Search

The time course of ovarian and pituitary endocrine events throughout the menstrual cycle in the Vervet monkey and the role of circulating luteinizing hormone (LH) are evaluated. The characteristics and regulation of the ovarian cycle in vervets are similar to those in women with pituitary gonadotropin hormones that determine the cyclicity.

During the formation of the insect peripheral nervous system (PNS), the cell adhesion receptor fasciclin II has been shown to play a prominent role in axonal fasciculation and synapse formation during motor neuron outgrowth. In the moth Manduca, fasciclin II (MFas II) is expressed both as a transmembrane isoform (TM-MFas II) and a glycosyl phosphatidylinositol-linked isoform (GPI-MFas II). By using RNA and antibody probes, we have shown that these two isoforms are expressed in nonoverlapping patterns: TM-MFas II is expressed exclusively by neurons and becomes localized to their most motile regions, while GPI-MFas II is expressed primarily by the glial cells that ensheath the peripheral nerves. This cell-type specificity of expression allowed us to monitor the nature of neuronal--glial interactions during PNS development. The outgrowth of TM-MFas II-positive axons in many regions preceded the arrival of GPI-MFas II-expressing glial processes that enwrapped them. In a few key locations, however, GPI-MFas II-positive glial cells differentiated before the arrival of the first axons and prefigured their subsequent trajectories. Prior inhibition of GPI-MFas II expression disrupted the subsequent outgrowth of axons at these locations but not elsewhere in the PNS. Our results suggest that the two isoforms of MFas II play distinct roles with respect to cellular motility and nerve formation. [C] 2001 Academic Press Key Words: growth cone; fasciculation; adhesion; insect; Manduca sexta.

During the formation of the enteric nervous system (ENS) of the moth Manduca sexta, identified populations of neurons and glial cells participate in precisely timed waves of migration. The cell adhesion receptor fasciclin II is expressed in the developing ENS and is required for normal migration. Previously, we identified two isoforms of Manduca fasciclin II (MFas II), a glycosyl phosphatidylinositol-linked isoform (GPI-MFas II) and a transmembrane isoform (TM-MFas II). Using RNA and antibody probes, we found that these two isoforms were expressed in cell type-specific patterns: GPI-MFas II was expressed by glial cells and newly generated neurons, while TM-MFas II was confined to differentiating neurons. The expression of each isoform also corresponded to the motile state of the different cell types: GPI-MFas II was detected on tightly adherent or slowly spreading cells, while TM-MFas II was expressed by actively migrating neurons and was localized to their most motile regions. Manipulations of each isoform in embryo culture showed that they played distinct roles: whereas GPI-MFas II acted strictly as an adhesion molecule, TM-MFas II promoted the motility of the EP cells as well as maintaining fasciculation with their pathways. These results indicate that precisely regulated patterns of isoform expression govern the functions of fasciclin II within the developing nervous system. [Copyright] 2000 Academic Press Key Words: migration; growth cone; motility; fasciculation; adhesion; fasciclin II; ENS; antisense; insect; moth; Manduca sexta.

Estrogen promotes the growth of some ovarian cancer cells at nanomolar concentrations, but has been shown to inhibit growth of normal ovarian surface epithelial (OSE) cells at micromolar concentrations (1 μg/ml). OSE cells express the estrogen receptor (ER)-α, and are the source of 90% of ovarian cancers. The potential sensitivity of OSE cells to estrogen stresses the importance of understanding the estrogen-dependent mechanisms at play in OSE proliferation and transformation, as well as in anticancer treatment. We investigated the effects of estradiol on cell proliferation in vitro, and demonstrate an intracellular locus of action of estradiol in cultured rhesus ovarian surface epithelial (RhOSE) cells. We show that ovarian and breast cells are growth-inhibited by micromolar concentrations of estradiol, and that this inhibition correlates with estrogen receptor expression. We further show that normal rhesus OSE cells do not activate ERK or Akt in response to estradiol, nor does estradiol block the ability of serum to stimulate ERK or induce cyclin D expression. Contrarily, estradiol inhibits serum-dependent retinoblastoma protein (Rb) phosphorylation and blocks DNA synthesis. This inhibition does not formally arrest cells, and is reversible within hours of estrogen withdrawal. Our data are consistent with growth inhibition by activation of Rb and indicate that sensitivity to hormone therapy in anticancer treatment can be modulated by cell cycle regulators downstream of the estrogen receptor. [Copyright &y& Elsevier]