The contribution of steroidal androgens and estrogens to reproductive maturation of the eastern mud snail Ilyanassa obsoleta.

Molluscs exposed to endocrine-disrupting chemicals (EDCs) have exhibited changes in reproductive tract development that are typically associated with androgen or estrogen signaling in vertebrates. However, a role for androgens and estrogens in molluscan reproductive endocrinology has yet to be established. In this study, we investigated putative roles for steroidal androgens and estrogens in recrudescence of the eastern mud snail Ilyanassa obsoleta. Our objectives were to: (1) identify associations among concentrations of testosterone and 17beta-estradiol, sex, and reproductive status in mud snails that suggest these hormones are involved in recrudescence; and (2) determine whether mud snails express NR3C4-like (androgen receptor) and NR3A-like (estrogen receptor) mRNAs in a manner indicative of a role in recrudescence. Temporal changes in testosterone levels in males were consistent with a positive role in recrudescence. Such a trend was not evident in females or for 17beta-estradiol in either sex. Efforts to identify an androgen receptor from the mud snail using targeted, degenerate RT-PCR were unsuccessful. However, an estrogen receptor (ER) cDNA was identified that is highly similar to known ERs of other molluscs. Studies with the ER of other molluscs have shown that this protein does not actually bind estrogens. We therefore considered the possibility that the mud snail ER may regulate reproductive maturation as a ligand-independent transcription factor based upon its tissue abundance. Males expressed greater levels of ER mRNA than did females over the entire reproductive cycle, and this difference was most evident during recrudescence. ER mRNA levels were significantly elevated during recrudescence in males but not females. In conclusion, testosterone may have a role in male reproductive tract recrudescence; however, this putative activity is independent of a NR3C4-type androgen receptor. The ER also may function in male recrudescence, though apparently independent of 17beta-estradiol. The retinoid signaling pathway is discussed as a possible alternative hormone/receptor-mediated signaling pathway that regulates male recrudescence.