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The E. coli divE mutation, which differentially inhibits synthesis of certain proteins, is in tRNASer1.
Author(s) -
Tamura F.,
Nishimura S.,
Ohki M.
Publication year - 1984
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1984.tb01936.x
Subject(s) - biology , mutation , genetics , escherichia coli , escherichia coli proteins , computational biology , microbiology and biotechnology , gene
The temperature‐sensitive divE mutant of Escherichia coli cannot synthesize certain membrane and cytoplasmic proteins at a non‐permissive temperature. Growth of the mutant cells is arrested at a specific stage of the cell cycle when exposed to the non‐permissive conditions, suggesting that the divE mutant possesses a defect in cell division control. From sequence determination of a cloned 1.35‐kbp DNA fragment that complements the temperature‐sensitive divE42 mutation, we characterized two genes in the segment; one for tRNASer1 and the other for a 23 500 dalton protein. In parallel experiments we cloned the homologous 1.35‐kbp DNA fragment from the divE42 mutant and determined its entire nucleotide sequence. Comparison of the two sequences showed that the mutation site is located not in the protein gene, but in the tRNA gene, where A10 is replaced by G10 in the D‐stem. Lambda transducing phages carrying the subcloned tRNASer1 gene complemented the divE42 mutation, thereby confirming the conclusion obtained from sequence analyses of the fragments. This finding indicates that tRNASer1 is specifically involved in regulation of cell cycle‐specific protein synthesis, coupled with an important step in the process of cell division, or that usage of serine tRNA is functionally specific for the biosynthesis of certain proteins.