Developmental expression of LC3α and β: Absence of fibronectin or autophagy phenotype in LC3β knockout mice

Gordon M. Cann, Christophe Guignabert, Lihua Ying, Niru Deshpande, Janine M. Bekker, Lingli Wang, Bin Zhou, Marlene Rabinovitch

Research output: Contribution to journalArticlepeer-review

82 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)187-195
Number of pages9
JournalDevelopmental Dynamics
Issue number1
StatePublished - Jan 2008
Externally publishedYes


  • Autophagy
  • Fibronectin
  • LC3
  • RNA-binding protein
  • Transgenic mouse

ASJC Scopus subject areas

  • Developmental Biology


Dive into the research topics of 'Developmental expression of LC3α and β: Absence of fibronectin or autophagy phenotype in LC3β knockout mice'. Together they form a unique fingerprint.

Cite this