Sexual size dimorphism (SSD) has been the most common phenotypic dimorphism across taxa and theory has long suggested that the SSD is facilitated by chromosomes. However, 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 significantly fast and larger than males. 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? The aim of this project is to unravel the nature and mechanisms of SSD by integrating phenotypic experiments, genomic, epigenomic, and physiological approaches.
The whole genome of a XX genotype female yellow perch was sequenced using Illumina and PacBio platforms. We adopted hybrid assembly strategy to improve the assembly quality with the Illumina short and PacBio long reads. A total of 1326 high quality contigs were obtained, with 1.33 Gb in length and 2.8 Mb of N50. Of these, a total of 531.68 Mb (39.79 %) repeat sequences were identified and 45,608 consensus protein-coding genes were predicted in yellow perch genome. As a result, 43,296 predicted genes (94.93%) were successfully annotated. Using the genome as a reference, RNA-seq and related analysis of 96 samples of large females (LF), small females (SF) and regular males (RM) were performed. PCA plotting of three groups in liver showed that the SF was much closer to RM instead of LF, indicating that the gene expression patterns of liver in SF and RM were similar. Furthermore, it could be inferred that the growth rates of these two groups may be related to the gene regulation. Hormonal analysis of the three groups showed similar patterns. We also conducted RNA-Seq and hormonal analysis of males, females and neo-males and results showed that steroid exposure during the critical period of sexual differentiation could epigenetically modulate subsequent hormonal responses and gene expression. In addition, we performed BS-seq of the males, females and neo-males to exam how epigenetically-modulated hormonal responses and gene expression regulates SSD throughout the lifespan. The female samples showed different methylation patterns with the other two groups, and the numbers of C methylated in CpG context in female are much lower than neomales and males. These results support our hypotheses: 1) Sex-biased or sex-specific gene expression is partially responsible for SSD; 2) The differences in sex-biased or sex-specific gene expression are associated with or the results from estrogen-mediated regulation; 3) Steroid exposure during the critical period of sexual differentiation can epigenetically modulate subsequent hormonal responses and gene expression; and 4) Epigenetically-modulated hormonal responses and gene expression in turn regulates SSD throughout the lifespan.