Estradiol Upregulates the Expression of the TGF-β Receptors ALK5 and BMPR2 during the Gonadal Development of Schizothorax prenanti

TGF-β receptors play important roles in mediating TGF-β signals during gonadal development. To identify the functions of TGF-β receptors, including the type I receptor (activin receptor-like kinase 5, ALK5) and type II receptor (bone morphogenetic protein receptor 2, BMPR2), during the gonadal development of S. prenanti, the full-length cDNA sequences of ALK5 and BMPR2 were isolated and characterized. Their expression patterns in developing gonads and in the gonads of exogenous estradiol (E2) -fed fish were analyzed. The cDNAs of ALK5 and BMPR2 were 1925 bp and 3704 bp in length and encoded 501 and 1070 amino acid residues, respectively. ALK5 and BMPR2 were mostly expressed in gonads, particularly in cortical alveoli stage ovaries and mid-spermatogenic stage testes; however, the overall level of BMPR2 mRNA was higher than that of ALK5 during gonadal development. Furthermore, immunohistochemical signals of ALK5 and BMPR2 were mostly detected at chromatin nucleolar oocytes and perinuclear oocytes in ovaries and at spermatocytes and spermatogonia in testes. Exogenous E2 induces the gonadal expression of ALK5 and BMPR2, and BMPR2 is more responsive to E2 than ALK5. These results suggest that ALK5 and BMPR2 might play a potentially vital role in both folliculogenesis and spermatogenesis in S. prenanti.

Comparative Analysis of Streptococcus Agalactiae S03 and S07 Isolated From Schizothorax Prenanti With Different Antibiotic Resistance and Virulence

Streptococcus agalactiae (GBS), is an important Gram-positive pathogen of fish aquaculture worldwide. In this study, we performed a comparative analysis of GBS S03 and S07 isolated from Schizothorax prenanti and explored the association between phenotypic antibiotic resistance as well as virulence and the genomic characteristics. Antimicrobial sensitivity tests on 12 common antibiotics using the disc diffusion method revealed that the S03 showed resistance to seven antibiotics, while S07 showed sensitivity to the tested antibiotics. Pathogenicity analysis demonstrated greater virulence of S07 than S03. Then, the occurrence of antibiotic resistance and virulence genes was identified using whole-genome sequence (WGS) of S03 and S07. There were mefE, tetO, lnuB, lsaE, APH3', and sat-4 resistance genes present only in S03 genome. And just S03 had gyrA and parC genes mutations. In addition to 51 virulence genes in both S03 and S07 genomes, S07 additionally carried virulence genes associated with invasion, such as SAN_1519, rfbA and cylE genes. There was complete concordance between genotypic evidence and phenotypic characteristics. Virulence factors and phylogenetic analysis showed that S03 and human sources shared an extremely close evolutionary relationship. Our findings provide important proof for using WGS as an effective tool of phenotypic predictions of GBS.