Disease relevance of femA

• Survey of the methicillin resistance-associated genes mecA, mecR1-mecI, and femA-femB in clinical isolates of methicillin-resistant Staphylococcus aureus [1].
• Various auxilliary genes are known to affect methicillin resistance expression, and one of these genes, femA, was necessary for the expression of this faster rate of autolysis [2].
• We developed, validated, and implemented real-time polymerase chain reaction (PCR) detection of the femA gene for Staphylococcus aureus and the mecA gene for methicillin resistance directly from BACTEC (Becton Dickinson, Sparks, MD) blood culture bottles showing gram-positive cocci in clusters [3].
• The triplex qPCR assay measures simultaneously the following targets: (i) mecA gene, conferring methicillin resistance, common to both S. aureus and Staphylococcus epidermidis; (ii) femA gene from S. aureus; and (iii) femA gene from S. epidermidis [4].
• Molecular characterization of femA from Staphylococcus hominis and Staphylococcus saprophyticus, and femA-based discrimination of staphylococcal species [5].

High impact information on femA

• S. aureus strains carrying mutations in the femA, femB, femAB, or the femAX genes synthesize altered cross-bridges, and each of these strains displayed decreased sorting activity [6].
• The S. aureus assay uses a femA marker to identify cells as S. aureus and a mecA marker to probe for methicillin resistance [7].
• Mutations in femA, the gene required for incorporation of the second and third glycines into the cross bridge, were found following PCR amplification and nucleotide sequence analysis [8].
• Complementation of lysostaphin-resistant mutants with pBBB31, which encodes femA, restored the phenotype of oxacillin resistance and lysostaphin susceptibility [8].
• This strong conservation of femA suggests an important role for femA in cell wall metabolism and methicillin resistance [1].

Biological context of femA

• All strains containing an intact mec element in their chromosomes were found to be defective in adhesion to fibrinogen and fibronectin immobilized on polymethylmethacrylate coverslips, regardless of the presence or absence of additional mutations in the femA, femB, or femC gene, known to decrease expression of methicillin resistance in S. aureus [9].
• Sequencing and analysis of the femA region of mutants isolated by chemical mutagenesis and selection for lysostaphin resistance revealed point mutations leading to the expression of truncated FemA proteins [10].
• The inactivation of FemB by insertion of Tn551 in the central part of the femB open reading frame was shown to increase susceptibility of methicillin-resistant Staphylococcus aureus strains toward beta-lactam antibiotics to the same extent as did inactivation of femA [11].
• Strains in which femA was inactivated by insertion of Tn551 into the control region of the femAB operon still expressed about 10% of the protein compared to their parent strains [12].
• On this basis, a consensus sequence of the femA gene was defined and interspecies variations were exploited to design strategies for staphylococci species-specific identification, including multiplex PCR amplification and a reverse hybridization assay [5].

Anatomical context of femA

• Both femA and femB are involved in the formation of cell wall peptidoglycan pentaglycine cross-bridges [13].

Associations of femA with chemical compounds

• The methicillin susceptibility of this particular strain was presumably due to a spontaneous femA-like mutation [1].
• Complementation of the femAB null mutant by either femA or femAB resulted in the extension of the cross-bridges to a triglycine or a pentaglycine, respectively [14].
• Inactivation of either femA or femB causes decreased resistance to methicillin, increased resistance to lysostaphin, and decreased glycine content in the interpeptide chains of peptidoglycan [15].
• These results and those of previous studies suggest that Triton X might act on factors other than the mecA or femA products [16].

Analytical, diagnostic and therapeutic context of femA

• These results were completely consistent with the results of femA detection using standard PCR and subsequent Southern blot hybridization [17].
• Molecular epidemiology of Staphylococcus spp. contamination in the ward environment: study on mecA and femA genes in methicillin-resistant strains [18].

References