High impact information on FST

• Molecular characterization of Xenopus embryo heparan sulfate. Differential structural requirements for the specific binding to basic fibroblast growth factor and follistatin [1].
• Follistatin and a BMP6 neutralizing antibody, which antagonized the anti-apoptotic effects of BMP15 and BMP6, respectively, whether alone or combined, blocked approximately 50% of the anti-apoptotic actions of oocytes [2].
• When we tested the TGF-beta effect on FS mRNA in different granulosa cell states, TGF-beta1 regulation was associated with progesterone production only in freshly isolated cells [3].
• Transforming growth factor beta1 regulates follistatin mRNA expression during in vitro bovine granulosa cell differentiation [3].
• The specificity of the BMP response was further explored by coincubating cells with BMPs and several potential BMP antagonists, chordin, gremlin, and follistatin [4].

Biological context of FST

• Complete bovine follistatin cDNA coding sequences are presented including 1,029 bases of open reading frame, the 5' translational start codon, and the 3' translational stop codon [5].
• Estimation of population subdivision using Wright's FST index showed that the average proportion of genetic variation explained by breed differences was 9% [6].
• Our results suggest a slightly higher population differentiation across the candidate genes (FST = 0.108) than across microsatellites (FST = 0.095), possibly because of selection and stochastic effects [7].
• Based on Wright's F-statistics, 4 loci were discarded, and the remaining 15 loci (FIT = 0.101, FST = 0.089, and FIS = 0.013) were used to compute the likelihood that each multilocus genotype of the total sample was drawn from its true breed instead of another breed [8].
• Moreover, the binding protein was shown to inhibit the spontaneous FSH release from cultured pituitary cells as does follistatin [9].

Anatomical context of FST

• We showed a positive regulation of FS mRNA after TGF-beta1 (1 ng/ml) treatment of freshly isolated granulosa cells from small-medium antral follicles (2-8 mm) [3].
• Follistatin had a dose-dependent inhibitory effect on blastocyst yield from COCs (67% reduction, p < 0.05) and opposed the stimulatory effect of activin (p < 0.05) [10].
• In summary, the degree of immunohistochemical expression of follistatin was phase specific for both follicles and corpora lutea [11].
• In contrast, addition of 1-100 ng/ml follistatin significantly reduced the percentage of zygotes developing to morulae and blastocysts (29-31% and 17-20%, respectively) compared with no addition (41% and 28%, respectively) [12].
• Follistatin was distributed in the perinuclear cytoplasm of granulosa and luteal cells but not in theca cells [11].

Associations of FST with chemical compounds

• Each protein was found to have the same NH2-terminus and its sequence was identical to that of follistatin, which is a specific inhibitor of identical to that of follistatin, which is a specific inhibitor of FSH release [9].
• Between 48-96 h and 96-144 h, FSH promoted (P < 0.0001) increases in output of inh A (6-fold), act A (15-fold), FS (6-fold), and E2 (18-fold), with maximal responses (in parentheses) elicited by 0.33 ng/ml FSH during the final period [13].
• Addition of oocytes to FSH-stimulated cells dose-dependently suppressed (P < 0.0001) inh A (6-fold maximum suppression), act A (5.5-fold), FS (3.6-fold), E(2) (4.6-fold), and P(4) (2.4-fold), with suppression increasing with FSH dose [14].
• Neither progesterone nor mifepristone affected inhibin A, activin A or follistatin production [15].
• Treatment with testosterone, but not dihydrotestosterone, decreased (P < 0.05) endogenous follistatin and increased (P < 0.05) the activin A:follistatin ratio in maturation medium [15].

Other interactions of FST

• Follistatin was not detectable in the corpus luteum during metestrus (Day 3 postovulation) or proestrus (Day >/= 17 postovulation) [11].
• Pituitary follicular cells secrete both vascular endothelial growth factor and follistatin [16].
• These results suggest that myostatin inhibits bovine preadiopocyte differentiation through suppressing PPARgamma and C/EBPalpha mRNA expressions and that follistatin counteracts the suppressive effect of myostatin [17].
• The dominant follicle (DF) is distinguishable from other subordinate follicles by its enhanced capacity to produce oestradiol, maintenance of low intrafollicular concentrations of insulin-like growth factor binding proteins-2, -4 and -5 and follistatin and an increase in free intrafollicular concentrations of IGF-I as well as an increase in size [18].

Analytical, diagnostic and therapeutic context of FST

• Stoichiometric inhibition as shown by gel filtration analysis indicates that activin-binding protein binds activin to form an inactive equimolar complex having neither stimulatory nor inhibitory activity for FSH secretion by the pituitary [9].
• Although these cells showed a similar effect on FS mRNA expression after treatment with activin-A, a soluble form of activin receptor type IIA was unable to inactivate the TGF-beta effect [3].
• A sensitive and specific heterologous radioimmunoassay for FSH-suppressing protein (FSP or follistatin) was applied to ovine plasma [19].
• Immunoassays were used to measure total FS, act-A, inh-A, oestradiol (E) and progesterone (P) levels; immunoblotting was used to quantify the relative abundance of different FS isoforms [20].
• Active immunization against follistatin and its effect on FSH, follicle development and superovulation in heifers [21].

References