HH Flor

Bio: HH Flor is an academic researcher. The author has contributed to research in topics: Rust. The author has an hindex of 1, co-authored 1 publications receiving 664 citations.

Current Status of the Gene-For-Gene Concept

Abstract: One of the most successful means of controlling plant diseases has been the development of varieties with major or vertical resistance genes. This type of resistance is easily manipulated in a breeding program and is efIec­ tive until strains of the pathogen to which it does not confer resistance be­ come established. Then, if another gene that conditions resistance to the new strains of the pathogen is available, this resistance gene may be incorporated into the variety by the plant breeder. In doing this, the breeder either con­ sciously or unconsciously is applying the principle of the gene-far-gene hypothesis. Plants resistant to races that are virulent on old varieties possess the new resistance gene. With the diseases of some crops, this process has becn repeated at relatively frequent intervals (4D, 42, 82). However, in some instances a single gene has conferred adequate resistance for many years 80,82). In plant diseases caused by living organisms, the same phenomena: in­ fection type in rusts, percent of infected plants in smuts of cereals, fleck or lesion in apple scab, are criteria of both the reaction of the host and the pathogenicity of the parasite. They indicate the relative resistance or sus­ ceptibility of the host and the relative avirulence or virulence of the para­ site. The gene-for-gene hypothesis was proposed (20,25) as the simplest ex­ planation of the results of studies on the inheritance of pathogenicity in the .flax rust fungus, M elampsora lini. On varieties of flax, Linum usitatissimum that have one gene for resistance to the avirulent parent race, F 2 cultures of the fungus segregate into monofactorial ratios. On varieties having 2, 3, or 4 genes for resistance to the avirulent parent race, the F2 cultures segregate into bi-, trio, or tetra factorial ratios (20-22) respectively. This suggests that for each gene that conditions reaction in the host there is a correspond­ ing gene in the parasite that conditions pathogenicity. Each gene in either member of a host-parasite system may be identified only by its counterpart in the other member of the system.

The Complementary Genic Systems in Flax and Flax Rust

Abstract: Publisher Summary The type of pustule developed on a host variety following inoculation with a race of rust is the criterion both of the reaction of that variety to the race and of the pathogenicity of that race to the variety. Races of rust—genes for pathogenicity—are identified by the reaction of a series of varieties termed “rust differentials.” Genes for rust reaction are identified by the pathogenicity of races of rust. Rust resistance in flax is inherited as a dominant character although with some genes, dominance is not complete. Virulence in flax rust, melampsora lini, with one exception, is inherited as a recessive character. F 2 cultures of hybrids among races of flax rust segregated for pathogenicity on the differential varieties in accordance with the number of genes in the differential that conditioned resistance to the avirulent parent race.

The root knot nematode resistance gene Mi from tomato is a member of the leucine zipper, nucleotide binding, leucine-rich repeat family of plant genes.

Abstract: The Mi locus of tomato confers resistance to root knot nematodes. Tomato DNA spanning the locus was isolated as bacterial artificial chromosome clones, and 52 kb of contiguous DNA was sequenced. Three open reading frames were identified with similarity to cloned plant disease resistance genes. Two of them, Mi-1.1 and Mi-1.2, appear to be intact genes; the third is a pseudogene. A 4-kb mRNA hybridizing with these genes is present in tomato roots. Complementation studies using cloned copies of Mi-1.1 and Mi-1.2 indicated that Mi-1.2, but not Mi-1.1, is sufficient to confer resistance to a susceptible tomato line with the progeny of transformants segregating for resistance. The cloned gene most similar to Mi-1.2 is Prf, a tomato gene required for resistance to Pseudomonas syringae. Prf and Mi-1.2 share several structural motifs, including a nucleotide binding site and a leucine-rich repeat region, that are characteristic of a family of plant proteins, including several that are required for resistance against viruses, bacteria, fungi, and now, nematodes.

Elicitors, Effectors, and R Genes: The New Paradigm and a Lifetime Supply of Questions

Abstract: The plant basal immune system can detect broadly present microbe-associated molecular patterns (MAMPs, also called PAMPs) and induce defenses, but adapted microbes express a suite of effector proteins that often act to suppress these defenses. Plants have evolved other receptors (R proteins) that detect these pathogen effectors and activate strong defenses. Pathogens can subsequently alter or delete their recognized effectors to avoid defense elicitation, at risk of a fitness cost associated with loss of those effectors. Significant research progress is revealing, among other things, mechanisms of MAMP perception, the host defense processes and specific host proteins that pathogen effectors target, the mechanisms of R protein activation, and the ways in which pathogen effector suites and R genes evolve. These findings carry practical ramifications for resistance durability and for future resistance engineering. The present review uses numerous questions to help clarify what we know and to identify areas that are ripe for further investigation.

Plant Disease Resistance Genes: Function Meets Structure.

Abstract: The coevolution of interacting plants and microbes has given rise to a diverse array of exchanged signals and responses. Microbes that elicit a host response can be met variously with hospitable acceptance (as is the case with symbionts such as nitrogen-fixing Rhizobium bacteria), with tardy recognition and moderately effective defenses (as for most interactions that result in disease), or with a strong and rapid defense response that blocks further infection (Dixon and Lamb, 1990; Keen, 1990; Long and Staskawicz, 1993). This latter form of disease resistance forms the subject of this review and is known variously as race-specific resistance, gene-for-gene resistance, or hypersensitive resistance. Activation of gene-for-gene resistance typically depends on specific recognition of the invading pathogen by the plant (Keen, 1990). Numerous individual plant genes have been identified that control gene-for-gene resistance, and these genes are known as resistance (R) genes. Study of gene-for-gene resistance might be justified solely by the intrigue of plant-pathogen coevolution or as a model for signal transduction research in which an organism perceives and responds to its environment. However, the topic takes on greater interest dueto its pivotal impact on crop health and food production. Plant diseases cause billions of dollars in lost harvest annually, and in some instances, these losses have severe consequences for humans (Agrios, 1988; Schumann, 1991). One of the most convenient, inexpensive, and environmentally sound ways to control plant disease is to utilize disease-resistam varieties, and plant breeders make extensive use of classically defined R genes (Agrios, 1988). Recent work has revealed the structure of a number of plant R genes, and a striking degree of similarity among these genes has been observed. After briefly introducing the subject of R genes and avirulence (Avo genes, this review provides an overview of the conserved structural components that are predicted in the proteins encoded by R genes. The cloning of R genes has stimulated additional research that is also discussed, including structure-function analysis of R gene-encoded proteins, isolation of additional R genes, identification of functionally related components of the defense signal transduction cascade, and engineering of improved disease resistance in plants. RESISTANCE GENES, AVIRULENCE GENES, AND PLANT DEFENSE