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Date of Award
Thesis - Pacific Access Restricted
Master of Science (M.S.)
First Committee Member
Second Committee Member
Vulval differentiation in Caenorhabditis elegans is a well characterized developmental system in which three vulval precursor cells divide, generating the 22 nuclei that form the functional wild type vulva. Additionally, the combined formation of the vulva and the uterus is a model for organogenesis. Hermaphrodites homozygous for a lin-11 mutation are unable to form a functional vulva due to abnormal mitotic divisions in two of the three vulval precursor cells that contribute cells to the vulva.
Laser microsurgery was used to ablate the two abnormal vulval precursor cells and other vulval precursor cells that could take on their developmental fate. These cells were believed to be responsible for the inability of hermaphrodites homozygous for a lin- 11 mutation to form a functional vulva. The results show that ablated hermaphrodites homozygous for a lin-11 mutation are rarely able to lay eggs, suggesting that there are other defects in the egg-laying apparatus in addition to the vulval precursor cells.
To ensure that the ablated animals did not form a functional vulva and fail to lay eggs due to defects in the neurons regulating egg-laying, ablated lin-11 mutant animals were exposed to serotonin, imipramine or nicotine. These drugs are able to induce egglaying in wild type and ablated wild type animals. Ablated hermaphrodites homozygous for a lin-11 mutation exposed to the drug treatments were not able to lay eggs. Therefore, the abnormal secondary cells are not entirely responsible for the lack of a functional vulva and the inability to lay eggs, suggesting that either uterine cells or other vulval cells are also abnormal.
White, Arron D.. (2000). The role of the C. elegans transcription factor LIN-11 in cell fate specification. University of the Pacific, Thesis - Pacific Access Restricted. https://scholarlycommons.pacific.edu/uop_etds/533
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