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Developmental expression of LC3α and β: Absence of fibronectin or autophagy phenotype in LC3β knockout mice
Author(s) -
Cann Gordon M.,
Guignabert Christophe,
Ying Lihua,
Deshpande Niru,
Bekker Janine M.,
Wang Lingli,
Zhou Bin,
Rabinovitch Marlene
Publication year - 2008
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21392
Subject(s) - biology , autophagy , fibronectin , microbiology and biotechnology , knockout mouse , gene isoform , phenotype , messenger rna , embryonic stem cell , embryogenesis , embryo , genetics , gene , extracellular matrix , apoptosis
Murine light chain 3 (LC3) exists as two isoforms, LC3α and β: LC3β is an RNA‐binding protein that enhances fibronectin (FN) mRNA translation, and is also a marker of autophagy. We report embryonic expression patterns for LC3α and LC3β, with some overlap but notable differences in the brain, and in tissues of non‐neuronal origin. LC3β knockout (−/−) mice develop normally without a compensatory increase in LC3α. LC3β−/− 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 LC3β−/−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 LC3β, ensuring proper FN accumulation and autophagy during fetal and neonatal life. Developmental Dynamics 237:187–195, 2008. © 2007 Wiley‐Liss, Inc.