Eukaryotic cells assemble an actomyosin ring during cytokinesis to function as a force-generating machine to drive membrane invagination, and to counteract the intracellular pressure and the cell surface tension. How the extracellular matrix affects actomyosin ring contraction has not been fully explored. While studying the S. pombe 1,3− β-glucan-synthase mutant cps1-191, which is defective in division septum synthesis and arrests with a stable actomyosin ring and, we found that weakening of the extracellular glycan matrix caused the generated spheroplasts to divide at the non-permissive condition. This non-medial slow division was dependent on a functional actomyosin ring and vesicular trafficking, but independent of normal septum synthesis. Interestingly, the high intracellular turgor pressure appears to play minimal roles in inhibiting ring contraction in the absence of cell wall remodeling in cps1-191 mutants as decreasing the turgor pressure alone did not enable spheroplast division. We propose that during cytokinesis, the extracellular glycan matrix restricts actomyosin ring contraction and membrane ingression, and remodeling of the extracellular components through division septum synthesis relieves the inhibition and facilitates actomyosin ring contraction.

真核细胞在胞质分裂过程中组装一个肌动球蛋白环，以作为产生力的机器来驱动膜的内陷，并抵消细胞内压力和细胞表面张力。细胞外基质如何​​影响肌动球蛋白环收缩尚未完全探讨。在研究粟酒裂殖酵母 1,3-β-葡聚糖合酶突变体cps1时-191，它在分隔隔膜的合成中是有缺陷的，并被稳定的放线菌素环阻滞，我们发现细胞外聚糖基质的弱化导致所生成的原生质球在非允许条件下分裂。这种非中间缓慢分裂取决于功能性肌动球蛋白环和囊泡运输，但不依赖于正常的隔膜合成。有趣的是，在不存在cps1的细胞壁重塑的情况下，高细胞内膨胀压力似乎在抑制环收缩中起着最小的作用。-191突变体仅由于降低了鼻腔压力而无法进行原生质球分裂。我们提出，在胞质分裂过程中，细胞外聚糖基质限制了肌动球蛋白环的收缩和膜的进入，通过分裂中隔合成的细胞外成分的重塑减轻了抑制作用，并促进了肌动球蛋白的环收缩。