@article{PAR00008489, title = {{P}ituitary gonadotropins {FSH} and {LH} are oppositely regulated by the activin/follistatin system in a basal teleost, the eel}, author = {{A}roua, {S}. and {M}augars, {G}. and {J}eng, {S}. {R}. and {C}hang, {C}. {F}. and {W}eltzien, {F}. {A}. and {R}ousseau, {K}. and {D}ufour, {S}ylvie}, abstract = {{E}uropean eels are blocked at a prepubertal silver stage due to a deficient production of pituitary gonadotropins. {W}e investigated the potential role of activin/follistatin system in the control of eel gonadotropins. {T}hrough the development of q{PCR} assays for {E}uropean eel activin beta({B}) and follistatin, we first analyzed the tissue distribution of the expression of these two genes. {B}oth activin beta({B}) and follistatin are expressed in the brain, pituitary and gonads. {I}n addition, a striking expression of both transcripts was also found in the retina and in adipose tissue. {T}he effects of recombinant human activins and follistatin on eel gonadotropin gene expression were studied using primary cultures of eel pituitary cells. {A}ctivins {A} and {B} strongly stimulated {FSH} beta subunit expression in a time- and dose-dependent manner. {I}n contrast, activin reduced {LH} beta expression, an inhibitory effect which was highlighted in the presence of testosterone, a known activator of eel {LH} beta expression. {N}o effect of activin was observed on other pituitary hormones. {F}ollistatin antagonized both the stimulatory and inhibitory effects of activin on {FSH} beta and {LH} beta expression, respectively. {A}ctivin is the first major stimulator of {FSH} expression evidenced in the eel. {T}hese results in a basal teleost further support the ancient origin and strong conservation of the activin/follistatin system in the control of {FSH} in vertebrates. {I}n contrast, the opposite regulation of {FSH} and {LH} may have emerged in the teleost lineage.}, keywords = {{A}ctivin ; {F}ollistatin ; {P}ituitary hormones ; {A}nguilla ; {T}eleost}, journal = {{G}eneral and {C}omparative {E}ndocrinology}, volume = {175}, numero = {1}, pages = {82--91}, ISSN = {0016-6480}, year = {2012}, DOI = {10.1016/j.ygcen.2011.10.002}, URL = {http://www.documentation.ird.fr/hor/{PAR}00008489}, }