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Wnt信号通路使皮质肌动蛋白聚合极化,以增加子细胞的不对称性。

Wnt signaling polarizes cortical actin polymerization to increase daughter cell asymmetry.

作者信息

Chai Yongping, Tian Dong, Zhu Zhiwen, Jiang Yuxiang, Huang Shanjin, Wu Dou, Ou Guangshuo, Li Wei

机构信息

Tsinghua-Peking Center for Life Sciences, Beijing Frontier Research Center for Biological Structure, McGovern Institute for Brain Research, School of Life Sciences and MOE Key Laboratory for Protein Science, Tsinghua University, Beijing, China.

School of Life Sciences, Tsinghua University, Beijing, China.

出版信息

Cell Discov. 2022 Mar 1;8(1):22. doi: 10.1038/s41421-022-00376-4.

Abstract

Asymmetric positioning of the mitotic spindle contributes to the generation of two daughter cells with distinct sizes and fates. Here, we investigated an asymmetric division in the Caenorhabditis elegans Q neuroblast lineage. In this division, beginning with an asymmetrically positioned spindle, the daughter-cell size differences continuously increased during cytokinesis, and the smaller daughter cell in the posterior eventually underwent apoptosis. We found that Arp2/3-dependent F-actin assembled in the anterior but not posterior cortex during division, suggesting that asymmetric expansion forces generated by actin polymerization may enlarge the anterior daughter cell. Consistent with this, inhibition of cortical actin polymerization or artificially equalizing actin assembly led to symmetric cell division. Furthermore, disruption of the Wnt gradient or its downstream components impaired asymmetric cortical actin assembly and caused symmetric division. Our results show that Wnt signaling establishes daughter cell asymmetry by polarizing cortical actin polymerization in a dividing cell.

摘要

有丝分裂纺锤体的不对称定位有助于产生两个大小和命运不同的子细胞。在此,我们研究了秀丽隐杆线虫Q神经母细胞谱系中的一种不对称分裂。在这种分裂中,从不对称定位的纺锤体开始,子细胞大小差异在胞质分裂过程中持续增加,后部较小的子细胞最终发生凋亡。我们发现,Arp2/3依赖性F-肌动蛋白在分裂期间在前皮质而非后皮质组装,这表明肌动蛋白聚合产生的不对称扩张力可能会扩大前侧子细胞。与此一致的是,抑制皮质肌动蛋白聚合或人为使肌动蛋白组装均衡会导致对称细胞分裂。此外,Wnt梯度或其下游成分的破坏会损害不对称皮质肌动蛋白组装并导致对称分裂。我们的结果表明,Wnt信号通过在分裂细胞中极化皮质肌动蛋白聚合来建立子细胞不对称性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1212/8885824/97aada3ee774/41421_2022_376_Fig1_HTML.jpg

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