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A glutamate receptor-interacting protein homolog organizes muscle guidance in Drosophila.

ABSTRACT: During Drosophila embryogenesis, developing muscles extend growth-cone-like structures to navigate toward specific epidermal attachment sites. Here, we show that the homolog of Glutamate Receptor-Interacting Proteins (DGrip) acts as a key component of proper muscle guidance. Mutations in dgrip impair patterning of ventral longitudinal muscles (VLMs), whereas lateral transverse muscles (LTMs) that attach to intrasegmental attachment sites develop normally. Myoblast fusion, stabilization of muscle contacts, and general muscle function are not impaired in the absence of DGrip. Instead, the proper formation of cellular extensions during guidance fails in dgrip mutant VLMs. DGrip protein concentrates at the ends of VLMs while these muscles guide toward segment border attachment sites. Conversely, LTMs overexpressing DGrip form ectopic cellular extensions that can cause attachment of these muscles to other muscles at segment borders. Our data suggest that DGrip participates in the reception of an attractive signal that emanates from the epidermal attachment sites to direct the motility of developing muscles. This dgrip phenotype should be valuable to study mechanistic principles of Grip function.

SUBMITTER: Swan LE

PROVIDER: S-EPMC324427 | biostudies-literature | 2004 Jan

REPOSITORIES: biostudies-literature

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A glutamate receptor-interacting protein homolog organizes muscle guidance in Drosophila.

Swan Laura E LE Wichmann Carolin C Prange Ulrike U Schmid Andreas A Schmidt Manuela M Schwarz Tobias T Ponimaskin Evgeni E Madeo Frank F Vorbrüggen Gerd G Sigrist Stephan J SJ

Genes & development 20040116 2

During Drosophila embryogenesis, developing muscles extend growth-cone-like structures to navigate toward specific epidermal attachment sites. Here, we show that the homolog of Glutamate Receptor-Interacting Proteins (DGrip) acts as a key component of proper muscle guidance. Mutations in dgrip impair patterning of ventral longitudinal muscles (VLMs), whereas lateral transverse muscles (LTMs) that attach to intrasegmental attachment sites develop normally. Myoblast fusion, stabilization of muscle ...[more]

PMID: 14729572

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Project description:AimsIt has been reported that the G-alpha interacting protein (GAIP) interacting protein, C terminus 1 (GIPC1/GIPC) engages in vesicular trafficking, receptor transport and expression, and endocytosis. However, its role in epilepsy is unclear. Therefore, in this study, we aimed to explore the role of GIPC1 in epilepsy and its possible underlying mechanism.MethodsThe expression patterns of GIPC1 in patients with temporal lobe epilepsy (TLE) and in mice with kainic acid (KA)-induced epilepsy were detected. Behavioral video monitoring and hippocampal local field potential (LFP) recordings were carried out to determine the role of GIPC1 in epileptogenesis after overexpression of GIPC1. Coimmunoprecipitation (Co-IP) assay and high-resolution immunofluorescence staining were conducted to investigate the relationship between GIPC1 and metabotropic glutamate receptor 7 (mGluR7). In addition, the expression of mGluR7 after overexpression of GIPC1 was measured, and behavioral video monitoring and LFP recordings after antagonism of mGluR7 were performed to explore the possible mechanism mediated by GIPC1.ResultsGIPC1 was downregulated in the brain tissues of patients with TLE and mice with KA-induced epilepsy. After overexpression of GIPC1, prolonged latency period, decreased epileptic seizures and reduced seizure severity in behavioral analyses, and fewer and shorter abnormal brain discharges in LFP recordings of KA-induced epileptic mice were observed. The result of the Co-IP assay showed the interaction between GIPC1 and mGluR7, and the high-resolution immunofluorescence staining also showed the colocalization of these two proteins. Additionally, along with GIPC1 overexpression, the total and cell membrane expression levels of mGluR7 were also increased. And after antagonism of mGluR7, increased epileptic seizures and aggravated seizure severity in behavioral analyses and more and longer abnormal brain discharges in LFP recordings were observed.ConclusionGIPC1 regulates epileptogenesis by interacting with mGluR7 and increasing its expression.

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A glutamate receptor-interacting protein homolog organizes muscle guidance in Drosophila.

Publications

A glutamate receptor-interacting protein homolog organizes muscle guidance in Drosophila.

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