Caenorhabiditis elegans seam cells (SC) are multipotent neuroectodermal cells that undergo both symmetrical and asymmetrical divisions throughout larval development, thus providing a valuable model system to gain mechanistic insights into the regulation of asymmetric divisions and the switch between the symmetric and asymmetric modes of division. Reiterative SC asymmetric division typically produces a differentiative anterior daughter that moves out of the seam line and joins the hyp7 syncytium and a proliferative posterior daughter that retains seam fate and carries on dividing. Non-muscle myosin II (NMY II) has emerged as a key regulator in the asymmetric divisions of the C. elegans zygote, the C. elegans Q neuroblast, and the Drosophila neuroblast systems. In addition to being an essential player in cytokinesis, nmy-2's roles in cell adhesion and migration processes further underline its potential as a regulator of seam cell asymmetric divisions. In this thesis work, I investigated the role of NMY-2 in C. elegans seam cell divisions. I found that nmy-2 is expressed in the seam and its protein localization is dynamic during SC divisions. Post-embryonic nmy-2 knockdown using a combination of temperature sensitive mutants and RNA interference robustly reduces terminal SC number. This reduction is due to progressive SC loss after each asymmetric division as a consequence of aberrant cell fate determination. I identified three classes of cell fate transformation phenotypes following nmy-2 knockdown, and sought to dissect the cell molecular basis of these phenotypes using a dual-color fate reporter strain. Although prevalent in nmy-2 knockdown, cytokinesis defects are not the only cause of SC losses. nmy-2 also does not appear to regulate SC divisions by affecting spindle positioning. In summary, nmy-2 function is crucial to ensure the proper division and fate specification in post-embryonic SC development.</p
