Journal
EMBO JOURNAL
Volume 22, Issue 5, Pages 1199-1209Publisher
WILEY
DOI: 10.1093/emboj/cdg103
Keywords
eIF4E; IRES; prion; Ure2p; [URE3]
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Funding
- NIGMS NIH HHS [GM26796, R01 GM026796] Funding Source: Medline
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The [URE3] phenotype in Saccharomyces cerevisiae is caused by the inactive, altered (prion) form of the Ure2 protein (Ure2p), a regulator of nitrogen catabolism. Ure2p has two functional domains: an N-terminal domain necessary and sufficient for prion propagation and a C-terminal domain responsible for nitrogen regulation. We show here that the mRNA encoding Ure2p possesses an IRES (internal ribosome entry site). Internal initiation leads to the synthesis of an N-terminally truncated active form of the protein (amino acids 94-354) lacking the prion-forming domain. Expression of the truncated Ure2p form (94-354) mediated by the IRES element cures yeast cells of the [URE3] phenotype. We assume that the balance between the full-length and truncated (94-354) Ure2p forms plays an important role in yeast cell physiology and differentiation.
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