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RbfA, a 30S ribosomal binding factor, is a cold‐shock protein whose absence triggers the cold‐shock response
Author(s) -
Jones Pamela G.,
Inouye Masayori
Publication year - 1996
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1996.tb02582.x
Subject(s) - cold shock domain , biology , ribosome , ribosomal protein , protein biosynthesis , mutant , polysome , translation (biology) , shock (circulatory) , 30s , heat shock , 50s , microbiology and biotechnology , ribosomal rna , messenger rna , heat shock protein , biochemistry , rna , gene , medicine
Summary The cold‐shock response, characterized by a specific pattern of gene expression, is induced upon a downshift in temperature and in the presence of inhibitors of ribosomal function. Here, we demonstrate that RbfA of Escherichia coli , considered to be involved in ribosomal maturation and/or initiation of translation, is a cold‐shock protein. Shifting the rbfA mutant to a lower temperature resulted in a constitutive induction of the cold‐shock response accompanied by slower growth at low temperatures, while shifting the rbfA mutant that overproduces wild‐type RbfA resulted in an increase in total protein synthesis accompanied by faster growth adaptation to the lower temperature. Furthermore, the cold‐shock response was also constitutively induced in a cold‐sensitive 16S rRNA mutant at low temperatures. Accompanying the transient induction of the cold‐shock response, we also report that shifting E. coli from 37°C to 15°C resulted in a temporary inhibition of initiation of translation, as evidenced by the transient decrease in polysomes accompanied by the transient increase in 70S monosomes. The accumulative data indicate that the inducing signal for the cold‐shock response is the increase in the level of cold‐unadapted non‐translatable ribo‐somes which are converted to cold‐adapted translatable ribosomes by the association of cold‐shock proteins such as RbfA. Therefore, the expression of the cold‐shock response, and thus cellular adaptation to low temperature, is regulated at the level of translation. The data also indicate that cold‐shock proteins can be translated by ribosomes under conditions that are not translatable for most mRNAs.