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ExploNL1

Financiado

Exploring the role of Neuroligin-1 in synapse formation and function

"Controlling the precise balance between excitation and inhibition (E/I balance) is critical for information processing in the brain. This equilibrium is regulated at the level of individual synapses, which can be either excitator... ver más

31/08/2026

CNRS

196K€

Presupuesto del proyecto: 196K€

Líder del proyecto

CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-05-10

HORIZON-MSCA-2022-PF-01-01: MSCA Postdoctoral Fellowships 2022 ExpectedOutcome:

I+D

Cerrada hace 2 años

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2 Participantes

CNRS

195.91K€ | Lider

UBx

N.D. | Participante

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Duración del proyecto: 39 meses Fecha Inicio: 2023-05-10
Fecha Fin: 2026-08-31

Líder del proyecto

CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 196K€

Descripción del proyecto "Controlling the precise balance between excitation and inhibition (E/I balance) is critical for information processing in the brain. This equilibrium is regulated at the level of individual synapses, which can be either excitatory or inhibitory depending of the type of neurotransmitter released. It is well established that cell adhesion molecules such as neurexins (NRXs) and neuroligins (NLs) play important roles in synapse formation and specification. In humans, several genetic mutations in NLs are associated with Autism Spectrum Disorders (ASD) but how those mutations act in the establishment of those disorders remains unclear. One hypothesis is that mutations found in ASD patients can affect the interactions of NLs to specific protein binding partners and/or alter signaling pathways, which could contribute to disrupt the E/I balance. Interestingly, the host group recently discovered a molecular mechanism in which the phosphorylation of unique tyrosine residue located in the intracellular domain of NL1 regulates the differential assembly of excitatory versus inhibitory synapses. Furthermore, in the absence of highly specific antibodies compatible with immunostaining of native adhesion molecules, little is known about the precise distribution of endogenous NL1 within the synapse. In this project we will #1) decipher the localization of endogenous NL1 and its modulation between excitatory and inhibitory synapses based on its phosphorylation state by using a new transgenic knock-in mouse line in which endogenous NL1 has been tagged with a small biotin acceptor peptide (BAP-NL1); #2) we will uncover how ASD-linked mutations in NL1 affect synaptic changes at the morphological and functional levels, in both physiological and ASD conditions. ExploNL1 will shed light on the basic molecular mechanisms regulating the differentiation of excitatory and inhibitory synapses, and as a consequence the underlying pathological basis of ASDs."

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