Disease relevance of fabZ

• The suppressor mutation, named sfhC21, that allows Escherichia coli ftsH null mutant cells to survive was found to be an allele of fabZ encoding R-3-hydroxyacyl-ACP dehydrase, involved in a key step of fatty acid biosynthesis, and appears to upregulate the dehydrase [1].
• These genes show homology to fabZ and accB from E. coli and Bacillus subtilis, respectively, both involved in fatty acids biosynthesis [2].
• Preliminary evaluation of the use of the sefA fimbrial gene to elicit immune response against Salmonella enterica serotype Enteritidis in chickens [3].

High impact information on fabZ

• A mutation, sabA1, that reverses the MacConkey sensitivity phenotype of asmB1 maps within fabZ (whose product is needed for phospholipid synthesis from a precursor) is also required for lipid A synthesis [4].
• Cloning and sequence analysis of chromosomal DNA downstream of lpxD revealed the presence of the fabZ and lpxA genes [5].
• The tolZ21 mutant was found to have a suppressor mutation, named sfhC, which allowed cells to survive [6].
• Primer extension analysis of sefABC revealed two major transcription start sites located upstream of sefA [7].
• Transcription of sefBC also initiated from the sefA promoter region [7].

Biological context of fabZ

• The nucleotide sequence of the sefA gene shared no homology with the Salmonella fimA gene encoding type 1 fimbriae, and these genes showed distinct patterns of distribution within salmonellae [8].
• By contrast, an ftsH null mutant carrying the suppressor mutation sfhC did not affect partitioning of the plasmid [9].

References