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Blocks in elongation and initiation of protein synthesis induced by interferon treatment in mouse L cells
Abstract:
Synthesis of polypeptide chains coded by exogenous messenger RNAs is inhibited in cell-free extracts from interferon-treated mouse L cells, due to a "deficiency" in some specific tRNA species. A detailed analysis shows that polypeptide chain elongation is blocked and incomplete chains are formed. After a few minutes, however, initiation of new polypeptide chains is also blocked. Messenger RNA still binds to ribosomes but initiator Met-tRNA(FMET) binding is inhibited. The block in initiation appears to be secondary to the block in elongation.
Insights
Interferon treatment of mouse cells inhibits protein synthesis by blocking polypeptide chain elongation due to a tRNA deficiency. This subsequently halts the initiation of new protein chains, even though messenger RNA still binds to ribosomes.
Area of Science:
- Molecular Biology
- Virology
- Cell Biology
Background:
- Interferons are key antiviral proteins.
- Protein synthesis is crucial for cellular function and viral replication.
- Previous studies suggested interferon's antiviral effects involve protein synthesis inhibition.
Purpose of the Study:
- To investigate the mechanism of protein synthesis inhibition in interferon-treated cells.
- To identify the specific molecular defects causing this inhibition.
Main Methods:
- Utilized cell-free extracts from interferon-treated mouse L cells.
- Analyzed polypeptide chain synthesis, elongation, and initiation.
- Assessed messenger RNA and initiator transfer RNA (tRNA) binding to ribosomes.
Main Results:
- Protein synthesis was inhibited in cell-free extracts from interferon-treated cells.
- A deficiency in specific transfer RNA (tRNA) species was identified as the cause.
- Polypeptide chain elongation was blocked, leading to incomplete chains.
- Initiation of new polypeptide chains was subsequently inhibited, with impaired initiator Met-tRNA(FMET) binding.
Conclusions:
- Interferon treatment induces a tRNA deficiency that impairs protein synthesis.
- The block in elongation precedes and likely causes the block in initiation.
- This mechanism contributes to interferon's antiviral activity by limiting viral protein production.