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Functional redundancy of necrotrophic effectors - consequences for exploitation for breeding.

Tan KC, Phan HT, Rybak K, John E, Chooi YH, Solomon PS, Oliver RP - Front Plant Sci (2015)

Bottom Line: As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex.Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate.This indicates that one or more further effectors are secreted into the culture filtrate.

View Article: PubMed Central - PubMed

Affiliation: Centre for Crop Disease Management, Department of Environment and Agriculture, Curtin University, Bentley WA, Australia.

ABSTRACT
Necrotrophic diseases of wheat cause major losses in most wheat growing areas of world. Tan spot (caused by Pyrenophora tritici-repentis) and septoria nodorum blotch (SNB; Parastagonospora nodorum) have been shown to reduce yields by 10-20% across entire agri-ecological zones despite the application of fungicides and a heavy focus over the last 30 years on resistance breeding. Efforts by breeders to improve the resistance of cultivars has been compromised by the universal finding that resistance was quantitative and governed by multiple quantitative trait loci (QTL). Most QTL had a limited effect that was hard to measure precisely and varied significantly from site to site and season to season. The discovery of necrotrophic effectors has given breeding for disease resistance new methods and tools. In the case of tan spot in West Australia, a single effector, PtrToxA and its recogniser gene Tsn1, has a dominating impact in disease resistance. The delivery of ToxA to breeders has had a major impact on cultivar choice and breeding strategies. For P. nodorum, three effectors - SnToxA, SnTox1, and SnTox3 - have been well characterized. Unlike tan spot, no one effector has a dominating role. Genetic analysis of various mapping populations and pathogen isolates has shown that different effectors have varying impact and that epistatic interactions also occur. As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex. We have deleted the three effectors in a strain of P. nodorum and measured effector activity and disease potential of the triple knockout mutant. The culture filtrate causes necrosis in several cultivars and the strain causes disease, albeit the overall levels are less than in the wild type. Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate. This indicates that one or more further effectors are secreted into the culture filtrate. We conclude that the in vitro-secreted necrotrophic effectors explain a very large part of the disease response of wheat germplasm and that this method of resistance breeding promises to further reduce the impact of these globally significant diseases.

No MeSH data available.


Related in: MedlinePlus

Reactions of 46 Australian wheat cultivars to effectors [∧, from Tan et al. (2014)] and the Parastagonospora nodorum toxa13-6 culture filtrate [#, this study].∗SNB disease rating was obtained from Shackley et al. (2013). VS, very susceptible; S-VS, susceptible-very susceptible; S, susceptible; MS-S, moderately susceptible-susceptible; MS, moderately susceptible; MR-MS, moderately resistant-moderately susceptible. Effector sensitivity scores are described in Supplementary Table S1.
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Figure 2: Reactions of 46 Australian wheat cultivars to effectors [∧, from Tan et al. (2014)] and the Parastagonospora nodorum toxa13-6 culture filtrate [#, this study].∗SNB disease rating was obtained from Shackley et al. (2013). VS, very susceptible; S-VS, susceptible-very susceptible; S, susceptible; MS-S, moderately susceptible-susceptible; MS, moderately susceptible; MR-MS, moderately resistant-moderately susceptible. Effector sensitivity scores are described in Supplementary Table S1.

Mentions: The activity of the toxa13-6 culture filtrate was assessed on 46 Australian commercial wheat cultivars (Figure 2). Ten cultivars are highly sensitive to the culture filtrate, resulting in significant chlorosis and necrosis whereas nine were mildly sensitive. It was observed that Cv. Magenta segregated in sensitivity to the culture filtrate.


Functional redundancy of necrotrophic effectors - consequences for exploitation for breeding.

Tan KC, Phan HT, Rybak K, John E, Chooi YH, Solomon PS, Oliver RP - Front Plant Sci (2015)

Reactions of 46 Australian wheat cultivars to effectors [∧, from Tan et al. (2014)] and the Parastagonospora nodorum toxa13-6 culture filtrate [#, this study].∗SNB disease rating was obtained from Shackley et al. (2013). VS, very susceptible; S-VS, susceptible-very susceptible; S, susceptible; MS-S, moderately susceptible-susceptible; MS, moderately susceptible; MR-MS, moderately resistant-moderately susceptible. Effector sensitivity scores are described in Supplementary Table S1.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4495316&req=5

Figure 2: Reactions of 46 Australian wheat cultivars to effectors [∧, from Tan et al. (2014)] and the Parastagonospora nodorum toxa13-6 culture filtrate [#, this study].∗SNB disease rating was obtained from Shackley et al. (2013). VS, very susceptible; S-VS, susceptible-very susceptible; S, susceptible; MS-S, moderately susceptible-susceptible; MS, moderately susceptible; MR-MS, moderately resistant-moderately susceptible. Effector sensitivity scores are described in Supplementary Table S1.
Mentions: The activity of the toxa13-6 culture filtrate was assessed on 46 Australian commercial wheat cultivars (Figure 2). Ten cultivars are highly sensitive to the culture filtrate, resulting in significant chlorosis and necrosis whereas nine were mildly sensitive. It was observed that Cv. Magenta segregated in sensitivity to the culture filtrate.

Bottom Line: As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex.Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate.This indicates that one or more further effectors are secreted into the culture filtrate.

View Article: PubMed Central - PubMed

Affiliation: Centre for Crop Disease Management, Department of Environment and Agriculture, Curtin University, Bentley WA, Australia.

ABSTRACT
Necrotrophic diseases of wheat cause major losses in most wheat growing areas of world. Tan spot (caused by Pyrenophora tritici-repentis) and septoria nodorum blotch (SNB; Parastagonospora nodorum) have been shown to reduce yields by 10-20% across entire agri-ecological zones despite the application of fungicides and a heavy focus over the last 30 years on resistance breeding. Efforts by breeders to improve the resistance of cultivars has been compromised by the universal finding that resistance was quantitative and governed by multiple quantitative trait loci (QTL). Most QTL had a limited effect that was hard to measure precisely and varied significantly from site to site and season to season. The discovery of necrotrophic effectors has given breeding for disease resistance new methods and tools. In the case of tan spot in West Australia, a single effector, PtrToxA and its recogniser gene Tsn1, has a dominating impact in disease resistance. The delivery of ToxA to breeders has had a major impact on cultivar choice and breeding strategies. For P. nodorum, three effectors - SnToxA, SnTox1, and SnTox3 - have been well characterized. Unlike tan spot, no one effector has a dominating role. Genetic analysis of various mapping populations and pathogen isolates has shown that different effectors have varying impact and that epistatic interactions also occur. As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex. We have deleted the three effectors in a strain of P. nodorum and measured effector activity and disease potential of the triple knockout mutant. The culture filtrate causes necrosis in several cultivars and the strain causes disease, albeit the overall levels are less than in the wild type. Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate. This indicates that one or more further effectors are secreted into the culture filtrate. We conclude that the in vitro-secreted necrotrophic effectors explain a very large part of the disease response of wheat germplasm and that this method of resistance breeding promises to further reduce the impact of these globally significant diseases.

No MeSH data available.


Related in: MedlinePlus