Bovine FSH(Follicle Stimulating Hormone) ELISA Kit

To select new Large White line with high number of piglets born, genotypes of estrogen receptor (ESR), the follicle stimulating hormone b subunit (FSHb), catenin alpha like 1 (CTNNAL1) and miR-27a were tested in 472 Large White sows. The associations of different genotypes with litter size traits were also studied. The results showed ESRBB and FSH beta(BB) sows produced 0.41-1.49 more pigs per litter (p<.05) for total number born (TNB) and number born alive (NBA) than did other corresponding genotypes. TNB of CTNNAL1(CG) sows is 0.50 more pigs per litter (p<.05) than that of CTNNAL1(GG) sows with the dominance effect of 0.25 pigs per litter (p<.05). miR-27aBB sows had a less estimated breeding value (EBV) to TNB and had a more number of mummified pigs (NM) than did miR-27aAA or miR27aAB sows (p<.05). Therefore, ESRB, FSH beta(B), CTNNAL1(G), miR-27a(A) allele was favorable for litter size traits. Furthermore, combined genetic effect analysis showed ESRAAFSH beta(BB), ESRAACTNNAL1(CG), ESR(AA)miR-27a(AA), FSH beta(BB)CTNNAL1(CC), FSH beta(BB)miR-27a(AA) and CTNNAL1(CG) miR-27a(AB) was the favorable combined genotype for litter size traits. These results identified favorable alleles and genotypes for litter size traits and suggested a potential selection scheme for litter size in Large White pigs.

Reproductive function is controlled by the pulsatile release of hypothalamic gonadotropin-releasing hormone (GnRH), which regulates the expression of the gonadotropins luteinizing hormone and FSH in pituitary gonadotropes. Paradoxically, Fshb gene expression is maximally induced at lower frequency GnRH pulses, which provide a very low average concentration of GnRH stimulation. We studied the role of secreted factors in modulating gonadotropin gene expression. Inhibition of secretion specifically disrupted gonadotropin subunit gene regulation but left early gene induction intact. We characterized the gonadotrope secretoproteome and global mRNA expression at baseline and after G alpha(s) knockdown, which has been found to increase Fshb gene expression (1). We identified 1077 secreted proteins or peptides, 19 of which showed mRNA regulation by GnRH or/and G alpha(s) knockdown. Among several novel secreted factors implicated in Fshb gene regulation, we focused on the neurosecretory protein VGF. Vgf mRNA, whose gene has been implicated in fertility (2), exhibited high induction by GnRH and depended on G alpha(s). In contrast with Fshb induction, Vgf induction occurred preferentially at high GnRH pulse frequency. We hypothesized that a VGF-derived peptide might regulate Fshb gene induction. siRNA knockdown or extracellular immunoneutralization of VGF augmented Fshb mRNA induction by GnRH. GnRH stimulated the secretion of the VGF-derived peptide NERP1. NERP1 caused a concentration-dependent decrease in Fshb gene induction. These findings implicate a VGF-derived peptide in selective regulation of the Fshb gene. Our results support the concept that signaling specificity from the cell membrane GnRH receptor to the nuclear Fshb gene involves integration of intracellular signaling and exosignaling regulatory motifs.