The marine yeast strain Metschnikowia saccharicola DD21-2, isolated from sediments in the Yalu River, produces a killer toxin with a lethal effect on Metschnikowia bicuspidate strain WCY, a pathogenic yeast strain that infects crabs. In this study, the killer toxin was purified and characterized. After sequential purification, the purity of the killer toxin was increased 72.2-fold over the purity of the yeast cell culture supernatant. The molecular weight of the purified killer toxin was 47.0 kDa. The optimal pH and temperature for killing activity were 5.5°C and 16°C, respectively. The killing activity was stable over a pH range of 4.0-6.5 and temperature range of 0°C-40°C. The purified killer toxin was only effective against toxin-sensitive integral cells and had no killing effect on the protoplasts of toxin-sensitive cells. When exerting the killing effect, the toxin bind to a cell wall receptor of the treated strain, disrupted cell wall integrity and eventually caused death. The amino acid sequence identified by mass spectroscopy indicated that the purified killer toxin might be a protein kinase, but did not show β-1,3-glucanase activity, consistent with the laminarin hydrolysis results. These findings provide a basis for disease prevention and control in marine aquaculture.
Phycobiliprotein biosynthesis was investigated in four strains of the unicellular rhodophyte, Cyandium caldarium, with different pigment phenotypes. All strains were incapable of synthesizing phycobiliproteins when grown in the dark. Westem blotting experiments showed that dark-grown cells of the wild-type and mutant GGB synthesized the a and jt subunit polypeptides of allophyocyanin and phycocyanin after exposure to light for 24 hours, whereas cells of mutant IIIC and GGBY did not. Similarly, light promoted the appearance of allophycocyanin and phycocyanin mRNAs in the wild-type and GGB but not in IIIC and GGBY. However, Southern blots of restricted genomic DNA from the wild type, IIIC, GGBY, and GGB, all hybridized with heterologous phycobiliprotein gene probes and revealed that all four strains contained identical Pst, EcoRI, and Dral restriction fragments containing allophycocyanin and phycocyanin genes. Cells of the wild type and GGB incubated in the dark with the heme precursor. 6-aminolevulinate, synthesized allophycocyanin and phycocyanin apoproteins providing strong evidence for the role of a tetrapyrrole in regulation of phycobiliprotein gene expression. However, cells of IIIC and GGBY incubated in the dark with 5-aminolevulinate did not contain detectable quantities of allophycocyanin or phycocyanin apoproteins. The possible role of a tetrapyrrole in phycobiliprotein gene expression and basis for the genetic lesion in mutants IIIC and GGBY is discussed.
We present a 64-year-old woman who developed symptoms of acute pericarditis three days after undergoing intravesical instillation of mitomycin C following transurethral bladder tumor resection. Mitomycin C is a chemotherapeutic agent which acts by alkylation of DNA and is known to be cardiotoxic when systemically administered. Despite classic pericarditis symptoms, the patient underwent an urgent coronary angiogram due to elevated cardiac troponin I level, EKG changes, and wall motion abnormalities on her echocardiogram. During her angiogram, it was found that she had multiple stenotic coronary artery lesions, with no acute total coronary occlusions, and percutaneous coronary intervention (PCI) was done with placement of a single drug-eluting stent for a 95% stenotic lesion in the left anterior descending artery. The patient was discharged after an uneventful hospitalization on dual antiplatelet therapy with aspirin and prasugrel, and colchicine for pericarditis. It is likely that the patient's presentation was the result of a perimyocardial inflammatory process secondary to intravesically administered mitomycin C, rather than an acute coronary syndrome. While the pathophysiological basis of cardiotoxicity of systemically administered mitomycin C is well documented, more studies are needed to determine whether intravesical MMC may cause cardiotoxicity.
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