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通过动力蛋白介导的皮层肌球蛋白 II 去除实现的极性弛豫。

Polar relaxation by dynein-mediated removal of cortical myosin II.

机构信息

Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, Coventry, UK.

Hokkaido University, Sapporo, Japan.

出版信息

J Cell Biol. 2020 Aug 3;219(8). doi: 10.1083/jcb.201903080.

Abstract

Nearly six decades ago, Lewis Wolpert proposed the relaxation of the polar cell cortex by the radial arrays of astral microtubules as a mechanism for cleavage furrow induction. While this mechanism has remained controversial, recent work has provided evidence for polar relaxation by astral microtubules, although its molecular mechanisms remain elusive. Here, using C. elegans embryos, we show that polar relaxation is achieved through dynein-mediated removal of myosin II from the polar cortexes. Mutants that position centrosomes closer to the polar cortex accelerated furrow induction, whereas suppression of dynein activity delayed furrowing. We show that dynein-mediated removal of myosin II from the polar cortexes triggers a bidirectional cortical flow toward the cell equator, which induces the assembly of the actomyosin contractile ring. These results provide a molecular mechanism for the aster-dependent polar relaxation, which works in parallel with equatorial stimulation to promote robust cytokinesis.

摘要

近六十年前,Lewis Wolpert 提出,星状微管的放射状阵列通过松弛极性细胞皮层,作为分裂沟诱导的一种机制。虽然这一机制一直存在争议,但最近的研究为星状微管介导的极性松弛提供了证据,尽管其分子机制仍难以捉摸。在这里,我们使用秀丽隐杆线虫胚胎表明,极性松弛是通过动力蛋白介导的将肌球蛋白 II 从极性皮层中去除来实现的。将中心体定位在更靠近极性皮层的突变体加速了沟的诱导,而抑制动力蛋白的活性则延迟了沟的形成。我们表明,动力蛋白介导的将肌球蛋白 II 从极性皮层中去除,引发了一个朝向细胞赤道的双向皮层流,从而诱导了肌动球蛋白收缩环的组装。这些结果为星状依赖性极性松弛提供了一个分子机制,它与赤道刺激平行工作,以促进强大的胞质分裂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/95f3/7401816/b5472ad5246c/JCB_201903080_Fig1.jpg

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