Journal
DEVELOPMENTAL DYNAMICS
Volume 237, Issue 1, Pages 187-195Publisher
WILEY
DOI: 10.1002/dvdy.21392
Keywords
LC3; RNA-binding protein; fibronectin; autophagy; transgenic mouse
Categories
Funding
- NHLBI NIH HHS [R01 HL074186] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL074186] Funding Source: NIH RePORTER
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Murine light chain 3 (LC3) exists as two isoforms, LC3 alpha and beta: LC3 beta 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 alpha and LC3 beta, with some overlap but notable differences in the brain, and in tissues of non-neuronal origin. LC3 beta knockout (-/-) mice develop normally without a compensatory increase in LC3 alpha LC3 beta-/- 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 beta-/-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 beta, ensuring proper FN accumulation and autophagy during fetal and neonatal life.
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