A first look at the genome structure of hexaploid "Mitcham" peppermint (Mentha × piperita L.).

Peppermint, Mentha × piperita L., is a hexaploid (2n = 6x = 72) and the predominant cultivar of commercial mint oil production in the US. This cultivar is threatened because of high susceptibility to the fungal disease verticillium wilt, caused by Verticillium dahliae.

Biochemical basis for the formation of organ-specific volatile blends in mint.

Above-ground material of members of the mint family is commercially distilled to extract essential oils, which are then formulated into a myriad of consumer products. Most of the research aimed at characterizing the processes involved in the formation of terpenoid oil constituents has focused on leaves. We now demonstrate, by investigating three mint species, peppermint ( ˣ L.

Chromosome-level genome assembly of Mentha longifolia L. reveals gene organization underlying disease resistance and essential oil traits.

Mentha longifolia (L.) Huds., a wild, diploid mint species, has been developed as a model for mint genetic and genomic research to aid breeding efforts that target Verticillium wilt disease resistance and essential oil monoterpene composition.

Dynamic Tissue-Specific Transcriptome Changes in Response to in Wild Mint Species .

is a wild mint species being used as a model to study the genetics of resistance to the fungal wilt pathogen . We used high-throughput Illumina sequencing to study gene expression in response to inoculation in two USDA accessions with contrasting phenotypes: wilt-resistant CMEN 585 and wilt-susceptible CMEN 584. Roots and stems were sampled at two early post-inoculation time points, four hours and twenty-four hours, and again at ten days and twenty days post-inoculation.

Persistence of the Host-Selective Toxin Ptr ToxB in the Apoplast.

The necrotrophic fungus Pyrenophora tritici-repentis is responsible for the disease tan spot of wheat. Ptr ToxB (ToxB), a proteinaceous host-selective toxin, is one of the effectors secreted by P. tritici-repentis.

Solution NMR structures of Pyrenophora tritici-repentis ToxB and its inactive homolog reveal potential determinants of toxin activity.

Pyrenophora tritici-repentis Ptr ToxB (ToxB) is a proteinaceous host-selective toxin produced by Pyrenophora tritici-repentis (P. tritici-repentis), a plant pathogenic fungus that causes the disease tan spot of wheat. One feature that distinguishes ToxB from other host-selective toxins is that it has naturally occurring homologs in non-pathogenic P.

Comparative genomics of a plant-pathogenic fungus, Pyrenophora tritici-repentis, reveals transduplication and the impact of repeat elements on pathogenicity and population divergence.

Pyrenophora tritici-repentis is a necrotrophic fungus causal to the disease tan spot of wheat, whose contribution to crop loss has increased significantly during the last few decades. Pathogenicity by this fungus is attributed to the production of host-selective toxins (HST), which are recognized by their host in a genotype-specific manner. To better understand the mechanisms that have led to the increase in disease incidence related to this pathogen, we sequenced the genomes of three P.

Host-selective toxins of Pyrenophora tritici-repentis induce common responses associated with host susceptibility.

Pyrenophora tritici-repentis (Ptr), a necrotrophic fungus and the causal agent of tan spot of wheat, produces one or a combination of host-selective toxins (HSTs) necessary for disease development. The two most studied toxins produced by Ptr, Ptr ToxA (ToxA) and Ptr ToxB (ToxB), are proteins that cause necrotic or chlorotic symptoms respectively. Investigation of host responses induced by HSTs provides better insight into the nature of the host susceptibility.

Host-selective toxins, Ptr ToxA and Ptr ToxB, as necrotrophic effectors in the Pyrenophora tritici-repentis-wheat interaction.

Host-selective toxins (HSTs) are effectors produced by some necrotrophic pathogenic fungi that typically confer the ability to cause disease. Often, diseases caused by pathogens that produce HSTs follow an inverse gene-for-gene model where toxin production is required for the ability to cause disease and a single locus in the host is responsible for toxin sensitivity and disease susceptibility. Pyrenophora tritici-repentis represents an ideal pathogen for studying the biological significance of such inverse gene-for-gene interactions, because it displays a complex race structure based on its production of multiple HSTs.

Analysis of transcriptome changes induced by Ptr ToxA in wheat provides insights into the mechanisms of plant susceptibility.

To obtain greater insight into the molecular events underlying plant disease susceptibility, we studied transcriptome changes induced by a host-selective toxin of Pyrenophora tritici-repentis, Ptr ToxA (ToxA), on its host plant, wheat. Transcriptional profiling of ToxA-treated leaves of a ToxA-sensitive wheat cultivar was performed using the GeneChip Wheat Genome Array. An improved and up-to-date annotation of the wheat microarray was generated and a new tool for array data analysis (BRAT) was developed, and both are available for public use via a web-based interface.

A Combination of Phenotypic and Genotypic Characterization Strengthens Pyrenophora tritici-repentis Race Identification.

ABSTRACT Pyrenophora tritici-repentis, causal agent of tan spot of wheat, produces multiple host-selective toxins (HSTs), including Ptr ToxA, Ptr ToxB, and Ptr ToxC. The specific complement of HSTs produced by a particular isolate determines its host cultivar specificity. Each unique specificity profile, represented by the differential induction of necrosis or chlorosis on a standard set of wheat differentials, defines a unique race.

UVB dose-toxicity thresholds and steady-state DNA-photoproduct levels during chronic irradiation of inbred Xenopus laevis tadpoles.

Environmental stressors that severely impact some species more than others can alter ecosystems and threaten biodiversity. Genotoxic stress, such as solar UV-B irradiance, may induce levels of DNA damage at rates that exceed repair capacities in some species but remain below repair capacities in other species. Repair rates would seem to establish toxicity thresholds.

Fluoroimaging-based immunoassay of DNA photoproducts in ultraviolet-B-irradiated tadpoles.

Sensitive and accurate measurement of photoproducts induced in DNA by natural or artificial ultraviolet-B (UVB; and UVC) light is essential to evaluate the toxic and mutagenic effects of this radiation. Monoclonal antibodies specific for the two major classes of photoproducts-cyclobutane pyrimidine dimers (CPDs) and pyrimidine-[6-4]-pyrimidinone photoproducts ([6-4]PPs)-have made possible highly specific and sensitive assays. Described here is the use of these primary antibodies with fluorescent secondary antibodies to generate 96-spot arrays.