Competition between bacteriophage f2 RNA and bacteriophage T4 messenger RNA

In an $\text{Escherichia coli}$ cell-free protein synthesis assay, mRNA isolated from cells late after infection by phage T4 out-competes bacteriophage f2 RNA. Addition of a saturating or subsaturating amount of T4 mRNA inhibits translation of f2 RNA, while even an excess of f2 RNA has no effect on translation of T4 mRNA. Peptide mapping of reaction products labeled with formyl-[³⁵S]-methionyl-tRNA was used to quantitate f2 and T4 protein products synthesized in the same reaction. We suggest that messenger RNA competition might be one mechanism by which T4 superinfection of cells infected with phage f2 blocks translation of f2 RNA and possibly host mRNA.     

Autogenous regulatory site on the bacteriophage T4 gene 32 messenger RNA

We have identified the binding site on the bacteriophage T4 gene 32 mRNA responsible for autogenous translational regulation. We demonstrate that this site is largely unstructured and overlaps the initiation codon of gene 32 as previously predicted. Co-operative binding of gene 32 protein to this site specifically blocks the formation of 30 S-tRNA(fMet)-gene 32 mRNA ternary complexes and initiation of translation. The translational operator is bound co-operatively by gene 32 protein and this binding is facilitated by a nucleation site far upstream from the initiation codon. A similar unstructured mRNA lacking this nucleation site is also bound co-operatively, but only at concentrations of gene 32 protein higher than those needed to repress binding of ribosomes to the gene 32 mRNA. Some sequence-specific interactions may also influence this binding. Comparison of the bacteriophage T2, T4 and T6 gene 32 operator sequences leads us to propose that the nucleation site is a pseudoknot.     

Dexamethasone-mediated inhibition of human T cell growth factor and gamma-interferon messenger RNA

Glucocorticoids suppress the proliferation of human T lymphocytes. Activated T lymphocytes require T cell growth factor (TCGF) for proliferation. TCGF is produced by a subset of T lymphocytes, and this production is regulated at the TCGF mRNA level. Dexamethasone, a synthetic glucocorticoid, strongly inhibits the synthesis of TCGF mRNA in human normal peripheral blood lymphocytes stimulated in culture with phytohemagglutinin. It also inhibits the accumulation of gamma-interferon mRNA in these cells. This dual effect may in part explain some of the immunosuppressive and anti-inflammatory effects of glucocorticoids.