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非肌肉肌球蛋白 II 对于秀丽隐杆线虫体节细胞分裂中正确的命运特化是必需的。

Non-muscle myosin II is required for correct fate specification in the Caenorhabditis elegans seam cell divisions.

机构信息

Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, United Kingdom.

Institution of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, Du Cane Road, London, W12 0NN, United Kingdom.

出版信息

Sci Rep. 2017 Jun 14;7(1):3524. doi: 10.1038/s41598-017-01675-7.

Abstract

During development, cell division often generates two daughters with different developmental fates. Distinct daughter identities can result from the physical polarity and size asymmetry itself, as well as the subsequent activation of distinct fate programmes in each daughter. Asymmetric divisions are a feature of the C. elegans seam lineage, in which a series of post-embryonic, stem-like asymmetric divisions give rise to an anterior daughter that differentiates and a posterior daughter that continues to divide. Here we have investigated the role of non-muscle myosin II (nmy-2) in these asymmetric divisions. We show that nmy-2 does not appear to be involved in generating physical division asymmetry, but nonetheless is important for specifying differential cell fate. While cell polarity appears normal, and chromosome and furrow positioning remains unchanged when nmy-2 is inactivated, seam cell loss occurs through inappropriate terminal differentiation of posterior daughters. This reveals a role for nmy-2 in cell fate determination not obviously linked to the primary polarity determination mechanisms it has been previously associated with.

摘要

在发育过程中,细胞分裂通常会产生具有不同发育命运的两个子细胞。不同的子细胞身份可能源于物理极性和大小不对称本身,以及随后在每个子细胞中激活不同的命运程序。不对称分裂是秀丽隐杆线虫 seam 谱系的一个特征,在后胚胎阶段,一系列类似于干细胞的不对称分裂产生一个分化的前子细胞和一个继续分裂的后子细胞。在这里,我们研究了非肌肉肌球蛋白 II(nmy-2)在这些不对称分裂中的作用。我们表明,nmy-2 似乎不参与产生物理分裂不对称性,但对指定细胞命运的差异仍然很重要。虽然细胞极性似乎正常,并且当 nmy-2 失活时染色体和沟的定位保持不变,但 seam 细胞的丢失是通过后子细胞的不当终端分化发生的。这揭示了 nmy-2 在细胞命运决定中的作用,与它以前与之相关的主要极性决定机制没有明显联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d521/5471188/4ae95026178a/41598_2017_1675_Fig1_HTML.jpg

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