Differential effects of lesion mimic mutants in barley on disease development by facultative pathogens

McGrann, Graham R. D.; Steed, Andrew; Burt, Christopher; Nicholson, P.; Brown, J. K. M.

doi:10.1093/jxb/erv154

Cited by 46 publications

(37 citation statements)

References 55 publications

(116 reference statements)

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“…The latter possibility raises the concern that there may be a cost to the plant in some other respect, for example loss of yield, susceptibility to abiotic stress or other pathogens. Fitness trade‐offs have been identified with other recessive genes in terms of enhanced susceptibility to other pathogens, lesion‐mimic phenotypes, and yield losses (McGrann et al ., ). No yield costs have been reported for expression of xa5 .…”

Section: Discussionmentioning

confidence: 97%

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The broadly effective recessive resistance gene xa5 of rice is a virulence effector‐dependent quantitative trait for bacterial blight

Huang

Antony

et al. 2016

The Plant Journal

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Mutations in disease susceptibility (S) genes, here referred to as recessive resistance genes, have promise for providing broad durable resistance in crop species. However, few recessive disease resistance genes have been characterized. Here, we show that the broadly effective resistance gene xa5,for resistance to bacterial blight of rice (Oryza sativa), is dependent on the effector genes present in the pathogen. Specifically, the effectiveness of xa5 in preventing disease by strains of Xanthomonas oryzae pv. oryzae is dependent on major transcription activation-like (TAL) effector genes, and correlates with reduced expression of the cognate S genes. xa5 is ineffective in preventing disease by strains containing the TAL effector gene pthXo1, which directs robust expression of the S gene OsSWEET11, a member of sucrose transporter gene family. Incompatibility is associated with major TAL effectors that target the known alternative S genes OsS-WEET14 and OsSWEET13. Incompatibility is defeated by transfer of pthXo1 to otherwise xa5-incompatible strains or by engineering a synthetic designer TAL effector to boost SWEET gene expression. In either case, compatible or incompatible, target gene expression and lesion formation are reduced in the presence of xa5. The results indicate that xa5 functions as a quantitative trait locus, dampening effector function, and, regardless of compatibility, target gene expression. Resistance is hypothesized to occur when S gene expression, and, by inference, sucrose leakage, falls below a threshold level.

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Section: Discussionmentioning

confidence: 97%

“…other pathogens. Fitness trade-offs have been identified with other recessive genes in terms of enhanced susceptibility to other pathogens, lesion-mimic phenotypes, and yield losses (McGrann et al, 2015). No yield costs have been reported for expression of xa5.…”

Section: Discussionmentioning

confidence: 99%

The broadly effective recessive resistance gene xa5 of rice is a virulence effector‐dependent quantitative trait for bacterial blight

Huang

Antony

et al. 2016

The Plant Journal

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“…Necrotrophic parasites can exploit mechanisms of resistance to biotrophs and thereby establish disease (91), mechanisms of resistance to different kinds of parasites may interfere with one another (49,95,145), and there may be complex interactions of defense with regulation of plant growth and development (113,116). The implication of such trade-offs for plant breeding is that it may not be possible to maximize resistance to all important diseases.…”

Section: Costs and Trade-offsmentioning

confidence: 99%

“…It causes necrotic flecking on leaves, reduces yield, reduces leaf size, increases susceptibility to several nonbiotrophic fungal pathogens, and reduces mycorrhizal colonization (24,94,95). Despite its importance to a major crop and the length of time for which it has been studied, the biology of its complex phenotype is poorly understood.…”

Section: Costs and Trade-offsmentioning

confidence: 99%

Durable Resistance of Crops to Disease: A Darwinian Perspective

Brown

2015

Annu. Rev. Phytopathol.

244

233

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This review takes an evolutionary view of breeding crops for durable resistance to disease. An understanding of coevolution between hosts and parasites leads to predictors of potentially durable resistance, such as corresponding virulence having a high fitness cost to the pathogen or resistance being common in natural populations. High partial resistance can also promote durability. Whether or not resistance is actually durable, however, depends on ecological and epidemiological processes that stabilize genetic polymorphism, many of which are absent from intensive agriculture. There continues to be no biological, genetic, or economic model for durable resistance. The analogy between plant breeding and natural selection indicates that the basic requirements are genetic variation in potentially durable resistance, effective and consistent selection for resistance, and an efficient breeding process in which trials of disease resistance are integrated with other traits. Knowledge about genetics and mechanisms can support breeding for durable resistance once these fundamentals are in place.

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“…Over the past several decades, many lesion mimic mutants (LMMs) and related candidate genes have been isolated from Arabidopsis, rice, maize, and barley (Bruggeman et al, 2015;Wang et al, 2015b,c). LMMs display spontaneous lesions similar to the pathogen infection-induced hypersensitive response mediated through programmed cell death (PCD) (McGrann et al, 2015). PCD is essential for plant developmental programs and response to environmental stimuli by eliminating unnecessary cells; the process is finely controlled by multiple signaling molecules such as reactive oxygen species (ROS) and various hormones (Dominguez & Cejudo, 2014;Petrov et al, 2015;Serrano et al, 2015;Van Hautegem et al, 2015;Van Durme & Nowack, 2016).…”

Section: Introductionmentioning

confidence: 99%

Excessive UDPG resulting from the mutation of UAP1 causes programmed cell death by triggering reactive oxygen species accumulation and caspase‐like activity in rice

Xiao

Zhou

et al. 2017

New Phytologist

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Lesion mimic mutants are valuable to unravel the mechanisms governing the programmed cell death (PCD) process. Uridine 5'-diphosphoglucose-glucose (UDPG) functions as a signaling molecule activating multiple pathways in animals, but little is known about its function in plants. Two novel allelic mutants of spl29 with typical PCD characters and reduced pollen viability were obtained by ethane methyl sulfonate mutagenesis in rice cv Kitaake. The enzymatic analyses showed that UDP-N-acetylglucosamine pyrophosphorylase 1 (UAP1) irreversibly catalyzed the decomposition of UDPG. Its activity was severely destroyed and caused excessive UDPG accumulation, with the lesion occurrence associated with the enhanced caspase-like activities in spl29-2. At the transcriptional level, several key genes involved in endoplasmic reticulum stress and the unfolded protein response were abnormally expressed. Moreover, exogenous UDPG could aggravate lesion initiation and development in spl29-2. Importantly, exogenous UDPG and its derivative UDP-N-acetylglucosamine could induce reactive oxygen species (ROS) accumulation and lesion mimics in Kitaake seedlings. These results suggest that the excessive accumulation of UDPG, caused by the mutation of UAP1, was a key biochemical event resulting in the lesion mimics in spl29-2. Thus, our findings revealed that UDPG might be an important component involved in ROS accumulation, PCD execution and lesion mimicking in rice, which also provided new clues for investigating the connection between sugar metabolism and PCD process.

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Differential effects of lesion mimic mutants in barley on disease development by facultative pathogens

Abstract: HighlightDifferent pathways that regulate cell death have distinct effects on diverse pathogens. MLO and NEC1, which both suppress cell death, interact with one another in their effects on pathogenic fungi.

Cited by 46 publications

References 55 publications

The broadly effective recessive resistance gene xa5 of rice is a virulence effector‐dependent quantitative trait for bacterial blight

The broadly effective recessive resistance gene xa5 of rice is a virulence effector‐dependent quantitative trait for bacterial blight

Durable Resistance of Crops to Disease: A Darwinian Perspective

Excessive UDPG resulting from the mutation of UAP1 causes programmed cell death by triggering reactive oxygen species accumulation and caspase‐like activity in rice

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