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Title: Control of endoderm development in Caenorhabditis elegans
Author: Clucas, Caroline
ISNI:       0000 0001 3559 2817
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 2003
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The intestine (or gut) of Caenorhabditis elegans consists of 20 cells and is exclusively derived from the E-cell blastomere, by a precise pattern of cell divisions. During post- embryonic development no cell divisions occur in the E-lineage. Instead a nuclear division occurs, such that most cells are binucleate. In addition, endoreduplication occurs once during each larval stage, resulting in a DNA content of 32C in adult intestinal cell nuclei. Although much research has focussed on E-cell specification, not much is known about genes involved in the execution of the E-cell lineage. In this thesis, I have identified and characterised 4 classes of mutants with various E-cell lineage defects. These are mutants with an altered E-cell lineage, a mutant that fails to execute the LI nuclear division, mutants that undergo additional post embryonic nuclear divisions, and a mutant with an abnormal gut morphology. Most of the work in this thesis focussed on the class with an altered E-cell lineage. Two independent genes were identified in this class, Un-60(ij48) and lin-62(ij52), the behaviour of these mutant alleles is genetically very distinct, lin-60 is a maternal gene and ij48 is a gain-of-function allele whereas lin-62 is a zygotic gene and ij52 is a loss-of-function allele. By cell lineage analysis, I showed that extra intestinal cells were generated from the E blastomere in each mutant. Additionally, I have shown that the ij48 lesion creates deregulation of the cell cycle in the E-cell lineage, resulting in a hyperplasia of intestinal cells, while other aspects of intestinal cell function are retained. Using a novel RNA-mediated interference (RNAi) approach, I cloned the wild-type copy of the gene identified by lin-60(ij48) and found that it encoded a previously identified homologue of the cell cycle control gene, Cdc25 (cdc-25.1). While gain of cdc-25.1 created intestinal hyperplasia, loss of the wild-type cdc-25.1 by RNAi caused a failure of proliferation of intestinal and other cell types. I found that the site of the cdc-25.1 mutation in iJ48 mutants identifies a conserved motif However, the distribution of CDC-25.1 protein in ij48 animals does not explain the intestinal hyperplasia.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available