Disease relevance of rrmJ

• To investigate whether overexpression of other E. coli genes can restore the severe growth defect observed in rrmJ null mutants, we constructed an overexpression library from the rrmJ deletion strain and cloned and identified the E. coli genes that were capable of rescuing the rrmJ mutant phenotype [1].

High impact information on rrmJ

• Null mutations in ftsJ show a dramatically altered ribosome profile, a severe growth disadvantage, and a temperature-sensitive phenotype [2].
• We identify FtsJ, the first encoded protein of the ftsJ-hflB heat shock operon, as an Escherichia coli methyltransferase of the 23 S rRNA [3].
• We have recently identified RrmJ, the first encoded protein of the rrmJ-ftsH heat shock operon, as being the Um(2552) methyltransferase of 23S rRNA, and reported that rrmJ-deficient strains exhibit growth defects, reduced translation rates and reduced stability of 70S ribosomes [4].
• In the present study, we show that a lack of U2552 methylation, obtained in rrmJ-deficient mutants, results in a decrease in programmed +1 and -1 translational frameshifing and a decrease in readthrough of UAA and UGA stop codons [4].

Biological context of rrmJ

• We recently identified RrmJ (alias FtsJ), the first encoded protein of the rrmJ-hflB heat shock operon, as an Um(2552) methyltransferase of the 23S rRNA [5].
• We also identified another gene (ftsJ) affecting cell division in the region upstream of the ftsH gene [6].

References