G2-arrested marine invertebrate oocytes are triggered to re-enter the cell cycle by different extracellular signals (sperm, hormones and rnimetics). They respond to competent signals either by germinal vesicle breakdown (for those arrested in prophase I) or by polar body emission (for those arrested in metaphase I or 11). These cellular responses b e easy to observe and quantify thus making of meiosis reinitiation an attractive model to study the transduction of signals endogenous to oocytes. Given the universal character of transmembrane coupling molecules and intracellular effectors, the specificity of cell and, in particular, oocyte response to an extracellular signal are mediated by the presence of specific receptors and by a specific set of intmcellular effectors that are activated by them. In this paper we discuss the current limitations in molecular and pharmacological identification and characterization of invertebrate oocyte receptors. We next analyze signalling pathways triggered by activation of relevant receptors and the cross-talk existing between them. The above aspects are discussed on the examples of serotonin-induced meiosis reinitiation in prophase I-arrested oocytes of Spisula solidissima and on KC1-induced meiosis reinitiation of metaphase I-arrested Mytilus galloprovincialis oocytes taken as paradigms.
Bivalve oocytes constitute an excellent model to study the mechanisms which control cell division, since they arrest at different stages of tile meiotic process and respond quite synchronously to various external signals regulating their evolution. Different situations were observed, according to the species, which required a more careful analysis. For example, the same serotonin (5-HT) signal was found to drive prophase-arrested oocytes of Spisula to the female pronucleus stage, whereas Ruditapes oocytes stopped in metaphase 1. In this last species, 5-HT treatment thus represents a necessary prerequisite for further development since sperm cannot penetrate prophase-arrested oocytes, in contrast to the situation found in Spisula. The reasons for these differences cannot be found at the level of the receptors and second messengers. In both species, we found that Ca -'+ was involved as a second messenger and required to release oocytes from their blocks in prophase and metaphase 1. This is an unexpected and puzzling situation since MPF is activated by the prophase Ca-" surge and inactivated during metaphase-anaphase transition. The mechanisms underlying these paradoxical situations are discussed, taking into account results from previous observations and experiments. Briefly, our data suggest: i) that the absence of K + sensitive voltage-gated Ca -'+ channels may be responsible for the unfertilizability of prophasearrested Ruditapes oocytes; and ii) that functional variations in the network of activated kinases present in prophase and metaphase oocytes may be responsible for the divergent responses exhibited by Spisula and Ruditapes oocytes. In particular, these oocytes differ in their sensitivity to Ca 2'/calmodulin antagonists and in tyrosine phosphorylation of their activated p34 cJ~-' kinase. calcium stores / oocyte maturation / serotonin / pelecypod molluscs
The possible role of immunomodulatory peptide somatostatin (SRIF) in measles virus (MV)-induced immunopathology was addressed by analysis of SRIF receptors and their coupling to adenylyl cyclase in mitogen-stimulated Jurkat T cells and human peripheral blood mononuclear cells (PBMC). SRIF-specific receptors were assayed in semipurified membrane preparations by using SRIF14 containing iodinated tyrosine at the first position in the amino acid chain ([125I]Tyr1) as a radioligand. A determination of receptor number by saturation of radioligand binding at equilibrium showed that in Jurkat cells, MV infection led to a dramatic decrease in the total receptor number. The virus-associated disappearance of one (Ki2 = 12 +/- 4 nM [mean +/- standard error of the mean [SEM]]; n = 4) of two somatostatin binding sites identified in control Jurkat cells (Ki1 = 78 +/- 3 pM and Ki2 = 12 +/- 4 nM [mean +/- SEM]; n = 4) was also observed. Almost identical results were obtained for phytohemagglutinin-activated human PBMC. In the absence of MV infection, two somatostatin binding sites were present (Ki1 = 111 +/- 31 pM and Ki2 = 17 +/- 2 nM [mean +/- SEM]; n = 2), whereas in MV-infected cells, only the high-affinity (Ki1 = 48 +/- 15 pM [mean +/- SEM]; n = 2) binding site remained. In addition, MV infection reinforced the inhibitory effects of SRIF on adenylyl cyclase activity, since maximal inhibition at 1 microM peptide was 11% +/- 4% in control cells versus 25% +/- 3% (P < 0.05) in infected Jurkat cells. Moreover, MV infection severely impaired the capacity of adenylyl cyclase to be activated directly (by forskolin) or indirectly (via Gs protein-coupled vasoactive intestinal peptide receptor). An assessment of [methyl-3H]thymidine incorporation showed that SRIF increased proliferative responses to mitogens only in control cells, not in MV-infected cells. Altogether, our data emphasize that MV-associated alteration of SRIF transduction appears to be related to the loss of SRIF-dependent increase of mitogen-induced proliferation.
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