EXPRESSION OF THE GENES FOR ALPHA-INHIBIN, BETA-A INHIBIN AND FOLLISTATIN IN THE OVARIES OF BOOROOLA EWES WHICH WERE HOMOZYGOTES OR NONCARRIERS OF THE FECUNDITY GENE FEC(B)

Ovine cDNA probes for the alpha and beta-A inhibin subunits and for follistatin were used to investigate the mRNA species for these hormones in ovaries obtained during the luteal phase of the oestrous cycle, from Booroola ewes which were homozygous carriers (BB) or noncarriers (++) of the Fec(B) gene. BB ewes had significantly higher concentrations of peripheral FSH and LH immunoreactivity than ++ ewes, but the peripheral inhibin immunoreactivity and ovarian inhibin and progesterone secretion rates were not significantly different between genotypes. No gene-specific differences in the number or size of mRNA transcripts detected by Northern blotting were noted for any of these genes. A single alpha inhibin mRNA species at 1.5 kb was observed in the follicle RNA from ++ and BB ovaries. Low amounts of alpha inhibin hybridization were discerned occasionally in ++ and BB stroma and also in BB, but not in ++, corpora lutea. The beta-A inhibin gene was expressed only in the follicles from both ++ and BB ovaries. At least three beta-A inhibin transcripts were observed; one at 7.5 kb and at least two between 1.4 and 5.0 kb. The follistatin cDNA probe detected two major transcripts at 2.7 and 1.5 kb and a minor band at 0.5 kb in both follicle and corpora lutea RNA. Densitometry of the Northern blots revealed no significant gene-specific differences in the levels of alpha inhibin and follistatin gene mRNA transcripts. However, significantly greater amounts of total beta-A inhibin hybridization were detected in follicle RNA from BB compared with ++ ovaries (P<0.001) and this Fec(B)-specific difference appeared to be associated with the 7.5 kb transcript. We conclude that the Booroola Fec(B) gene does not influence the synthesis of the alpha inhibin subunit or follistatin during the luteal phase of the oestrous cycle, but may affect inhibin or activin synthesis in the ovaries of Fec(B) carriers, by increasing the transcription or stability of the beta-A inhibin mRNA species.