High impact information on 17,10beta-P

• Like 17alpha,20beta-DP, cytochalasin B (10 microg/ml) induced both complete dispersion of the aggregation and translational activation of cyclin B mRNA, forcing the oocytes to undergo GVBD without 17alpha,20beta-DP [1].
• When oocytes were treated with 17alpha,20beta-DP, a meshwork of microfilaments in the oocyte cortex disappeared and the aggregation of cyclin B mRNA dispersed just prior to the initiation of cyclin B synthesis and germinal vesicle breakdown (GVBD) [1].
• These results, which are identical to those in goldfish, strongly suggest that cyclin B is synthesized from stored (masked) mRNA after 17alpha,20beta-DP stimulation and that its binding to the preexisting cdc2 allows cdk7 to activate MPF [2].
• To know the reason growing oocytes fail to mature upon 17alpha,20beta-DP treatment, we investigated changes in the components of machinery responsible for MPF activation during zebrafish oogenesis [2].
• When treated with 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP), a natural maturation-inducing hormone in fishes, fully grown zebrafish oocytes are induced to mature via the activation of the maturation-promoting factor (MPF), which consists of cdc2 (a catalytic subunit) and cyclin B (a regulatory subunit) [2].

Biological context of 17,10beta-P

• Therefore, the unresponsiveness of growing oocytes to 17alpha,20beta-DP is attributable to a deficiency in the processes leading to cyclin B synthesis, which include 17alpha,20beta-DP reception on the oocyte surface, subsequent signal transduction pathways, and unmasking the stored cyclin B mRNA [2].
• A cDNA encoding a nuclear 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP, spermiation-inducing hormone in fish) receptor (DPR) was, for the first time, isolated from an eel testis cDNA library [3].
• We then examined the polyadenylation state of cyclin B mRNA during 17alpha,20beta-DP-induced oocyte maturation by means of a PCR poly (A) test, and found that cyclin B mRNA is polyadenylated during oocyte maturation [4].

Anatomical context of 17,10beta-P

• In contrast, 17alpha,20beta-DP is unable to induce growing (previtellogenic and vitellogenic) oocytes to mature [2].
• These results indicate that the cDNA encodes a functional eel DPR, and show that 17alpha,20beta-DP has a nuclear receptor-mediated action in eel testes [3].
• A cDNA encoding 20beta-hydroxysteroid dehydrogenase (20beta-HSD), the enzyme that converts 17alpha-hydroxyprogesterone to 17alpha,20beta-DP, was cloned from the ovarian follicle of Nile tilapia [5].
• Furthermore, specific 17alpha,20beta-DP binding to plasma membranes was higher in postvitellogenic immature oocytes than in ovulated eggs [6].
• In spermatogenically active testes, the seminiferous tubules and the interstitium readily synthesized androgens from labelled C21 steroid precursor; seminiferous tubules also produced significant amounts of 17alpha,20alpha-dihydroxyprogesterone [7].

Associations of 17,10beta-P with other chemical compounds

• In addition, in vitro hormonal regulation by the maturation-inducing steroid 17,20beta-dihydroxy-4-pregnen-3-one (17,20betaP), gonadotropin, and estradiol were studied [8].
• In the teleost Fundulus heteroclitus, serotonin (5-HT) reversibly inhibits oocyte maturation induced in vitro by the maturation-inducing steroid (MIS) 17,20beta-dihydroxy-4-pregnen-3-one (17,20betaP) [9].
• Cycloheximide-treated oocytes failed to undergo meiotic maturation in response to 17alpha,20beta-DP; in this group neither cyclin B nor 34-kDa active cdc2 was detectable in oocytes [4].
• Testicular development and plasma levels of sex steroids (11-ketotestosterone (11-KT), testosterone (T) and 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P)) were investigated for the first time in cultured male Senegalese sole Solea senegalensis [10].
• In the present study we have characterized the membrane progestin receptor in Arctic char (Salvelinus alpinus) and show that the 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P) receptor also binds several xenobiotics, thus rendering oocyte maturation sensitive to environmental pollutants [11].

Gene context of 17,10beta-P

• Conversely, disturbance of the aggregation of cyclin B mRNA with a low concentration (1 microg/ml) of cytochalasin B inhibited 17alpha,20beta-DP-induced GVBD [1].
• Conversely, the injection of goldfish c-mos antisense RNA inhibited both Mos synthesis and MAPK activation in the 17alpha,20beta-DP-treated oocytes, but these oocytes underwent GVBD [12].
• Previous studies demonstrated that two teleost MISs, the progestins 17,20beta,21-trihydroxy-4-pregnen-3-one (20beta-S) and 17,20beta-dihydroxy-4-pregnen-3-one (DHP) can induce maturation of black porgy oocytes in vitro [13].

Analytical, diagnostic and therapeutic context of 17,10beta-P

• Free and conjugated (sulfates and glucuronides) levels of the established teleost oocyte maturation inducing steroids (MIS), i.e. 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P) and 17,20beta,21-trihydroxy-4-pregnen-3-one (17,20beta,21-P) were measured in the incubation media by high performance liquid chromatography [14].

References