Suppr超能文献

细胞内在的机械调节在胞质分裂沟处的质膜积累。

Cell-intrinsic mechanical regulation of plasma membrane accumulation at the cytokinetic furrow.

机构信息

Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455.

Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.

出版信息

Proc Natl Acad Sci U S A. 2024 Jul 16;121(29):e2320769121. doi: 10.1073/pnas.2320769121. Epub 2024 Jul 11.

Abstract

Cytokinesis is the process where the mother cell's cytoplasm separates into daughter cells. This is driven by an actomyosin contractile ring that produces cortical contractility and drives cleavage furrow ingression, resulting in the formation of a thin intercellular bridge. While cytoskeletal reorganization during cytokinesis has been extensively studied, less is known about the spatiotemporal dynamics of the plasma membrane. Here, we image and model plasma membrane lipid and protein dynamics on the cell surface during leukemia cell cytokinesis. We reveal an extensive accumulation and folding of the plasma membrane at the cleavage furrow and the intercellular bridge, accompanied by a depletion and unfolding of the plasma membrane at the cell poles. These membrane dynamics are caused by two actomyosin-driven biophysical mechanisms: the radial constriction of the cleavage furrow causes local compression of the apparent cell surface area and accumulation of the plasma membrane at the furrow, while actomyosin cortical flows drag the plasma membrane toward the cell division plane as the furrow ingresses. The magnitude of these effects depends on the plasma membrane fluidity, cortex adhesion, and cortical contractility. Overall, our work reveals cell-intrinsic mechanical regulation of plasma membrane accumulation at the cleavage furrow that is likely to generate localized differences in membrane tension across the cytokinetic cell. This may locally alter endocytosis, exocytosis, and mechanotransduction, while also serving as a self-protecting mechanism against cytokinesis failures that arise from high membrane tension at the intercellular bridge.

摘要

胞质分裂是母细胞的细胞质分裂为子细胞的过程。这是由肌动球蛋白收缩环驱动的,该收缩环产生皮质收缩性并驱动分裂沟内陷,导致形成薄的细胞间桥。虽然胞质分裂过程中的细胞骨架重排已经得到了广泛的研究,但对质膜的时空动力学知之甚少。在这里,我们在白血病细胞胞质分裂过程中对细胞表面的质膜脂质和蛋白质动力学进行成像和建模。我们揭示了在分裂沟和细胞间桥处质膜的广泛积累和折叠,同时在细胞极处质膜的耗竭和展开。这些膜动力学是由两种肌动球蛋白驱动的生物物理机制引起的:分裂沟的径向收缩导致明显的细胞表面积的局部压缩和沟处质膜的积累,而肌动球蛋白皮质流在沟内陷时将质膜拖向细胞分裂平面。这些效应的大小取决于质膜的流动性、皮质粘附和皮质收缩性。总的来说,我们的工作揭示了质膜在分裂沟处积累的细胞内在机械调节,这可能会在细胞分裂过程中产生细胞间膜张力的局部差异。这可能会局部改变内吞作用、外排作用和机械转导,同时也作为一种自我保护机制,防止由于细胞间桥处的高膜张力而导致的胞质分裂失败。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/afbf/11260091/d2ad55f26880/pnas.2320769121fig01.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验