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有丝分裂起始时的顶端缢缩逆转是细胞分裂产生不同形态发生结果的基础。

Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division.

机构信息

Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142.

出版信息

Mol Biol Cell. 2020 Jul 21;31(16):1663-1674. doi: 10.1091/mbc.E19-12-0673. Epub 2020 Mar 4.

Abstract

During development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled nonmitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

摘要

在发育过程中,协调的细胞形状变化和细胞分裂会塑造组织。虽然这些单个细胞行为已经得到了广泛的研究,但上皮细胞中同时发生的细胞形状变化和细胞分裂如何影响组织形状,人们了解得还比较少。我们在胚胎早期的两个背景下探讨了这个问题:中胚层内陷过程中的过早细胞分裂,以及顶端收缩性异位激活时的固有外胚层细胞分裂。利用定量活细胞成像,我们证明有丝分裂进入通过干扰中-顶端 RhoA 信号来逆转顶端收缩性。虽然过早的有丝分裂进入会抑制依赖于顶端收缩的中胚层内陷,但在人工收缩的外胚层中,有丝分裂进入会诱导异位组织内陷。异位内陷是由于相邻有丝分裂细胞中的中-顶端肌球蛋白丢失所致。这种肌球蛋白的丢失使非有丝分裂细胞能够通过有丝分裂细胞的拉伸进行顶端收缩。因此,有丝分裂进入的空间模式可以通过顶端收缩性和有丝分裂之间的信号干扰,差异调节组织形状。

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