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Type of Document	Dissertation
Author	Yu, Hui
URN	etd-11142004-223239
Persistent URL	http://resolver.caltech.edu/CaltechETD:etd-11142004-223239
Title	C. elegans male tail development
Degree	PhD
Option	Biology
Advisory Committee	Advisor Name Title Bruce A. Hay Committee Member David Anderson Committee Member Marianne Bronner-Fraser Committee Member Paul W. Sternberg Committee Member
Keywords	sexual differentiation pattern formation RFX factors Wnt pathway transcriptional regulation
Date of Defense	2004-09-10
Availability	restricted
Abstract The C. elegans hook sensillum is a male copulatory structure developed from the hook sensillum competence group (HCG), P(9-11).p. Male P(9-11).p each adopt one of three potential fates (1º, 2º, or 3º), forming an invariant spatial pattern of 3º-2º-1º. I examined HCG fate specification in various genetic backgrounds and found that both lin-17 Frizzled-like Wnt receptor and bar-1 [beta]-catenin are predominantly expressed in 1º P11.p. Activation of the bar-1 canonical Wnt pathway by a pry-1(Axin) mutation changes the competence of the anterior P(3-8).p cells and induces ectopic 1º HCG fate. I also found that the Hox gene mab-5 acts downstream of the Wnt pathway to determine HCG competence. Ectopic mab-5 expression, in conjunction with activated LIN-12 or EGF signaling, causes ectopic HCG fates in anterior P(1-8).p. Furthermore, epistatic interactions between lin-17 and lin-12 showed that generation of 2º HCG fate in P10.p by LIN-12/Notch activity depends on LIN-17-mediated Wnt signaling. Together these observations suggest that Wnt signaling is the major player that governs HCG patterning and functions in HCG competence, specification, and execution. Precise execution of the 2º HCG lineage leads to generation of all five major components of a functional hook sensillum that mediates vulva location behavior during male mating. Both sensory neurons of the hook sensillum, HOA and HOB, are necessary for efficient vulva location. From a genetic screen for altered expression of an HOB marker ceh-26::gfp or abnormal hook morphology, I isolated five mutants. Further analysis of one of these mutants identified an allele of egl-46, a zinc-finger transcription factor. EGL-46, and to some extent, another transcription factor EGL-44, regulate a group of HOB-specific genes. These targets include the homeodomain protein CEH-26, a neuropeptide-like protein NLP-8, a degenerin homologue T28F4.2, and two C. elegans polycystin homologs LOV-1 and PKD-2. Both egl-46 and egl-44 mutants exhibit defective vulva location behavior, suggesting impaired HOB function. The regulator of a general ciliogenic pathway, DAF-19, indirectly affects expression of HOB-specific genes. Expression of DAF-19, EGL-46, and EGL-44 is independent from one another, indicating that general and cell-specific regulatory factors act in parallel to produce cell specificities crucial for HOB sensory function.
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