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时空分离的皮质流和纺锤体几何形状在果蝇神经干细胞中建立了物理不对称性。

Spatio-temporally separated cortical flows and spindle geometry establish physical asymmetry in fly neural stem cells.

机构信息

Biozentrum, University of Basel, Klingelbergstrasse 50-70, CH-4056, Basel, Switzerland.

MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London, WC1E 6BT, UK.

出版信息

Nat Commun. 2017 Nov 9;8(1):1383. doi: 10.1038/s41467-017-01391-w.

DOI:10.1038/s41467-017-01391-w
PMID:29123099
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5680339/
Abstract

Asymmetric cell division, creating sibling cells with distinct developmental potentials, can be manifested in sibling cell size asymmetry. This form of physical asymmetry occurs in several metazoan cells, but the underlying mechanisms and function are incompletely understood. Here we use Drosophila neural stem cells to elucidate the mechanisms involved in physical asymmetry establishment. We show that Myosin relocalizes to the cleavage furrow via two distinct cortical Myosin flows: at anaphase onset, a polarity induced, basally directed Myosin flow clears Myosin from the apical cortex. Subsequently, mitotic spindle cues establish a Myosin gradient at the lateral neuroblast cortex, necessary to trigger an apically directed flow, removing Actomyosin from the basal cortex. On the basis of the data presented here, we propose that spatiotemporally controlled Myosin flows in conjunction with spindle positioning and spindle asymmetry are key determinants for correct cleavage furrow placement and cortical expansion, thereby establishing physical asymmetry.

摘要

不对称细胞分裂可产生具有不同发育潜力的姐妹细胞,这可以表现在姐妹细胞大小的不对称上。这种形式的物理不对称发生在几种后生动物细胞中,但潜在的机制和功能尚不完全清楚。在这里,我们使用果蝇神经干细胞来阐明建立物理不对称的机制。我们表明肌球蛋白通过两种不同的皮质肌球蛋白流重新定位到分裂沟:在后期开始时,极性诱导的基底定向肌球蛋白流从顶皮质中清除肌球蛋白。随后,有丝分裂纺锤体提示在侧神经母细胞质膜上建立肌球蛋白梯度,这对于触发向顶的流、从基底皮质中去除肌动球蛋白是必要的。根据这里呈现的数据,我们提出,时空控制的肌球蛋白流与纺锤体定位和纺锤体不对称性是正确分裂沟位置和皮质扩张的关键决定因素,从而建立物理不对称性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/788e050548f9/41467_2017_1391_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/c59b400cc537/41467_2017_1391_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/22cc06e94b0b/41467_2017_1391_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/8b33e67299a7/41467_2017_1391_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/f40e34ccc7bf/41467_2017_1391_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/5e7934b54132/41467_2017_1391_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/14920b5fbf3d/41467_2017_1391_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/dc1629963fba/41467_2017_1391_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/788e050548f9/41467_2017_1391_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/c59b400cc537/41467_2017_1391_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/22cc06e94b0b/41467_2017_1391_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/8b33e67299a7/41467_2017_1391_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/f40e34ccc7bf/41467_2017_1391_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/5e7934b54132/41467_2017_1391_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/14920b5fbf3d/41467_2017_1391_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/dc1629963fba/41467_2017_1391_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe99/5680339/788e050548f9/41467_2017_1391_Fig8_HTML.jpg

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Klp10A, a stem cell centrosome-enriched kinesin, balances asymmetries in male germline stem cell division.
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