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胚胎尾部弯曲是由不对称的脊索收缩驱动的,并通过上皮细胞增殖来协调。

embryonic tail bending is driven by asymmetrical notochord contractility and coordinated by epithelial proliferation.

机构信息

Sars-Fang Centre, MoE Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China.

Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, China.

出版信息

Development. 2020 Dec 23;147(24):dev185868. doi: 10.1242/dev.185868.

DOI:10.1242/dev.185868
PMID:33361090
Abstract

Ventral bending of the embryonic tail within the chorion is an evolutionarily conserved morphogenetic event in both invertebrates and vertebrates. However, the complexity of the anatomical structure of vertebrate embryos makes it difficult to experimentally identify the mechanisms underlying embryonic folding. This study investigated the mechanisms underlying embryonic tail bending in chordates. To further understand the mechanical role of each tissue, we also developed a physical model with experimentally measured parameters to simulate embryonic tail bending. Actomyosin asymmetrically accumulated at the ventral side of the notochord, and cell proliferation of the dorsal tail epidermis was faster than that in the ventral counterpart during embryonic tail bending. Genetic disruption of actomyosin activity and inhibition of cell proliferation dorsally caused abnormal tail bending, indicating that both asymmetrical actomyosin contractility in the notochord and the discrepancy of epidermis cell proliferation are required for tail bending. In addition, asymmetrical notochord contractility was sufficient to drive embryonic tail bending, whereas differential epidermis proliferation was a passive response to mechanical forces. These findings showed that asymmetrical notochord contractility coordinates with differential epidermis proliferation mechanisms to drive embryonic tail bending.This article has an associated 'The people behind the papers' interview.

摘要

胚胎尾部在囊胚中的腹侧弯曲是无脊椎动物和脊椎动物中进化上保守的形态发生事件。然而,脊椎动物胚胎的解剖结构复杂,使得实验鉴定胚胎折叠的机制变得困难。本研究调查了脊索动物胚胎尾部弯曲的机制。为了进一步了解每个组织的力学作用,我们还开发了一个具有实验测量参数的物理模型来模拟胚胎尾部弯曲。肌动球蛋白在脊索的腹侧不对称积累,并且在胚胎尾部弯曲过程中,背部尾表皮的细胞增殖比腹侧快。肌动球蛋白活性的遗传破坏和背部细胞增殖的抑制导致尾部弯曲异常,表明脊索中的不对称肌球蛋白收缩和表皮细胞增殖的差异对于尾部弯曲都是必需的。此外,不对称的脊索收缩足以驱动胚胎尾部弯曲,而表皮的差异增殖是对机械力的被动反应。这些发现表明,不对称的脊索收缩与表皮增殖机制协同作用,驱动胚胎尾部弯曲。本文有一个相关的“论文背后的人”访谈。

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