Colletotrichum shisoi sp. nov., an anthracnose pathogen of Perilla frutescens in Japan: molecular phylogenetic, morphological and genomic evidence.

Species of the fungal genus Colletotrichum are among the most devastating pathogens of agricultural crops in the world. Based on DNA sequence data (ITS, GAPDH, CHS-1, ACT, TUB2) and morphology, we revealed Colletotrichum isolates infecting the oil crop Perilla frutescens, commonly known as shiso, to represent a previously unknown species of the C. destructivum species complex and described it as C. shisoi. We found that C. shisoi appears to be able to adopt a hemibiotrophic lifestyle, characterised by the formation of biotrophic hyphae followed by severe necrotic lesions on P. frutescens, but is less virulent on Arabidopsis, compared to its close relative C. higginsianum which also belongs to the C. destructivum species complex. The genome of C. shisoi was sequenced, annotated and its predicted proteome compared with four other Colletotrichum species. The predicted proteomes of C. shisoi and C. higginsianum, share many candidate effectors, which are small, secreted proteins that may contribute to infection. Interestingly, C. destructivum species complex-specific secreted proteins showed evidence of increased diversifying selection which may be related to their host specificities.

Genome Sequence Resources for Four Phytopathogenic Fungi from the Colletotrichum orbiculare Species Complex.

Colletotrichum orbiculare species complex fungi are hemibiotrophic plant pathogens that cause anthracnose of field crops and weeds. Members of this group have genomes that are remarkably expanded relative to other Colletotrichum fungi and compartmentalized into AT-rich, gene-poor and GC-rich, gene-rich regions. Here, we present an updated version of the C. orbiculare genome, as well as draft genomes of three other members from the C. orbiculare species complex: the alfalfa pathogen C. trifolii, the prickly mallow pathogen C. sidae, and the burweed pathogen C. spinosum. The data reported here will be important for comparative genomics analyses to identify factors that play a role in the evolution and maintenance of the expanded, compartmentalized genomes of these fungi, which may contribute to their pathogenicity.

Draft Genome Assembly of Colletotrichum chlorophyti, a Pathogen of Herbaceous Plants.

Colletotrichum chlorophyti is a fungal pathogen that infects various herbaceous plants, including crops such as legumes, tomato, and soybean. Here, we present the genome of C. chlorophyti NTL11, isolated from tomato. Analysis of this genome will allow a clearer understanding of the molecular mechanisms underlying fungal host range and pathogenicity.

Apoptosis induction by T-2 toxin: activation of caspase-9, caspase-3, and DFF-40/CAD through cytosolic release of cytochrome c in HL-60 cells.

The molecules participating in apoptosis induced by T-2 toxin in human leukemia HL-60 cells were investigated. The rank order of the potency of trichothecene mycotoxins to induce internucleosomal DNA fragmentation was found to be T-2, satratoxin G, roridin A >> diacetoxyscirpenol > baccharin B-5 >> nivalenol, deoxynivalenol, 3-acetyldeoxynivalenol, fusarenon-X, baccharin B-4=vehicle control. Western blot analysis of caspase-3 in T-2-treated cells clearly indicated the appearance of its catalytically active fragment of 17-kDa. Increased caspase-3 activity was also detected by using a fluorogenic substrate, DEVD-AMC. Next, cells exposed to T-2 led to cleavage of PARP from its native 116-kDa form to the 85-kDa product. Moreover, DFF-45/ICAD were cleaved to give a 12.5-kDa fragment via T-2 treatment. T-2 caused the release of cytochrome c from mitochondria into the cytosol. Increased enzymic activity of caspase-9 on LEHD-AMC was shown. These data indicate that T-2-induced apoptosis involves activation of caspase-3 and DFF-40/CAD through cytosolic accumulation of cytochrome c along with caspase-9 activation.

Surgical treatment of tricuspid insufficiency in patients undergoing mitral valve replacement.

During the past eight years, 46 of the 106 patients who underwent mitral valve replacement were associated with tricuspid insufficiency. No surgical correction was performed (14 cases) in cases of slight tricuspid insufficiency. Tricuspid annuloplasty (11 cases) or valve replacement (21 cases) was employed according to the severity of insufficiency. In the non-repair group, the mortality rate was fairly low (21 per cent), but the postoperative status was the least satisfactory by the NYHA classification. Tricuspid insufficiency was significantly reduced only in two of these 14 cases after the mitral valve replacement. In the tricuspid annuloplasty group, although the technique of tricuspid annuloplasty did not always correct insufficiency completely, only one patient died of residual insufficiency. The cardiac output measured with Minnesota Impedance Cardiograph increased postoperatively in proportion to stress in this group. In the tricuspid valve replacement group, cardiac catheterization studies revealed hemodynamic improvement at rest in all, but cardiac output during exercise remained unchanged or decreased in some cases. Now we consider that tricuspid insufficiency with advanced mitral valve disease, even of a slight degree, should be surgically treated and that annuloplasty has more obvious hemodynamic benefits than valve replacement.