Disease relevance of mnmG

• This result shows clearly that E. coli oriC and flanking genes gidA and gidB have been translocated by the inversion of some 40 kb fragment [1].
• Global regulation by gidA in Pseudomonas syringae [2].
• Sequence analysis of a 34.7-kb DNA segment from the genome of Buchnera aphidicola (endosymbiont of aphids) containing groEL, dnaA, the atp operon, gidA, and rho [3].

High impact information on mnmG

• We compared phylogenies of host genes (the nuclear EF-1alphaF2 and mitochondrial COI/II) and Blochmannia genes (16S ribosomal DNA [rDNA], groEL, gidA, and rpsB), totaling more than 7 kilobases for each of 16 Camponotus species [4].
• The gidA* mutant releases a heat-stable, protease-resistant, small molecular weight molecule that acts in trans to inhibit aggregation and gene expression of wild-type cells during development [5].
• In both seqA- and dam- cells, gidA and dnaA continued to be transcribed after initiation, whereas the inhibition of mioC transcription before initiation was unaltered [6].
• Conversely, the active transcription of gidA and dnaA prior to initiation is consistent with their positive effects on initiation, and their shutdown after initiation could serve to limit premature reinitiation [7].
• Consistent with the finding that GidA is essential in Escherichia coli, we were unable to obtain a gidA mutant in H. pylori despite evidence that insertional mutagenesis had occurred [8].

Biological context of mnmG

• Site-specific recombination of a disrupted gidA gene into the chromosome resulted in the same phenotypic pattern as transposon insertion [2].
• Wild-type levels of reporter expression were restored by supplying an intact gidA gene on a plasmid [2].
• The mutations in the six group II mutants were complemented by introduction of the gidA gene, which may be involved in cell division [9].
• The salA gene, a copy number suppressor of the syringomycin-deficient phenotype in gacS and gacA mutants, was also found to suppress the antibiotic-negative phenotypes of gidA mutants, suggesting that gidA might play some role in salA regulation [2].
• Analysis of two virulence mutants of Pseudomonas syringae B728a revealed that the Tn 5 sites of insertion were within the gidA open reading frame (ORF) [2].

Regulatory relationships of mnmG

• However, the mechanisms involved are different: regulation of transcription in the case of asnA and asnC and post-transcriptional control of gidA [10].

Other interactions of mnmG

• Interestingly, high-performance liquid chromatography (HPLC) analysis shows that identical levels of the same undermodified form of U34 are present in tRNA hydrolysates from loss-of-function gidA and mnmE mutants [11].

References