Epidermal Function in the Nematode, Caenorhabditis elegans

McMahon, Laura Mary (1999) Epidermal Function in the Nematode, Caenorhabditis elegans. PhD thesis, University of Glasgow.

Abstract

Epithelial sheets create the forces which shape embryos during the development of all metazoans. The external epithelia, or hypodermis, of the nematode Caenorhabditis elegans plays an essential role in shape change during embryogenesis and also maintains body shape during postembryonic development. Embryonic shape change, known as elongation, is mediated by actin microfilaments in the hypodermis which align circumferentially and contract, causing the embryo to change from a ball of cells, to a long, thin worm shape. A prerequisite to elongation is the migration of the hypodermis around the embryo from the dorsal surface to completely cover the embryo in a layer of hypodermal cells, a process known as enclosure. At the end of embryogenesis, the hypodermis secretes a multi-layered, collagenous exoskeleton, known as the cuticle, which maintains the elongated worm shape postembryonically. In this thesis, I have characterised three elongation-defective mutants which arrest during embryogenesis, and have also looked at the pattern of a cuticular collagen, DPY-7, throughout development using a novel monoclonal antibody, DPY7-5a. One of the embryonic lethal mutations, w4, lies on Chromosome I, between positions 6.2 and 9.9 on the genetic map. The majority of w4 homozygotes are defective in enclosure. The other two embryonic lethal mutations, ijDf1 and ijDf2 are the result of large deficiencies which have been physically mapped. ijDf2 extends from around position -0.9 to 0.7 on chromosome V and is approximately 2.2Mb in size. ijDf1 homozygotes appear to have a pre-enclosure defect in cell adhesion. ijDf1 extends from around position 18 to 23.5 on the X chromosome and is approximately 1.6Mb in size. ijDf1 homozygotes arrest as 1.5-fold stage embryos and this early elongation defect was rescued by injection of the genomic overlap of cosmids K09A9 and K09E9, plus the whole of cosmid C02C6. However, inhibition of the function of predicted genes contained in these cosmids did not produce the mutant phenotype seen in the deficiency. The characterisation of the DPY7-5a antibody suggests localisation of DPY-7 in the cortical layer of the cuticle. The study of the antibody pattern in a dpy-7 mutant demonstrates a clear reduction in secreted DPY-7. These results suggest that there are many molecular components in the complex process of embryonic elongation and the DPY7-5a antibody provides a novel mechanism to study postembryonic shape change and mechanisms of cuticle organisation within the hypodermis.

• Item Type: Thesis (PhD)
• Qualification Level: Doctoral
• Additional Information: Adviser: Iain Johnstone
• Keywords: Parasitology
• Date of Award: 1999
• Depositing User: Enlighten Team
• Unique ID: glathesis:1999-75391
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 19 Nov 2019 20:19
• Last Modified: 19 Nov 2019 20:19
• URI: https://theses.gla.ac.uk/id/eprint/75391