Thesis (Ph. D.)--University of Hong Kong.

Thesis--M.D., University of Hong Kong, 1977. / Typescript.

Thesis (M. Phil.)--University of Hong Kong, 1978. / Typewritten.

Thesis (Ph. D.)--University of Hong Kong, 1967. / Typewritten.

Thesis (M. Sc.)--University of Hong Kong, 1969. / Typewritten.

Thesis (M. Med. Sc.)--University of Hong Kong, 2002. / Includes bibliographical references (46-49).

Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2003. / Includes bibliographical references (leaves 197-236). Also available in electronic version. Access restricted to campus users.

All animals must integrate internal and environmental information into an appropriate behavior that ultimately aims to increases fitness. In order to investigate the proximate and ultimate mechanisms underlying adaptive behavior, I examined the role of neuroendocrine molecules at three distinct levels of biological organization. At the level of the individual, I demonstrate that steroid hormone receptors play distinct roles in modulating adaptive behavior, physiology and brain gene expression in dominant and subordinate African cichlid fish. At the level of the social community, I investigate how the behavior and physiology of one individual can affect the behavior, physiology, and brain gene expression of other community members. I found striking covariance patterns that implicate identifiable neuroendocrine pathways as mediators of specific social signals, establishing an important model to investigate the molecular basis of how behavioral phenotypes spread through communities. Finally, I investigate how the neurochemistry of the five major vertebrate classes has changed in a way that covaries with sensory integration, life history, and mating strategy. To address this question, I have laid an important theoretical framework to study the evolution of behavior as well as establishing neuroanatomical brain homologies across vertebrate lineages. I show that variation in where neurochemicals (dopamine, steroids, neuropeptides) are produced in the brain varies across vertebrates while where signals are received (ie receptors) are conserved, providing a novel theory of social brain evolution. In summary, I use a multidisciplinary approach to study hormonal contributions to the proximate and ultimate mechanisms of social behavior on many levels of biological organization and have contributed important novel insights that have significantly increased our understanding of the evolution of behavior and its neural and molecular underpinnings. / text

In the red-eared slider turtle, Trachemys scripta, gonadal sex is determined by the incubation temperature during the mid-trimester of development; temperature effects can be overridden by exogenous ligands if they are administered during the temperature-sensitive period of development. How the physical signal of temperature is transduced into a biological signal that ultimately results in determining gonad sex is not known. My thesis research focuses on five candidate sex determining genes: cyp19a1 (aromatase), Forkhead box protein L2, R-spondin1, Doublesex mab3-related transcription factor 1, and Sex-determining Region on Y chromosome-box 9. The first three genes are markers of ovarian differentiation while the latter two genes are markers of testicular differentiation. Both in ovo (egg) and in vitro (gonadal explants) studies were conducted. Chapters 1 and 2 examine how exogenous steroid ligands interact with candidate genes as the gonads differentiate into testes or ovaries. Topical application of testosterone with aromatase inhibitor to eggs incubating at the female-producing temperature (31 ºC; FPT) suppresses expression of ovarian markers while increasing expression of testicular markers. Administration of 17β-estradiol (E2) to eggs incubating at a male-producing temperature (26 ºC; MPT) increases expression of ovarian markers while testicular markers are suppressed. This suggests that exogenous ligands modify gonadal trajectory by re-directing (suppression and activation) the expression of candidate genes. Chapter 3 identifies the gonad-specific promoter and the temperature-dependent DNA methylation signatures of the aromatase gene during gonadal differentiation. DNA methylation of the aromatase promoter is lowest at FPT relative to MPT. Exogenous E2 and certain polychlorinated biphenyls retain typical methylation patterns observed at MPT (Chapter 4). This suggests that despite the ability of exogenous ligands to alter the transcriptional profiles and gonad phenotypes, the MPT set the temperature typical epigenetic marks first at the beginning of TSP. Recruitment of modified histone proteins, H3K4me3 and H3K27me3, at the aromatase promoter is FPT-specific during gonad determination. Temperature shift experiments suggest a lack of histone enrichment is due to MPT cue, but is not reversible by FPT. Preliminary analysis of modified histones by Next-generation sequencing shows high duplication levels across samples, leaving room for technical improvement in future study.

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