisms to regulate cell geometry in response to osmotic, oxidative, or low glucose conditions.

Cells maintain an appropriate size to function, yet the mechanisms that enable size adaptation to environmental stress remain poorly understood. Fission yeast cells enter mitosis and divide at a threshold size when cyclin-dependent kinase (Cdk1) is activated through size- and time-dependent scaling of its regulators: Cdr2 kinase with cell surface area (SA), Cdc25 phosphatase with cell volume, and mitotic cyclin Cdc13 with time. This integrated size control network is characterized in nutrient-rich conditions, but under stress, it remains unclear which size parameters cells monitor, and which size- or time-sensing pathways mediate cell size changes. Using high-throughput image analysis, we quantified the geometry of dividing cells under osmotic, oxidative, and low glucose conditions. Wild-type cells increased their SA-to-volume (SA:Vol) ratio in low glucose but decreased it under osmotic or oxidative stress, revealing distinct stress-specific geometric responses. Genetic perturbations of size- and time-sensing pathways revealed that Cdc25 is required for volume-based expansion in oxidative and osmotic stress, Cdr2 promotes SA-based expansion in low glucose, and Cdc13 contributes to geometry changes under low glucose and osmotic stress. Although disrupting individual pathways altered normal geometric responses, cells remained viable, suggesting that a modular size control system enables flexible geometric responses to changing environments.