monensin and Disorders-of-Sex-Development

Gamete self-incompatibility in the hermaphrodite tunicate Ciona intestinalis is a useful system with which to study self-nonself recognition. We have used in vitro fertilization of oocytes isolated from the gonad of Ciona intestinalis to identify the cellular source of self-sterility elements present on the egg envelopes. Here we show for the first time that self-discrimination, which occurs on the egg vitelline coat, is established there in late oogenesis and is contributed or controlled by products of the overlying follicle cells. The acquisition of self-sterility by the oocyte is prevented by the ionophore monensin, which suggests that the follicle cell self-sterility controlling factor is a glycoprotein.

Topics: Animals; Ciona intestinalis; Disorders of Sex Development; Female; Fertilization; Glycoproteins; Gonads; Monensin; Oocytes; Oogenesis; Vitelline Membrane

Spermiogenesis in Caenorhabditis elegans involves the conversion of spherical, sessile spermatids into bipolar, crawling spermatozoa. In males, spermiogenesis is induced by mating, while in hermaphrodites, spermiogenesis occurs before the first oocytes are fertilized. Alternatively, spermiogenesis can be induced in vitro by treatment with monensin triethanolamine, or pronase. Treatment with the calmodulin inhibitors, trifluoperazine, chlorpromazine, or W7, also induces spermiogenesis in vitro with a half maximal effect at 20 microM. Upon initial activation, spermatids extend long, thin spikes and undergo extensive cellular movements. Eventually, a single motile pseudopod forms through the restructuring of one or more of these spikes. These transient spikes can be prolonged in vitro by removing triethanolamine as soon as the spermatids first form spikes. Spermatids from spe-8 and spe-12 spermatogenesis-defective (spe) mutants activate in vivo with male but not hermaphrodite sperm activator. In vitro, the mutant spermatids arrest spermiogenesis at the spike stage when activated with pronase, but form normal spermatozoa if subsequently or initially treated with monensin or triethanolamine. We present a model of spermiogenesis in which the mutant defects and the action of the pharmacological agents are ordered relative to one another.

Topics: Animals; Caenorhabditis; Chlorpromazine; Disorders of Sex Development; Ethanolamines; Hydrogen-Ion Concentration; Male; Microscopy, Electron; Monensin; Mutation; Pronase; Sperm Motility; Spermatids; Spermatogenesis; Spermatozoa; Sulfonamides; Trifluoperazine