Discriminación por razón de género y negociación colectiva tras la ley 3/2012

Este artículo describe y analiza la configuración jurídica del convenio colectivo como fuente reguladora y ga-rantista del derecho de igualdad y no dis-criminación por razón de género, tanto con carácter general como en el ámbito específico del acceso al empleo, formación y promoción en el trabajo y en las más relevantes condiciones en las relaciones laborales. A tal fin, y a partir de la doctrina establecida por la jurisprudencia constitucional, se estudian las causas de la desigualdad y las categorías que permiten una fundamentación razonable y objetiva para lograr la igualdad material. También se aportan datos cuantitativos acerca de la influencia de la Ley Orgánica 3/2007 en el régimen de los convenios convenios colectivos en esta materia.This paper work de-scribes and analyses the collective agree-ments legal configuration as regulating and guarantor source of the equality's right and no discrimination because of the sex, as much in general terms as in the specific field of accessing to a job, training and advance-ment in the job and in the main conditions in the labour relationships. According the established doctrine by the constitutional sentences, we study the inequality causes and the categories which give a reasonable and factual basis to reach a material equality. In addition, this work also provides quanti-tative facts about the influence of Organic Law 3/2007 in the collective agreements regime in this matte

Gata4 Is Required for Formation of the Genital Ridge in Mice

In mammals, both testis and ovary arise from a sexually undifferentiated precursor, the genital ridge, which first appears during mid-gestation as a thickening of the coelomic epithelium on the ventromedial surface of the mesonephros. At least four genes (Lhx9, Sf1, Wt1, and Emx2) have been demonstrated to be required for subsequent growth and maintenance of the genital ridge. However, no gene has been shown to be required for the initial thickening of the coelomic epithelium during genital ridge formation. We report that the transcription factor GATA4 is expressed in the coelomic epithelium of the genital ridge, progressing in an anterior-to-posterior (A-P) direction, immediately preceding an A-P wave of epithelial thickening. Mouse embryos conditionally deficient in Gata4 show no signs of gonadal initiation, as their coelomic epithelium remains a morphologically undifferentiated monolayer. The failure of genital ridge formation in Gata4-deficient embryos is corroborated by the absence of the early gonadal markers LHX9 and SF1. Our data indicate that GATA4 is required to initiate formation of the genital ridge in both XX and XY fetuses, prior to its previously reported role in testicular differentiation of the XY gonadHoward Hughes Medical Institut

Analysis of Medaka sox9 Orthologue Reveals a Conserved Role in Germ Cell Maintenance

The sex determining gene is divergent among different animal species. However, sox9 is up-regulated in the male gonads in a number of species in which it is the essential regulator of testis determination. It is therefore often discussed that the sex determining gene-sox9 axis functions in several vertebrates. In our current study, we show that sox9b in the medaka (Oryzias latipes) is one of the orthologues of mammalian Sox9 at syntenic and expression levels. Medaka sox9b affects the organization of extracellular matrices, which represents a conserved role of sox9, but does not directly regulate testis determination. We made this determination via gene expression and phenotype analyses of medaka with different copy numbers of sox9b. Sox9b is involved in promoting cellular associations and is indispensible for the proper proliferation and survival of germ cells in both female and male medaka gonads. Medaka mutants that lack sox9b function exhibit a seemingly paradoxical phenotype of sex reversal to male. This is explained by a reduction in the germ cell number associated with aberrant extracellular matrices. Together with its identified roles in other vertebrate gonads, a testis-determining role for Sox9 in mammals is likely to have been neofunctionalized and appended to its conserved role in germ cell maintenance

Oestrogen blocks the nuclear entry of SOX9 in the developing gonad of a marsupial mammal

<p>Abstract</p> <p>Background</p> <p>Hormones are critical for early gonadal development in nonmammalian vertebrates, and oestrogen is required for normal ovarian development. In contrast, mammals determine sex by the presence or absence of the <it>SRY </it>gene, and hormones are not thought to play a role in early gonadal development. Despite an XY sex-determining system in marsupial mammals, exposure to oestrogen can override <it>SRY </it>and induce ovarian development of XY gonads if administered early enough. Here we assess the effect of exogenous oestrogen on the molecular pathways of mammalian gonadal development.</p> <p>Results</p> <p>We examined the expression of key testicular (<it>SRY</it>, <it>SOX9</it>, <it>AMH </it>and <it>FGF9</it>) and ovarian (<it>WNT4</it>, <it>RSPO1</it>, <it>FOXL2 </it>and <it>FST</it>) markers during gonadal development in the marsupial tammar wallaby (<it>Macropus eugenii</it>) and used these data to determine the effect of oestrogen exposure on gonadal fate. During normal development, we observed male specific upregulation of <it>AMH </it>and <it>SOX9 </it>as in the mouse and human testis, but this upregulation was initiated before the peak in <it>SRY </it>expression and 4 days before testicular cord formation. Similarly, key genes for ovarian development in mouse and human were also upregulated during ovarian differentiation in the tammar. In particular, there was early sexually dimorphic expression of <it>FOXL2 </it>and <it>WNT4</it>, suggesting that these genes are key regulators of ovarian development in all therian mammals. We next examined the effect of exogenous oestrogen on the development of the mammalian XY gonad. Despite the presence of <it>SRY</it>, exogenous oestrogen blocked the key male transcription factor SOX9 from entering the nuclei of male somatic cells, preventing activation of the testicular pathway and permitting upregulation of key female genes, resulting in ovarian development of the XY gonad.</p> <p>Conclusions</p> <p>We have uncovered a mechanism by which oestrogen can regulate gonadal development through the nucleocytoplasmic shuttling of SOX9. This may represent an underlying ancestral mechanism by which oestrogen promotes ovarian development in the gonads of nonmammalian vertebrates. Furthermore, oestrogen may retain this function in adult female mammals to maintain granulosa cell fate in the differentiated ovary by suppressing nuclear translocation of the SOX9 protein.</p> <p>See commentary: http://www.biomedcentral.com/1741-7007/8/110</p

Sex Reversal in Zebrafish fancl Mutants Is Caused by Tp53-Mediated Germ Cell Apoptosis

The molecular genetic mechanisms of sex determination are not known for most vertebrates, including zebrafish. We identified a mutation in the zebrafish fancl gene that causes homozygous mutants to develop as fertile males due to female-to-male sex reversal. Fancl is a member of the Fanconi Anemia/BRCA DNA repair pathway. Experiments showed that zebrafish fancl was expressed in developing germ cells in bipotential gonads at the critical time of sexual fate determination. Caspase-3 immunoassays revealed increased germ cell apoptosis in fancl mutants that compromised oocyte survival. In the absence of oocytes surviving through meiosis, somatic cells of mutant gonads did not maintain expression of the ovary gene cyp19a1a and did not down-regulate expression of the early testis gene amh; consequently, gonads masculinized and became testes. Remarkably, results showed that the introduction of a tp53 (p53) mutation into fancl mutants rescued the sex-reversal phenotype by reducing germ cell apoptosis and, thus, allowed fancl mutants to become fertile females. Our results show that Fancl function is not essential for spermatogonia and oogonia to become sperm or mature oocytes, but instead suggest that Fancl function is involved in the survival of developing oocytes through meiosis. This work reveals that Tp53-mediated germ cell apoptosis induces sex reversal after the mutation of a DNA–repair pathway gene by compromising the survival of oocytes and suggests the existence of an oocyte-derived signal that biases gonad fate towards the female developmental pathway and thereby controls zebrafish sex determination

Mate choice influences differential introgression in a hybrid zone

Hybrid zones are widely recognized as important sources of genetic variation, and conduits for the exchange of genes from one species to another. How and which traits move, or introgress, is an important area of study in evolutionary biology. A hybrid zone between two manakin (Pipridae) species, Manacus candei and Manacus vitellinus, exists in Bocas del Toro Province, in western Panama. The hybrid zone is unique in that the plumage genes of Manacus vitellinus introgress up to 50 km beyond the genetic center of the hybrid zone, into populations that are morphologically and genetically similar to M. candei. M.vitellinus males are more aggressive than Manacus candei males in mixed leks where both species occur. If M. candei females preferred males with M. vitellinus plumage traits, introgression of M. vitellinus plumage genes would be explained by both intra- and inter-sexual selection. Manacus spp. have a lek mating system; males perform elaborate, acrobatic courtship displays on small arenas on the forest floor, producing loud ‘wingsnaps’ and maximizing the visibility of their colored throat feathers. We have recently shown that display performance is associated with female preference in M. vitellinus, with females perferring males that perform certain moves faster. Thus, we hypothesized that female choice based on courtship display drives asymmetrical trait introgression. We studied whether display performance differs between the two species. Using high speed videography to film courtship displays of males of the two species, we compared them for those traits which in M. vitellinus are correlated to female preference. Contrary to our expectations, we found that M. candei males outperform M. vitellinus males. We propose that vitellinus-like plumage is preferred by females, but only when it recombines with the candei morphometric background, and hence, the superior display ability of M. candei