egl-32 acts through sperm to regulate egg-laying in Caenorhabditis elegans

• Main Author: McGovern, Marie
• Format: Dissertation
• Language: English
• Subjects: biology, animal physiology; biology, cell; biology, genetics; biology, molecular
• ISBN: 9780542510533; 0542510537

A study of the egg-laying defective mutant, egl-32, in Caenorhabditis elegans has revealed that sperm have an active role in regulating egg-laying. Initially, our lab became interested in studying egl-32 because we believed it interacted directly with a TGF-beta pathway that regulates dauer development. In studying this mutant we hoped we would gain a better understanding of the role of the TGF-beta dauer pathway in egg-laying. We now believe that egl-32 and the TGF-beta pathway only interact indirectly. However, studying the egg-laying defective mutant, egl-32, has lead to the novel finding that sperm have an influence on egg-laying. In an attempt to determine the cellular and anatomical basis for the egl-32's egg laying defect it was found that egl-32 interacts with genes highly expressed in sperm. Here I present evidence that the cellular basis of the egl-32's egg-laying defective phenotype is due to a defect in sperm. I have investigated the possibility that sperm are playing an active role in egg-laying by performing simple mating experiments. These mating experiments have revealed the wild-type sperm can rescue the egg-laying defect of egl-32 mutant animals. Also, introduction of mutant egl-32 sperm into wild-type animals can induce an egg-laying defective phenotype. In an effort to determine the exact location of egl-32 a candidate gene, smn-1 was uncovered. A knockout of smn-1 was obtained and characterized. The knockout is homozygous lethal. Heterozygous animals are egg-laying defective and respond similarly to egl-32 in mating experiments. smn-1 was also determined to interact with the same sperm proteins as egl-32.