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.
Highlights
Asymmetric cell division generates two daughters that adopt distinct fates, a fundamental process in developmental biology that allows a single fertilised cell to give rise to a multi-cellular organism with diverse cell types[1,2,3]
We investigated the role of nmy-2 in C. elegans seam cell asymmetric divisions
We found that knocking down nmy-2 post-embryonically using a combination of RNA interference (RNAi) and ts mutations caused progressive seam cell loss after asymmetric divisions
Summary
Asymmetric cell division generates two daughters that adopt distinct fates, a fundamental process in developmental biology that allows a single fertilised cell to give rise to a multi-cellular organism with diverse cell types[1,2,3]. The term “asymmetrical cell division” itself encompasses multiple levels of asymmetry, including physical size asymmetry as well as downstream differential fate specification These two aspects of the division are linked yet somewhat separable. At the beginning of the second larval stage, V lineage seam cells undergo a single symmetric division (L2.1 division) before the L2 asymmetric division (L2.2 division) This symmetric division generates two proliferative seam daughters, thereby expanding the number of seam cells to 164. The V lineage cells undergo L1, L2.2, L3 and L4 asymmetric divisions (white lines) as well as the L2.1 symmetric division (brown lines) during larval development to generate a total of 16 terminal seam cells per side, which fuse to form a seam syncytium in adulthood, whilst contributing hypodermal cells to the hyp[7] syncytium to allow the worm to grow in size. During the L2.1 symmetrical seam cell division in which both daughters adopt the proliferative fate, POP-1 and WRM-1 asymmetry are still observed[17, 18]
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