Developmental expression of LC3alpha and beta: absence of fibronectin or autophagy phenotype in LC3beta knockout mice
| Autor: | Christophe Guignabert, Niru Deshpande, Marlene Rabinovitch, Janine M. Bekker, Lingli Wang, Bin Zhou, Gordon M. Cann, Lihua Ying |
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| Rok vydání: | 2007 |
| Předmět: |
Genetically modified mouse
Blotting Western Caveolin 1 RNA-binding protein Matrix metalloproteinase Nervous System Mesoderm Mice Autophagy Animals Humans Protein Isoforms Cells Cultured In Situ Hybridization Mice Knockout biology Wild type Gene Expression Regulation Developmental Fibroblasts Phenotype Molecular biology Survival Analysis Matrix Metalloproteinases Fibronectins Fibronectin embryonic structures Knockout mouse biology.protein biological phenomena cell phenomena and immunity Microtubule-Associated Proteins Developmental Biology |
| Zdroj: | Developmental dynamics : an official publication of the American Association of Anatomists. 237(1) |
| ISSN: | 1058-8388 |
| Popis: | Murine light chain 3 (LC3) exists as two isoforms, LC3 and : LC3 is an RNA-binding protein that enhances fibronectin (FN) mRNA translation, and is also a marker of autophagy. We report embryonic expression patterns for LC3 and LC3, with some overlap but notable differences in the brain, and in tissues of non-neuronal origin. LC3 knockout (/) mice develop normally without a compensatory increase in LC3. LC3/ embryonic fibroblasts (MEFs) exhibit reduced FN synthesis but maintain wild type (WT) levels of FN protein. No significant changes in proteins associated with FN turnover, i.e., caveolin-1, LRP-1, or matrix metalloproteinases were identified. Autophagosomes form in amino acid–starved LC3/MEFs, and Caesarean-delivered pups survive as long as WT pups without an increase in LC3-related proteins linked to autophagy. These results suggest novel compensatory mechanisms for loss of LC3, ensuring proper FN accumulation and autophagy during fetal and neonatal life. Developmental Dynamics 237:187–195, 2008. © 2007 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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