Stat5b Regulates Sexually Dimorphic Gene Expression in Zebrafish Liver

Abstract

Sexual size dimorphism is an interesting phenomenon occurred in many fish species. Wildtype zebrafish exhibits a significant sexual dimorphism in body size at the adult stage. Previous studies indicated that sexual size dimorphism was eliminated in stat5b-mutated zebrafish. Herein, the comparative transcriptome analysis was conducted to observe the genes and pathways involved in sexual size dimorphism. The number of male-biased and female-biased genes was much less in the liver of stat5b mutant zebrafish than in wildtype. Gene ontology (GO) enrichment and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis indicated that multiple pathways related to metabolism were affected upon loss of stat5b function. qRT-PCR results also validated that sexually dimorphic expression of a set of genes was lost when stat5b was mutated. Furthermore, the weighted correlation network analysis (WGCNA) detected many candidate genes related to the growth traits and stat5b function, such as greb1, lepr, and igf2b. Our data suggest that stat5b should regulate the sexually dimorphic gene expression in zebrafish liver and add in understanding of the molecular mechanisms underlying sexual size dimorphism in fish species.

Transcriptome analysis provides insights into differentially expressed genes and long noncoding RNAs involved in sex‐related differences in Amur sturgeon (Acipenser schrenckii)

“…The male‐specific pattern of liver gene expressions, for example, the male expression pattern of intermittent plasma GH and cytochrome P‐450 (CYP) have been observed in rat, and the STAT5b is required in this process (Park & Waxman, ). In zebrafish, the number of male‐biased and female‐biased genes was much less in the liver of Stat5b mutant individuals than in wild‐type and it suggested that Stat5b should regulate the sexually dimorphic gene expression in zebrafish liver (Huang et al, ). CYP belongs to a superfamily of proteins that contain a heme cofactor and STAT5 binding sites were identified in the 5′‐flank of the adult male‐expressed genes CYP2A2 , CYP4A2, and CYP2C11 (Park & Waxman, ).…”

“…Meanwhile, the transcriptome analysis of testes and ovaries from A. schrenckii had also been reported (Jin et al, ). Furthermore, Huang, Xiong, Kang, Mei, and Gui () found that some genes in the liver could also regulate sexually dimorphic in zebrafish. Especially, during the reproductive phase, the liver is one of the most sexually dimorphic organs, because of the different metabolic demands between the two sexes (Roy & Chatterjee, ).…”

“…Meanwhile, the transcriptome analysis of testes and ovaries from A. schrenckii had also been reported (Jin et al, 2015). Furthermore, Huang, Xiong, Kang, Mei, and Gui (2018) found that some genes in the liver could also regulate sexually dimorphic in zebrafish.…”

“…number of male-biased and female-biased genes was much less in the liver of Stat5b mutant individuals than in wild-type and it suggested that Stat5b should regulate the sexually dimorphic gene expression in zebrafish liver (Huang et al, 2018). CYP belongs to a superfamily of proteins that contain a heme cofactor and STAT5 binding sites were identified in the 5′-flank of the adult male-expressed genes CYP2A2, CYP4A2, and CYP2C11 (Park & Waxman, 2001).…”

Roles of Estrogens in the Healthy and Diseased Oviparous Vertebrate Liver

“…For instance, there is a significant body size difference between males and females in the adult zebrafish, which is not observed in stat5b -mutated fishes [ 44 ]. Interestingly, comparative whole transcriptome analysis in liver showed that the number of female-biased and male-biased genes was much lower in stat5b mutant zebrafish than in wild-type animals [ 45 ]. Several metabolic pathways were affected upon stat5b mutation, and the expression of candidate genes related to the growth traits and stat5b function, such as greb1 (growth regulating estrogen receptor binding 1—an estrogen receptor-regulated tumor promoter), lepr (leptin receptor—involved in the regulation of body weight), and igf2b (insulin-like growth factor 2b—diverse functions in organ development) was modified.…”