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Sunflower broomrape (Orobanche cumana Wallr.) parasitization on sunflower was first observed at the end of the 19th century and has continued since then jeopardizing sunflower cultivation in many areas of Europe and Asia. A distinctive characteristic of the O. cumana-sunflower parasitic system is that it is mainly governed by a gene-for-gene interaction. This determines complete resistance in the host controlled by dominant alleles at a single locus, which facilitates the management of the resistance for hybrid seed production. But on the other hand avirulence in the parasite is also controlled by dominant alleles at a single gene. Monogenic, dominant resistance exerts a strong selection pressure on the parasite that maximizes the probability of overcoming resistance mechanisms in a short period of time. This has in fact resulted in a number of physiological races that periodically surpass all the available resistance sources. The spread of populations to new areas and the subsequent hybridization between populations is another mechanism creating genetic diversity in sunflower broomrape and allegedly recombination of avirulences genes. After more than one century of coexistence, genetic resistance to broomrape in sunflower has to be focused under an integrated approach that considers not only the characterization of resistance mechanisms in the host, but also the genetic and physiological bases of avirulence in the parasite. From the perspective of genetic resistance in sunflower, most important is not relying only on single dominant genes, but following instead pyramiding strategies. These should give priority to combining complementary mechanisms of resistance under both qualitative (vertical) and quantitative (horizontal) genetic control. These aspects are discussed in the paper. [ABSTRACT FROM AUTHOR]

Molecular studies focusing on the interface between microbes and plant hosts have provided major insights into the basis underlying pathogenesis, symbiosis and plant defence and resistance mechanisms. A more recent focus on microbes, facilitated by the generation of complete genome sequences, has uncovered the sheer number of protein effectors microbes deliver in this interface as well as inside host cells to manipulate the plant immune system. Although studies on the characterization and roles of bacterial effectors are further advanced, in this review we focus on the current knowledge of fungal and oomycete effectors and their roles. Examples are given of effectors disarming plant defence enzymes, such as the apoplastic effector AVR2 from Cladosporium fulvum which inhibits the tomato defence cysteine protease. Other effectors interfere with the perception by the host of microbes exposing molecular determinants such as Phytophthora infestans INF1 protein. Many effectors alter gene expression induced by the host during defence, exemplified in fungi by Ustilago maydis Pit2 suppressing maize defence genes. Effectors recognized by resistance gene products, either directly or indirectly, and eliciting defence, represent the classical avirulence genes and almost 50 have now been cloned from fungi and oomycetes. Evolutionary adaptations and arms races have produced diversification in both pathogen and host, and in pathogens, are the cause of breaking crop resistance in agricultural settings. Molecular insight provides valuable information for applications. For example, some effectors are crucial for pathogenesis, thereby revealing targets for disease control and others interact with host resistance gene products and could be used to screen germplasm for novel sources of disease resistance. Variation among effectors will likely yield diagnostic tools for pathogen race identification. The study of model systems is providing insight into avenues by which other, major plant diseases can potentially be controlled. [ABSTRACT FROM AUTHOR]

Abstract: Host plant resistance is an efficient and environmentally friendly means of controlling insects, including aphids, but resistant-breaking biotypes have occurred in several plant–aphid systems. Our review of the genetic and molecular bases of aphid resistance in crop species emphasizes the limited number of aphid resistance genes and alleles. Inheritance of aphid resistance may be monogenic (dominant or recessive genes) or polygenic. Two dominant, aphid resistance genes have been isolated to date. They both encode NBS-LRR proteins involved in the specific recognition of aphids. Strategies to ensure aphid resistance effectiveness and durability are discussed. Innovative research activities are proposed. [Copyright &y& Elsevier]

Pathogenic rust fungi constitute a major disease threat to agriculture, but their obligate parasitic lifestyle makes them difficult to study. Research on the model flax rust disease system has contributed greatly to our knowledge of rust infection and, in particular, the mechanisms of rust resistance and susceptibility controlled by resistance (R) genes in the host and avirulence (Avr) genes in the pathogen. Twenty flax R genes have been isolated and encode cytoplasmic proteins with nucleotide-binding domains and leucine-rich repeat regions. These proteins act as a surveillance system for the recognition of specific pathogen Avr proteins as signals of invasion and subsequently activate plant defences. Several of these rust Avr proteins have also been isolated and were found to be small secreted proteins that are expressed in haustoria (specialized structures that penetrate the host cell wall) and delivered into the host cytoplasm during infection. The identification of flax R genes and the corresponding fungal Avr genes has allowed more detailed analysis of the recognition events that trigger resistance, revealing a direct interaction between R and Avr proteins as the basis of resistance specificity in flax rust disease. [ABSTRACT FROM AUTHOR]