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PubMed2006

17-beta-estradiol elicits genomic and non-genomic responses in mouse male germ cells.

Estrogens have been postulated to exert a detrimental effect on spermatogenesis in vivo. Since mouse male germ cells express estrogen receptors, we have investigated whether molecular pathways are activated by estrogen stimulation of these cells. Our results demonstrate that estrogen receptor beta is expressed in mitotic and meiotic male germ cells as well as in the spermatogonia derived GC-1 cell line. By using this cell line, we show that 17-beta-estradiol triggers activation of a transcriptional response that requires a functional estrogen receptor. Moreover, GC-1 cells respond to estrogens by transiently activating a signal transduction pathway that impinges on the mitogen-activated protein kinases (MAPK) ERK1 and -2. A similar dose-dependent transient activation of ERKs was also observed in primary mouse spermatocytes in culture. Activation by the estrogen was specific because other steroids such as progesterone and dihydrotestosterone were ineffective and because it could be blocked by the selective inhibitor of the ERK pathway and by competitive inhibitors of the estrogen receptor. Finally, we observed that 17-beta-estradiol does not affect spontaneous or induced apoptosis in cultured mouse spermatocytes, indicating that the apoptotic effects observed in vivo require additional testicular components.

Animals↗
PubMed1994

Genomic and non-genomic actions of progesterone in the control of female hamster sexual behavior.

Progesterone (P) in both the ventromedial hypothalamus (VMH) and the ventral tegmental area (VTA) is necessary to facilitate sexual receptivity in estrogen-primed hamsters. The mechanism of P may be different in the VMH and VTA, as there are many intracellular progestin receptors (PR) in the VMH but few in the VTA. Progesterone conjugated to bovine serum albumin (P-3-BSA) does not bind well to intracellular PR or permeate the surface of neuronal membranes. However, VTA application of P-3-BSA rapidly increases sexual receptivity if P has been applied earlier to the VMH. P-3-BSA is ineffective when applied to the VMH. The membrane-limited effect of P may be related to the ability of some progestins to modulate the GABAA-benzodiazepine receptor complex (GBRC). We have found that infusions of a GABAA agonist, muscimol, into the VTA enhance and a GABAA antagonist, bicuculline, inhibit receptivity. Because P itself is not highly effective at the GBRC, and since the most potent modulators of the GBRC, the 5 alpha-reduced progestins, do not bind well to PRs, progestin metabolites were applied to the VTA. Only the potent GBRC modulators facilitated sexual receptivity when applied to the VTA concurrent with P to the VMH. The reverse treatment, with a progestin metabolite implanted into the VMH, was ineffective. VTA infusions of an inhibitor of 5 alpha-reductase also attenuated behavioral estrus in hamsters.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1985

Membrane-bound virions of coxsackievirus B4: cellular localization, analysis of the genomic RNA, genome-linked protein, and effect on host macromolecular synthesis.

Hela cells infected with several group B coxsackieviruses contain, in addition to standard virions, a population of virus-specific ribonucleoprotein particles which we (5) designated membrane-bound virions (MBV). MBVs differ from standard virions in buoyant density, yield, appearance, protein composition and infectivity. Here we present several new features of MBVs of coxsackievirus B4. The MBVs are lighter (rho about 1.30) and are localized in rough membranes, intermixed with virions. They contain 35S virion RNA covalently linked with a small protein, VPg. The VPg contain two proteins of different charge. MBV VPg is considerably smaller than the 5300-dalton virion VPg. MBV RNA is homologous to the base sequence present in B4 virus double-stranded RNA. The T1 oligonucleotide fingerprint of MBV RNA is distinguishable from that of virion RNA by one oligonucleotide. Several oligonucleotides of virion RNA appear to occur in submolar quantities in MBV RNA. MBVs are 75 to greater than 200 times less infective; they inhibit host cell macromolecular synthesis less efficiently than virions. In coinfected cells, the extent of inhibition of host synthesis is less severe than in cells infected with virions alone, which suggest interference by MBV particles.

Cell Compartmentation↗
PubMed2002

Recessive resistance genes against potyviruses are localized in colinear genomic regions of the tomato ( Lycopersicon spp.) and pepper ( Capsicum spp.) genomes.

Resistance against both Potato virus Y (PVY) and Tobacco etch virus (TEV) was identified in the wild tomato relative Lycopersicon hirsutum PI247087. Analysis of the segregation ratio in F(2)/F(3) and BC(1) interspecific progenies indicated that a single recessive gene, or two very tightly linked recessive loci, are involved in resistance to both potyviruses. This locus was named pot-1. Using amplified fragment length polymorphism markers and a set of L. hirsutum introgression lines, pot-1 was mapped to the short arm of tomato chromosome 3, in the vicinity of the recessive py-1 locus for resistance to corky root rot. Because of the occurrence of phenotypically similar genes in pepper ( Capsicum spp.), the comparative genetics of resistance to potyviruses between tomato and pepper was investigated. Unlike most of the comparative genetic studies on resistance genes, pot-1 was tightly flanked by the same restriction fragment length polymorphism (RFLP) markers than the pvr2/pvr5 locus for resistance to PVY and TEV from pepper. These results may indicate that recessive resistance genes against potyviruses evolve less rapidly than the majority of the dominant genes cloned so far, and consequently may belong to a different family of resistance genes.

Journal Article↗
PubMed2005

Genomic and non-genomic actions of sex steroids in the growth plate.

Sex steroids, and particularly estrogens, are important regulators of bone growth and bone mass accrual. For a long time, it was thought that these effects were mainly caused by their modulatory effects on the somatotrophic axis. Data gathered in the past years have challenged this view and it is now widely accepted that many of the effects of sex steroids on growth and bone mass accrual are caused by direct effects on target cells in the growth plate and bone. This review summarizes and discusses some of our latest findings on the expression of sex steroid receptors in the growth plate, the source of the ligands activating these receptors, and their putatitive mechanism of action predominantly focusing on observations in the rat.

Animals↗