Disease relevance of colA

• In addition, a gene (colA) encoding a 120-kDa collagenase was cloned in Escherichia coli [1].
• To determine if the ability to produce collagenase was a significant virulence factor in cases of gas gangrene or clostridial myonecrosis that are caused by C. perfringens, a chromosomal colA mutant was constructed by homologous recombination and subsequently virulence tested in the mouse myonecrosis model [2].
• A novel gene that regulates the alpha-toxin (plc), kappa-toxin (colA), and theta;-toxin (pfoA) genes was identified using toxin-negative mutant strains of Clostridium perfringens [3].
• The tetanus toxin and a collagenase are encoded on a 74,082-bp plasmid, containing 61 ORFs [4].
• Humoral immune responses in Peyronie's disease patients receiving clostridial collagenase therapy [5].

High impact information on colA

• We found that the small 3'-portion of VR-RNA was sufficient for the activation of toxin genes, which suggested that VR-RNA itself could act as an RNA regulatory molecule for the plc and colA genes mediating the regulatory information from the VirR/VirS system in C. perfringens [6].
• The other gene, hyp7, whose transcript was positively regulated by the VirR/VirS system, was shown to activate the transcription of the colA (kappa-toxin) and plc (alpha-toxin) genes, but not the pfoA (theta-toxin) gene in C. perfringens [7].
• The liver cell suspension, prepared by perfusing the liver with collagenase, was treated with enterotoxin from Clostridium perfringens for 15 min [8].
• CcpA was also required for maximum synthesis of collagenase (kappa toxin) and acted as a repressor of polysaccharide capsule synthesis in the presence of glucose, but it did not regulate synthesis of the phospholipase PLC (alpha toxin) [9].
• Both colG and colA have a homologous gene, mscL, at their 3' ends [10].

Biological context of colA

• Nested deletions were used to define the coding region of colA, and this region was sequenced; from the nucleotide sequence, this gene encodes a protein of 1,104 amino acids (M(r), 125,966) [1].
• These results suggest that gene duplication and segment duplication have occurred in an ancestor cell common to C. histolyticum and C. perfringens and that further divergence of the parent gene produced colG and colA [10].
• Southern analysis revealed that the colA gene is located 6.5 kb downstream of the pbg gene in the chromosome of C. perfringens [11].
• It is suggested that the productivity of theta-toxin in these strains is diverse because of the multiple genetic backgrounds including single deletion of pfoA, large deletion of the pfoA-colA region and the putative point mutations [12].
• We also identified four other gelatinases (105, 82, 78, and 67 kDa) and determined their N-terminal amino acid sequences, all of which coincided with that of either ColG or ColH [10].

Anatomical context of colA

• 6. Toxin-induced contraction was diminished by pretreating aorta with collagenase or by rubbing the intimal surface to remove the endothelium [13].
• Some of these virulence factors, such as the alpha toxin, which is phospholipase C, and the kappa toxin, which is a collagenase, are enzymes that hydrolyze substances essential to the integrity of membranes or other body structures [14].

Associations of colA with chemical compounds

• The purified enzyme was identified as the major collagenase of the organism, and it cleaved typical collagenase substrates such as azocoll, a synthetic substrate (4-phenylazobenzyloxy-carbonyl-Pro-Leu-Gly-Pro-D-Arg [Pz peptide]), and a type I collagen fibril [1].
• The 105-kDa protein also showed activity against a typical collagenase substrate, azocoll, and was inhibited by EDTA and 1,10-phenanthroline [15].

Other interactions of colA

• The colA gene, which encodes the kappa-toxin, had two major promoters, only one of which was virR/virS-dependent [16].

Analytical, diagnostic and therapeutic context of colA

• Intralesional injection of 3,000 to 12,650 Units of collagenase induced an increase of two- to 10-fold in the IgG levels at one to two months in 88 per cent of patients [5].
• Pre, 1 and/or 2 month post treatment sera were analyzed in radioimmunoassays for human IgG and IgE antibodies using solid phase purified Cl. histolyticum collagenase to extract antibodies from serum and 125I-Protein A or rabbit anti-human IgE to detect bound IgG and IgE, respectively [5].

References