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Attenuation of insulin signalling contributes to FSN-1-mediated regulation of synapse development.


ABSTRACT: A neuronal F-box protein FSN-1 regulates Caenorhabditis elegans neuromuscular junction development by negatively regulating DLK-mediated MAPK signalling. In the present study, we show that attenuation of insulin/IGF signalling also contributes to FSN-1-dependent synaptic development and function. The aberrant synapse morphology and synaptic transmission in fsn-1 mutants are partially and specifically rescued by reducing insulin/IGF-signalling activity in postsynaptic muscles, as well as by reducing the activity of EGL-3, a prohormone convertase that processes agonistic insulin/IGF ligands INS-4 and INS-6, in neurons. FSN-1 interacts with, and potentiates the ubiquitination of EGL-3 in vitro, and reduces the EGL-3 level in vivo. We propose that FSN-1 may negatively regulate insulin/IGF signalling, in part, through EGL-3-dependent insulin-like ligand processing.

SUBMITTER: Hung WL 

PROVIDER: S-EPMC3680742 | biostudies-literature | 2013 Jun

REPOSITORIES: biostudies-literature

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Attenuation of insulin signalling contributes to FSN-1-mediated regulation of synapse development.

Hung Wesley L WL   Hwang Christine C   Gao Shangbang S   Liao Edward H EH   Chitturi Jyothsna J   Wang Ying Y   Li Hang H   Stigloher Christian C   Bessereau Jean-Louis JL   Zhen Mei M  

The EMBO journal 20130510 12


A neuronal F-box protein FSN-1 regulates Caenorhabditis elegans neuromuscular junction development by negatively regulating DLK-mediated MAPK signalling. In the present study, we show that attenuation of insulin/IGF signalling also contributes to FSN-1-dependent synaptic development and function. The aberrant synapse morphology and synaptic transmission in fsn-1 mutants are partially and specifically rescued by reducing insulin/IGF-signalling activity in postsynaptic muscles, as well as by reduc  ...[more]

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