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

被引:5
|
作者
Ding, Siyu Serena [1 ,2 ,3 ]
Woollard, Alison [1 ]
机构
[1] Univ Oxford, Dept Biochem, South Parks Rd, Oxford OX1 3QU, England
[2] Imperial Coll London, Inst Clin Sci, Fac Med, Du Cane Rd, London W12 0NN, England
[3] MRC London Inst Med Sci LMS, Hammersmith Hosp Campus,Du Cane Rd, London W12 0NN, England
来源
SCIENTIFIC REPORTS | 2017年 / 7卷
基金
英国惠康基金; 英国生物技术与生命科学研究理事会;
关键词
ANTERIOR-POSTERIOR POLARITY; CBF-BETA HOMOLOG; C-ELEGANS; ASYMMETRIC DIVISIONS; WNT; PROTEIN; PROLIFERATION; ESTABLISHMENT; KINASE; CENTRALSPINDLIN;
D O I
10.1038/s41598-017-01675-7
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页数:13
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