Lynn Epstein

A Kinase-START Gene Confers Temperature-Dependent Resistance to Wheat Stripe Rust

Stripe rust is a devastating fungal disease that afflicts wheat in many regions of the world. New races of Puccinia striiformis, the pathogen responsible for this disease, have overcome most of the known race-specific resistance genes. We report the map-based cloning of the gene Yr36 (WKS1), which confers resistance to a broad spectrum of stripe rust races at relatively high temperatures (25° to 35°C). This gene includes a kinase and a putative START lipid-binding domain. Five independent mutations and transgenic complementation confirmed that both domains are necessary to confer resistance. Yr36 is present in wild wheat but is absent in modern pasta and bread wheat varieties, and therefore it can now be used to improve resistance to stripe rust in a broad set of varieties.

Lifestyle transitions in plant pathogenic Colletotrichum fungi deciphered by genome and transcriptome analyses

Colletotrichum species are fungal pathogens that devastate crop plants worldwide. Host infection involves the differentiation of specialized cell types that are associated with penetration, growth inside living host cells (biotrophy) and tissue destruction (necrotrophy). We report here genome and transcriptome analyses of Colletotrichum higginsianum infecting Arabidopsis thaliana and Colletotrichum graminicola infecting maize. Comparative genomics showed that both fungi have large sets of pathogenicity-related genes, but families of genes encoding secreted effectors, pectin-degrading enzymes, secondary metabolism enzymes, transporters and peptidases are expanded in C. higginsianum. Genome-wide expression profiling revealed that these genes are transcribed in successive waves that are linked to pathogenic transitions: effectors and secondary metabolism enzymes are induced before penetration and during biotrophy, whereas most hydrolases and transporters are upregulated later, at the switch to necrotrophy. Our findings show that preinvasion perception of plant-derived signals substantially reprograms fungal gene expression and indicate previously unknown functions for particular fungal cell types.

MINIREVIEW—POLYPHENOLS AND OXIDASES IN SUBSTRATUM ADHESION BY MARINE ALGAE AND MUSSELS

Minireviews do not have abstracts.

One fungus, one name

In this letter, we advocate recognizing the genus Fusarium as the sole name for a group that includes virtually all Fusarium species of importance in plant pathology, mycotoxicology, medicine, and basic research. This phylogenetically guided circumscription will free scientists from any obligation to use other genus names, including teleomorphs, for species nested within this clade, and preserve the application of the name Fusarium in the way it has been used for almost a century. Due to recent changes in the International Code of Nomenclature for algae, fungi, and plants, this is an urgent matter that requires community attention. The alternative is to break the longstanding concept of Fusarium into nine or more genera, and remove important taxa such as those in the F. solani species complex from the genus, a move we believe is unnecessary. Here we present taxonomic and nomenclatural proposals that will preserve established research connections and facilitate communication within and between research communities, and at the same time support strong scientific principles and good taxonomic practice.

One fungus, one name: defining the genus Fusarium in a scientifically robust way that preserves longstanding use.

In this letter, we advocate recognizing the genus Fusarium as the sole name for a group that includes virtually all Fusarium species of importance in plant pathology, mycotoxicology, medicine, and basic research. This phylogenetically guided circumscription will free scientists from any obligation to use other genus names, including teleomorphs, for species nested within this clade, and preserve the application of the name Fusarium in the way it has been used for almost a century. Due to recent changes in the International Code of Nomenclature for algae, fungi, and plants, this is an urgent matter that requires community attention. The alternative is to break the longstanding concept of Fusarium into nine or more genera, and remove important taxa such as those in the F. solani species complex from the genus, a move we believe is unnecessary. Here we present taxonomic and nomenclatural proposals that will preserve established research connections and facilitate communication within and between research communities, and at the same time support strong scientific principles and good taxonomic practice.

Adhesion of Fungi to the Plant Surface

The initial process of attachment of fungal propagules to a host plant is essential to the successful establishment of pathogenesis. Attachment may be involved in recognition of the host surface, serve as a base around which the infection court can be altered, and may include adhesion of the propagule. It was considered initially that attachment was purely a chance event resulting from physical entrapment of the propagule or germling. We know now that attachment involves an active process of secretion of adhesive materials by the fungus that in some cases are highly specific for the recognition of, and binding to, a particular host species. Adhesive production may occur at a specific stage of conidium or germling development, but may best be considered a general phenomenon for the establishment of the fungus prior to penetration.

Adhesion of Spores and Hyphae to Plant Surfaces

Although fungal adhesion to plants has been recognized for over a century, this aspect of fungal-plant interaction has not been well characterized (Nicholson and Epstein 1991). The importance of adhesion has rarely been critically tested, no fungal adhesive compound that mediates attachment to plants has been fully characterized, and few data are available that describe the molecular bases of fungal-substratum binding. The detailed description of fungal-plant attachment is further complicated by the fact that adhesion occurs at multiple stages of fungal morphogenesis; adhesion can be associated with zoospores and their cysts, conidia, germlings, appressoria, and infection cushions (Nicholson 1984). In some species of rust and anthracnose fungi, several different types of cells (i.e., spores, germlings and appressoria) attach to the host surface before penetration (Chap. 2, this Vol.; Chap. 5, Vol. V, Part B).

Adhesion of ungerminated Colletotrichum musae conidia

Abstract Conidia of Colletotrichum musae adhered to a greater extent on hydrophobic than on hydrophilic substrata. Polystyrene was chosen as a model substratum to study adhesion of conidia since surface hydrophobicity on polystyrene and the banana fruit was similar and conidia adhered equally well to both surfaces. Conidia adhered several hours before germ tubes emerged. On polystyrene, 47% and 94% of the conidia adhered when incubated for 2 h at 1 and 24 °C, respectively. After 4 h at either temperature, > 84% conidia adhered. Concentrations of Triton X-100 and SDS which did not affect spore viability inhibited adhesion. Conidia were relatively non-adhesive when killed with heat, formaldehyde, or UV light. Conidia incubated with the proteolytic enzyme pronase E adhered significantly less than controls. Conidia that were treated with pronase E and then washed regained adhesiveness, suggesting that cell-surface protein(s) are involved in adhesion of conidia and that the adhesive material can be produced at more than one time prior to germ tube emergence.

Adhesion of Nectria haematococca macroconidia

Abstract Prior to germ tube emergence, macroconidia of the squash pathogen Nectria haematococca mating population I (anamorph, Fusarium solani f. sp. cucurbitae race 1) attach to polystyrene. We developed a radiological assay to quantify spore adhesion and to study the attachment process. Macroconidia adhere when harvested and allowed to attach at 24 °C, but not when harvested and allowed to attach at 1 °C. However, macroconidia adhere when harvested at 24 °C and allowed to attach at 1 °C. The data suggest that the process of macroconidial adhesion can be divided into two phases. The first phase is temperature-dependent. The second phase, in which the spores physically attach to the surface, is relatively temperature-independent. Adhesion is inhibited by sodium azide and cycloheximide, suggesting respiration and protein synthesis are required for macroconidial attachment. However, adhesion was not affected by tunicamycin, monensin or actinomycin D, indicating glycosylation, intracellular transport, and RNA synthesis are not required for spore adhesion. The data from the inhibitor and the temperature-shift experiments indicate that metabolism is required for the development of adhesive macroconidia, but not for the physical binding to the surface.

Wheat Stripe Rust Resistance Protein WKS1 Reduces the Ability of the Thylakoid-Associated Ascorbate Peroxidase to Detoxify Reactive Oxygen Species

The wheat WKS1 protein reduces the activity of a chloroplast enzyme that detoxifies reactive oxygen species and causes cell death in the infected regions, conferring partial resistance to stripe rust. Stripe rust is a devastating fungal disease of wheat caused by Puccinia striiformis f. sp tritici (Pst). The WHEAT KINASE START1 (WKS1) resistance gene has an unusual combination of serine/threonine kinase and START lipid binding domains and confers partial resistance to Pst. Here, we show that wheat (Triticum aestivum) plants transformed with the complete WKS1 (variant WKS1.1) are resistant to Pst, whereas those transformed with an alternative splice variant with a truncated START domain (WKS1.2) are susceptible. WKS1.1 and WKS1.2 preferentially bind to the same lipids (phosphatidic acid and phosphatidylinositol phosphates) but differ in their protein-protein interactions. WKS1.1 is targeted to the chloroplast where it phosphorylates the thylakoid-associated ascorbate peroxidase (tAPX) and reduces its ability to detoxify peroxides. Increased expression of WKS1.1 in transgenic wheat accelerates leaf senescence in the absence of Pst. Based on these results, we propose that the phosphorylation of tAPX by WKS1.1 reduces the ability of the cells to detoxify reactive oxygen species and contributes to cell death. This response takes several days longer than typical hypersensitive cell death responses, thus allowing the limited pathogen growth and restricted sporulation that is characteristic of the WKS1 partial resistance response to Pst.