Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions

<p>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 switc...

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Detaylı Bibliyografya
Yazar: Ding, S
Diğer Yazarlar: Woollard, A
Materyal Türü: Tez
Baskı/Yayın Bilgisi: 2015
Konular:
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author Ding, S
author2 Woollard, A
author_facet Woollard, A
Ding, S
author_sort Ding, S
collection OXFORD
description <p>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. <em>elegans</em> zygote, the C. <em>elegans</em> Q neuroblast, and the <em>Drosophila</em> neuroblast systems. In addition to being an essential player in cytokinesis, <em>nmy</em>-2's roles in cell adhesion and migration processes further underline its potential as a regulator of seam cell asymmetric divisions.</p> <p>In this thesis work, I investigated the role of NMY-2 in C. <em>elegans</em> seam cell divisions. I found that <em>nmy</em>-2 is expressed in the seam and its protein localization is dynamic during SC divisions. Post-embryonic <em>nmy</em>-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 <em>nmy</em>-2 knockdown, cytokinesis defects are not the only cause of SC losses. <em>nmy</em>-2 also does not appear to regulate SC divisions by affecting spindle positioning. In summary, <em>nmy</em>-2 function is crucial to ensure the proper division and fate specification in post-embryonic SC development.</p>
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spelling oxford-uuid:5b5cb805-327a-4a58-b3db-3787f5264efc2022-03-26T17:21:39ZElucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisionsThesishttp://purl.org/coar/resource_type/c_db06uuid:5b5cb805-327a-4a58-b3db-3787f5264efccell biologydevelopmental biologyORA Deposit2015Ding, SWoollard, A<p>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. <em>elegans</em> zygote, the C. <em>elegans</em> Q neuroblast, and the <em>Drosophila</em> neuroblast systems. In addition to being an essential player in cytokinesis, <em>nmy</em>-2's roles in cell adhesion and migration processes further underline its potential as a regulator of seam cell asymmetric divisions.</p> <p>In this thesis work, I investigated the role of NMY-2 in C. <em>elegans</em> seam cell divisions. I found that <em>nmy</em>-2 is expressed in the seam and its protein localization is dynamic during SC divisions. Post-embryonic <em>nmy</em>-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 <em>nmy</em>-2 knockdown, cytokinesis defects are not the only cause of SC losses. <em>nmy</em>-2 also does not appear to regulate SC divisions by affecting spindle positioning. In summary, <em>nmy</em>-2 function is crucial to ensure the proper division and fate specification in post-embryonic SC development.</p>
spellingShingle cell biology
developmental biology
Ding, S
Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title_full Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title_fullStr Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title_full_unstemmed Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title_short Elucidating the role of non-muscle myosin II in Caenorhabditis elegans stem-like seam cell divisions
title_sort elucidating the role of non muscle myosin ii in caenorhabditis elegans stem like seam cell divisions
topic cell biology
developmental biology
work_keys_str_mv AT dings elucidatingtheroleofnonmusclemyosiniiincaenorhabditiselegansstemlikeseamcelldivisions