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Synapses FXS

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Characterization of the molecular components of synapses in Fragile X mental ret...

Characterization of the molecular components of synapses in Fragile X mental retardation syndrome new insights into the FMRP regulatory mechanisms Fragile-X mental retardation syndrome (FXS) is caused by mutations in the Fmr1 gene that codes for the FMRP protein. FMRP is an RNA binding protein involved in mRNA metabolism. The translational dysregulation of a subset of FMRP t... ver más

31/05/2013

VLAAMS INSTITUUT...

220K€

Presupuesto del proyecto: 220K€

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TRL 4-5

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Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2013-05-31 No tenemos la información de la convocatoria

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Líder del proyecto

VIB VZW No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 220K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Fragile-X mental retardation syndrome (FXS) is caused by mutations in the Fmr1 gene that codes for the FMRP protein. FMRP is an RNA binding protein involved in mRNA metabolism. The translational dysregulation of a subset of FMRP target mRNAs is probably the major contribution to FXS. A hallmark of the FXS phenotype is the elevated spine density with immature morphology. We aim to understand the causes of this spine dysmorphogenesis by unraveling the molecular composition of synapses in a mouse model for FXS and also get insights into the fine-tune regulatory mechanisms of FMRP. This general aim will be tackled by the following objectives: (i) Characterization of the postsynaptic core proteome of hippocampal and cortical synapses in Fmr1 knock-out (KO) mouse model under synaptic plasticity activation at two developmental stages; (ii) Quantitative analysis of the synaptic mRNAs in Fmr1 KO; (iii) Study the function of synaptic microRNAs on mRNA expression and the role that FMRP plays in this miRNA-regulation, and (iv) identification of the regulatory dendritic translational machinery by isolation of the native Arc and PSD-95 mRNAs, two FMRP targets. These objectives will be approached by a novel combination of high sensitive techniques such as Tandem Affinity Purification (TAP) method, microarrays and RNA pull down in Fmr1 KO and TAP knock-in mouse models. The wide expertise of the host lab in mRNA metabolism and in FXS, the use of well characterized mouse models and the fine design of the experimental work-flow make this project with high rate of success. The main outcomes will be to list the dysregulated mRNAs and proteins in synapses of FXS, if this dysregulation is brain region specific and change during development and what mechanisms behind mRNA translation affect this dysregulation. All this will be very relevant to understand the ethiology of the disease and settle the bases for future drug design to ameliorate the grade of mental retardation in FXS patients.

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