Disease relevance of metE

• Salmonella typhimurium metE operator-constitutive mutations [1].

High impact information on metE

• The first is a complex surface consisting of residues important for alpha-DNA interactions, activation of both genes (residues 263, 293, and 320), and activation of either metE only (residues 260, 276, 302, 306, 309, and 322) or metH only (residues 258, 264, 290, 294, and 295) [2].
• We used both random mutagenesis and alanine scanning to identify alphaCTD residues that are crucial for MetR-dependent activation of metE and metH [2].
• The transcription start sites for the metR and metE genes were determined by mung bean nuclease mapping [3].
• A metE mutation was transduced into a cheR cheB double mutant, and the cells were starved for methionine [4].
• The metR and metE genes are divergently transcribed, with only 25 base pairs separating the transcription start sites [3].

Biological context of metE

• The formation of type II F' ilv cya metE plasmids from the Salmonella typhimurium Hfr strain SA722 occurs by general recombination between repeated rrn [5].
• In contrast, a corresponding cheR+ cheB+ metE mutant completely lost its chemotaxis ability after being starved for methionine [4].

Associations of metE with chemical compounds

• Aerobically, metE mutants of S. typhimurium need either methionine or cobalamin as a nutritional supplement for growth [6].

Other interactions of metE

• The growth response to cobalamin depends upon a cobalamin-requiring enzyme, encoded by the gene metH, that catalyzes the same reaction as the metE enzyme [6].
• The overlapping nature of the metR and metE promoters suggests that there may be common regulatory signals for the two genes [3].

References