[OFER-TRABEC] NAC: Se busca candidato para solicitar BECA PREDOCTORAL

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Boletín semanal de ofertas de empleo publico
http://administracion.gob.es/pag_Home/empleoBecas/empleo/boletinEmpleoPublico.html
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---Procedencia:
Institución:UB (Universidad de Barcelona)
Contacto correo-e:mendezzu@idibell.cat
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Se busca candidato para solicitar beca predoctoral a la Generalitat de Cataluña (BECAS FI-AGAUR), fecha límite de contacto 20 de septiembre 2016: mendezzu@idibell.cat

Beca PREDOCTORAL a solicitar: Beca FI-AGAUR, [CVE-DOGC-A-16251027-2016,Diari Oficial de la Generalitat de Catalunya (DOGC)]
Requisitos: los exigidos en la convocatoria (DOGC, 1 Sept 2016)
Expediente académico superior a 8,00.
Principal Investigator Ana Méndez Zunzunegui, mendezzu@idibell.cat




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Información complementaria de la oferta:
Title: molecular and cellular basis of the light response in retinal photoreceptor cells.
Brief description of the research lines/research project:
The main aim of our laboratory is to understand how photoreceptor cells of the retina respond to light, the adaptation mechanisms that allow them to operate in the highly varying ambient light intensities of the natural world and the mechanisms that sustain their extraordinary compartmentalization. Our ultimate goal is to undertand how genetic defects at this level lead to blindness in order to design new therapies for inherited retinal dystrophies. To that goal we combine the use of mouse genetics with biochemical, histological and functional analyses. We are now focused on the characterization of the organization, trafficking and in vivo regulation of the RD3/retGC/GCAPs protein complex, responsible for cGMP synthesis in rods and cones, both under physiological conditions and in response to mutations linked to blindness. Because cGMP is the second messenger in phototransduction -the first step in the light response- the function of this protein complex is absolutely req
uired for visual function. Autosomal recessive null mutations in retinal guanylate cyclase (retGC) or in the recently identified protein RD3 (rd3 gene) cause the most severe form of inherited retinal dystrophy: Leber Congenital Amaurosis (LCA), a congenital form of blindness in which rod and cone function is affected. There is no cure for this disease. Autosomal dominant mutations in retGC or in the guanylate cyclase activating proteins (GCAPs, genes GUCA1A and GUCA1B) cause cone and rod dystrophies. These age-related diseases lead to the loss of central vision and visual acuity, and eventually lead to complete blindness. We want to determine the molecular and cellular basis underlying the pathology in these scenarios in order to guide new therapies for patients.

Skills, technology and general abilities to be acquired by the predoctoral candidate:
The ability to design and undertake comparative proteomic analysis (IP or pull-down assays followed by mass spectrometry determinations by LC-MS/MS) to identify new protein interactors of key signaling proteins linked to blindness; fine co-localization studies by confocal microscopy, proximity ligation assays and super-resolution techniques; electron microscopy of retinal sections; the ability to undertake genetic approaches by transient transgenesis in the retina by in vivo DNA electroporation; visual function analysis in mouse models.
Publications:

López-del Hoyo N, López-Begines S, Rosa JL, Chen J, Méndez A. Functional EF-hands in neuronal calcium sensor GCAP2 determine its phosphorylation state and subcellular distribution in vivo, and are required for photoreceptor cell integrity. PLoS Genetics 2014.
López del Hoyo N, Fazioli L, López-Begines S, Fernández-Sánchez L, Cuenca N, Llorens J, Villa P, Méndez A. Overexpression of guanylate cyclase activating protein 2 in rod photoreceptors in vivo leads to morphological changes at the synaptic ribbon. PLoS One 2012;7:1-20.
Funded Projects:
Proyecto Fundación Ramón Areces, FRA-2015. Bases moleculares de la patología en ceguera hereditaria. IP: Ana Méndez. Duración: 2015-2017. Cuantía: 128.000.
SAF2013-49069-C2-2-R MINECO Identificación de dianas terapéuticas para distrofias de retina: caracterización funcional in vivo e in vitro de genes causantes de ceguera hereditaria. IP: Ana Méndez. Duración: 2014-2016. Cuantía: 100.000.
Proyecto ONCE 2015/300666 Estudio de las bases moleculares de retinosis pigmentarias y distrofias hereditarias de retina: caracterización funcional de proteínas causantes de enfermedad y de mecanismos de patogenicidad en modelos animales. IP: Ana Méndez. Duración: 2015. Cuantía: 7.000.
Proyecto Marató TV3: Dissecting protein trafficking in retinal neurodegeneration by super-resolution imaging on animal models and human iPSCs. IP: Roser González Duarte. Participación: investigador. Duración: 2015-2017. Cuantía: 400.000.