Translation elongation defects activate the <i>Caenorhabditis elegans</i> ZIP-2 bZIP transcription factor-mediated toxin defense.

ABSTRACT: The Caenorhabditis elegans bZIP transcription factor ZIP-2 is activated by toxins or mutations that inhibit translational elongation. The zip-2 DNA-binding protein is encoded in a downstream main open reading frame (mORF), but under normal translation elongation conditions only an upstream overlapping oORF -1 frameshifted from mORF is translated. Mutations or toxins that slow translational elongation, but not inhibitors of translational initiation or termination, activate ZIP-2. An mORF initiation codon mutation does not disrupt the normal zip-2 response to translational elongation defects, suggesting that zip-2 activation does not depend on this ATG. An mORF early termination mutant can be activated by strong translation elongation inhibition, suggesting that t

SUBMITTER: Kniazeva M 

PROVIDER: S-EPMC11831180 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature