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. 2011 Feb;12(2):105-22.
doi: 10.1111/j.1364-3703.2010.00656.x. Epub 2010 Aug 26.

Venturia Inaequalis: The Causal Agent of Apple Scab

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Free PMC article

Venturia Inaequalis: The Causal Agent of Apple Scab

Joanna K Bowen et al. Mol Plant Pathol. .
Free PMC article

Abstract

The fungus Venturia inaequalis infects members of the Maloideae, and causes the disease apple scab, the most important disease of apple worldwide. The early elucidation of the gene-for-gene relationship between V. inaequalis and its host Malus has intrigued plant pathologists ever since, with the identification of 17 resistance (R)-avirulence (Avr) gene pairings. The Avr gene products are presumably a subset of the total effector arsenal of V. inaequalis (predominantly proteins secreted in planta assumed to facilitate infection). The supposition that effectors from V. inaequalis act as suppressors of plant defence is supported by the ability of the pathogen to penetrate the cuticle and differentiate into large pseudoparenchymatous structures, termed stromata, in the subcuticular space, without the initiation of an effective plant defence response. If effectors can be identified that are essential for pathogenicity, the corresponding R genes will be durable and would add significant value to breeding programmes. An R gene cluster in Malus has been cloned, but no V. inaequalis effectors have been characterized at the molecular level. However, the identification of effectors is likely to be facilitated by the resolution of the whole genome sequence of V. inaequalis.

Taxonomy: Teleomorph: Venturia inaequalis Cooke (Wint.); Kingdom Fungi; Phylum Ascomycota; Subphylum Euascomycota; Class Dothideomycetes; Family Venturiaceae; genus Venturia; species inaequalis. Anamorph: Fusicladium pomi (Fr.) Lind or Spilocaea pomi (Fr.). LIFE CYCLE: V. inaequalis is a hemibiotroph and overwinters as pseudothecia (sexual fruiting bodies) following a phase of saprobic growth in fallen leaf tissues. The primary inoculum consists of ascospores, which germinate and penetrate the cuticle. Stromata are formed above the epidermal cells but do not penetrate them. Cell wall-degrading enzymes are only produced late in the infection cycle, raising the as yet unanswered question as to how V. inaequalis gains nutrients from the host. Conidia (secondary inoculum) arise from the upper surface of the stromata, and are produced throughout the growing season, initiating multiple rounds of infection. VENTURIA INAEQUALIS AS A MODEL PATHOGEN OF A WOODY HOST: V. inaequalis can be cultured and is amenable to crossing in vitro, enabling map-based cloning strategies. It can be transformed readily, and functional analyses can be conducted by gene silencing. Expressed sequence tag collections are available to aid in gene identification. These will be complemented by the whole genome sequence, which, in turn, will contribute to the comparative analysis of different races of V. inaequalis and plant pathogens within the Dothideomycetes.

Figures

Figure 1
Figure 1
Formation of stromata during leaf infection by Venturia inaequalis: at 5 days post‐inoculation, with stromata beginning to form (a), and 10 days post‐inoculation, with sporulating stromata (b). Scale bar represents 50 µm. (Reprinted from Bowen et al., 2009. Copyright 2009 with permission from John Wiley & Sons.)
Figure 2
Figure 2
Typical scab symptoms on apple fruit caused by Venturia inaequalis.
Figure 3
Figure 3
The life cycle of Venturia inaequalis. Subcuticular mycelium = stroma. (This diagram was published in Agrios, Plant Pathology, p. 506. Copyright Elsevier 2005.)
Figure 4
Figure 4
(a) A spore of Venturia inaequalis 9 h post‐inoculation, with germination from the apical end of the conidium and formation of an appressorium adhering to the leaf surface. Scale bar represents 5 µm. (b) A germinated conidium and appressorium of V. inaequalis adhering to a slide coated in apple wax, 24 h post‐inoculation; mr, melanized ring at the base of the penetration peg beneath the appressorium. Scale bar represents 10 µm.
Figure 5
Figure 5
Cross‐section of an infected leaf at 14 days post‐ioculation, stained with aniline blue, showing the increased thickness of the cuticle (double arrow). Scale bar represents 10 µm; sh, subcuticular hyphae. (Reprinted from Kucheryava et al., 2008. Copyright 2008 with permission from Elsevier.)
Figure 6
Figure 6
Characteristic scab resistance reactions on apple leaves: pin‐point pit, hypersensitive response conditioned by the Rvi4 gene (left); stellate necrosis by the Rvi2 gene (middle); and chlorosis with limited sporulation conditioned by the Rvi6 gene (right) under glasshouse conditions.
Figure 7
Figure 7
Microscopic interference blue autofluorescence observations, demonstrating the hypersensitive response involving the epidermis and the palisade mesophyll conditioned by the Rvi5 gene. Several hypersensitive responses are shown, each initiated by a Venturia inaequalis spore (sp) at its centre. Scale bar represents 200 µm.

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