A genetic and molecular analysis of spermiogenesis initiationin Caenorhabditis elegans

Persistent Link:
http://hdl.handle.net/10150/290524
Title:
A genetic and molecular analysis of spermiogenesis initiationin Caenorhabditis elegans
Author:
Muhlrad, Paul Jay
Issue Date:
2001
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
How do cells acquire and regulate their specialized forms and functions? This is the fundamental question underlying the experiments described in this dissertation. To examine this question, I have peered deeply into an exquisitely specialized cell from a genetically tractable organism: the spermatozoon of the nematode, Caenorhabditis elegans. C. elegans sperm orchestrate a fantastic morphogenetic transformation under severe constraints of time and cellular resources. In response to an external signal, spermatids reorganize their membranes and cytoskeleton to form crawling spermatozoa. This maturation, termed spermiogenesis, ensues without any new gene expression. To better understand this signaling pathway, I isolated suppressors of a mutation in spe-27, another gene in the pathway. These suppressors are described in Chapters II and III. The suppressors bypass the requirement for spe-27 and three other genes in this pathway, spe-8, -12, and -29. Eighteen of the suppressors are new alleles of spe-6, a previously characterized gene required for an early stage of spermatogenesis. The original spe-6 alleles are loss-of-function mutations, which prevent Major Sperm Protein assembly into fibrous body-membranous organelles of spermatocytes, and arrest development in meiosis. I isolated the spe-6 gene, and found that it encodes a predicted protein-serine/threonine kinase, similar to casein kinase 1. The suppressors appear to be reduction-of-function mutations. I propose a model whereby SPE-6, along with its role in spermatocyte development, inhibits spermiogenesis until the activation signal is received. The signal is transduced through SPE-8, -12, -27, and -29 to relieve SPE-6 repression, triggering the formation of spermatozoa. Chapter IV describes continuing efforts to understand the spermiogenesis signaling pathway by identifying the spe-8 gene. To find spe-8 I exploited spermatogenesis-specific gene expression data obtained through microarray technology. SPE-8, like SPE-6, is a protein kinase, but of the non-receptor protein tyrosine kinase class. I identified mutations in all but one of the spe-8 mutants. Most are in the kinase domain; one is in an associated protein-binding (SH2) domain. Both SPE-6 and SPE-8 are members of large multigene families in C. elegans, many members of which appear to be spermatogenesis-specific or enriched. I discuss this and other ramifications of my research in Chapter V.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Biology, Molecular.; Biology, Genetics.; Biology, Cell.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Molecular and Cellular Biology
Degree Grantor:
University of Arizona
Advisor:
Ward, Samuel

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleA genetic and molecular analysis of spermiogenesis initiationin Caenorhabditis elegansen_US
dc.creatorMuhlrad, Paul Jayen_US
dc.contributor.authorMuhlrad, Paul Jayen_US
dc.date.issued2001en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractHow do cells acquire and regulate their specialized forms and functions? This is the fundamental question underlying the experiments described in this dissertation. To examine this question, I have peered deeply into an exquisitely specialized cell from a genetically tractable organism: the spermatozoon of the nematode, Caenorhabditis elegans. C. elegans sperm orchestrate a fantastic morphogenetic transformation under severe constraints of time and cellular resources. In response to an external signal, spermatids reorganize their membranes and cytoskeleton to form crawling spermatozoa. This maturation, termed spermiogenesis, ensues without any new gene expression. To better understand this signaling pathway, I isolated suppressors of a mutation in spe-27, another gene in the pathway. These suppressors are described in Chapters II and III. The suppressors bypass the requirement for spe-27 and three other genes in this pathway, spe-8, -12, and -29. Eighteen of the suppressors are new alleles of spe-6, a previously characterized gene required for an early stage of spermatogenesis. The original spe-6 alleles are loss-of-function mutations, which prevent Major Sperm Protein assembly into fibrous body-membranous organelles of spermatocytes, and arrest development in meiosis. I isolated the spe-6 gene, and found that it encodes a predicted protein-serine/threonine kinase, similar to casein kinase 1. The suppressors appear to be reduction-of-function mutations. I propose a model whereby SPE-6, along with its role in spermatocyte development, inhibits spermiogenesis until the activation signal is received. The signal is transduced through SPE-8, -12, -27, and -29 to relieve SPE-6 repression, triggering the formation of spermatozoa. Chapter IV describes continuing efforts to understand the spermiogenesis signaling pathway by identifying the spe-8 gene. To find spe-8 I exploited spermatogenesis-specific gene expression data obtained through microarray technology. SPE-8, like SPE-6, is a protein kinase, but of the non-receptor protein tyrosine kinase class. I identified mutations in all but one of the spe-8 mutants. Most are in the kinase domain; one is in an associated protein-binding (SH2) domain. Both SPE-6 and SPE-8 are members of large multigene families in C. elegans, many members of which appear to be spermatogenesis-specific or enriched. I discuss this and other ramifications of my research in Chapter V.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectBiology, Molecular.en_US
dc.subjectBiology, Genetics.en_US
dc.subjectBiology, Cell.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMolecular and Cellular Biologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorWard, Samuelen_US
dc.identifier.proquest3023500en_US
dc.identifier.bibrecord.b4195757xen_US
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