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Add To Calendar 20/02/2017 15:30:0020/02/2017 15:50:00America/ChicagoAquaculture America 2017GENOMIC REGULATION AND EPIGENOMIC MODIFICATION OF SEXUAL SIZE DIMORPHISM IN FISH   Room 11The World Aquaculture Societyjohnc@was.orgfalseanrl65yqlzh3g1q0dme13067DD/MM/YYYY

GENOMIC REGULATION AND EPIGENOMIC MODIFICATION OF SEXUAL SIZE DIMORPHISM IN FISH  

Han-Ping Wang, Zhi-Gang Shen, Hong Yao, Paul O'Bryant, and Dean Rapp
Aquaculture Genetics and Breeding Laboratory, The Ohio State University South Centers, 1864 Shyville Rd, Piketon, OH, USA, 45661, wang.900@osu.edu

Sexual size dimorphism (SSD) has been the most common phenotypic dimorphism across taxa. Because sex chromosomes are the only portions of the genome that differ between males and females, theory has long suggested that the development of SSD is facilitated by the chromosomes. Contrarily, our recent studies showed that hormonal-induced neo-males with female genotype (XX♂) and normal males (XY♂) exhibited no SSD in yellow perch, where females naturally grow much fast and larger than females. Why are phenotypic traits correlated with phenotypic sex instead of genotype (chromosomes) sex of an organism? Does steroid exposure in early life epigenetically modulate subsequent gene expression which in turn regulates lifetime SSD?  What is the mechanism of sex-bias gene regulation of this nature and fish SSD evolution in general?

Yellow perch display a distinct SSD pattern, and females outgrow males from 8-11 cm total length. Yellow perch have an XY mating system. Uniquely, yellow perch females only have one ovary, and thus sex-reversed neo-males develop a single testis also. Contrary to the prevailing view that slower growth of one sex in species is due to earlier maturation, our preliminary data indicates that female perch growing faster and bigger is not because females mature late; instead, early/year-1 maturing females (Type 1♀) grow much faster and bigger than males and late or year-2 maturing females (Type 2♀), and that males and late/year-2 maturing females have similar growth and mean size. The overall goal of the proposed project is to unravel the nature and mechanisms of SSD by integrating phenotypic experiments, genomic, epigenomic, and physiological approaches. Specifically, we will address the following objectives and hypotheses:

1) Sex-biased or sex-specific gene expression is partially responsible for SSD.

2) The magnitude of sexual dimorphism in the phenotype is associated with the magnitude of sex-biased expression;

3)      The differences in sex-biased or sex-specific gene expression are associated with or the results from estrogen-mediated regulation.

4)      Steroid exposure during the critical period of sexual differentiation can epigenetically modulate subsequent hormonal responses and gene expression

5)      Epigenetically-modulated hormonal responses and gene expression in turn regulates SSD throughout the lifespan.

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