Cells control the size of their organelles to play a fundamental role in maintaining cellular homeostasis, ensuring proper function, and adapting to various environmental and physiological conditions. However, the mechanisms behind organelle size control remain largely unknown, partly due to the complexity of many organelles, which makes these mechanisms challenging to study. Eukaryotic cilia and flagella, being microtubule-based organelles with relatively simple structures, serve as ideal models for studying size regulation mechanisms. Several theoretical models have been proposed to understand the mechanism of flagellar length control. In this study, we experimentally tested the diffusion model using Chlamydomonas . According to the diffusion model, a signaling molecule is released at the tip of the flagellum and diffuses back to its base. This model hinges on the diffusion gradient of a signal molecule produced at the flagellar tip and consumed in the cytoplasm. We focused on kinesin as the signaling molecule. Kinesin drives anterograde intraflagellar transport (IFT) from the flagellar base to the tip but diffuses back to the base. To experimentally test the kinesin diffusion model, we reduced the diffusion rate of kinesin by trapping it on axonemes using a chemically induced dimerization system. Despite reducing the kinesin diffusion rate, the length of the flagella and the IFT behavior were mostly unchanged. This observation does not support the diffusion model based on kinesin diffusion.
Ishikawa et al. (2026) studied this question.