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Plant disease resistance

About: Plant disease resistance is a research topic. Over the lifetime, 12952 publications have been published within this topic receiving 381820 citations. The topic is also known as: plant innate immunity.


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Journal ArticleDOI
TL;DR: Analyses of whole-genome sequences have and will continue to provide new insight into the dynamics of resistance gene evolution.

350 citations

Journal ArticleDOI
29 Jun 2017-Cell
TL;DR: The identification of a natural allele of a C2H2-type transcription factor in rice that confers non-race-specific resistance to blast is reported, highlighting this novel allele as a strategy for breeding durable resistance in rice.

350 citations

Journal ArticleDOI
TL;DR: A novel mutation in Arabidopsis, hlm1, which causes aberrant regulation of cell death, manifested by a lesion-mimic phenotype and an altered HR, segregated as a single recessive allele exhibited increased resistance to a virulent strain of Pseudomonas syringae pv tomato.
Abstract: The hypersensitive response (HR) in plants is a programmed cell death that is commonly associated with disease resistance. A novel mutation in Arabidopsis, hlm1, which causes aberrant regulation of cell death, manifested by a lesion-mimic phenotype and an altered HR, segregated as a single recessive allele. Broad-spectrum defense mechanisms remained functional or were constitutive in the mutant plants, which also exhibited increased resistance to a virulent strain of Pseudomonas syringae pv tomato. In response to avirulent strains of the same pathogen, the hlm1 mutant showed differential abilities to restrict bacterial growth, depending on the avirulence gene expressed by the pathogen. The HLM1 gene encodes a cyclic nucleotide–gated channel, CNGC4. Preliminary study of the HLM1/CNGC4 gene pro-duct in Xenopus oocytes (inside-out patch-clamp technique) showed that CNGC4 is permeable to both K+ and Na+ and is activated by both cGMP and cAMP. HLM1 gene expression is induced in response to pathogen infection and some pathogen-related signals. Thus, HLM1 might constitute a common downstream component of the signaling pathways leading to HR/resistance.

350 citations

Journal ArticleDOI
TL;DR: It is demonstrated that host-induced gene silencing (HIGS) targeting the fungal sterol 14α-demethylase (CYP51) genes restricts Fusarium infection in plants, demonstrating that HIGS is a powerful tool, which could revolutionize crop plant protection.
Abstract: Head blight, which is caused by mycotoxin-producing fungi of the genus Fusarium, is an economically important crop disease. We assessed the potential of host-induced gene silencing targeting the fungal cytochrome P450 lanosterol C-14α-demethylase (CYP51) genes, which are essential for ergosterol biosynthesis, to restrict fungal infection. In axenic cultures of Fusarium graminearum, in vitro feeding of CYP3RNA, a 791-nt double-stranded (ds)RNA complementary to CYP51A, CYP51B, and CYP51C, resulted in growth inhibition [half-maximum growth inhibition (IC50) = 1.2 nM] as well as altered fungal morphology, similar to that observed after treatment with the azole fungicide tebuconazole, for which the CYP51 enzyme is a target. Expression of the same dsRNA in Arabidopsis and barley rendered susceptible plants highly resistant to fungal infection. Microscopic analysis revealed that mycelium formation on CYP3RNA-expressing leaves was restricted to the inoculation sites, and that inoculated barley caryopses were virtually free of fungal hyphae. This inhibition of fungal growth correlated with in planta production of siRNAs corresponding to the targeted CYP51 sequences, as well as highly efficient silencing of the fungal CYP51 genes. The high efficiency of fungal inhibition suggests that host-induced gene-silencing targeting of the CYP51 genes is an alternative to chemical treatments for the control of devastating fungal diseases.

347 citations

Journal ArticleDOI
30 Sep 2004-Nature
TL;DR: It is shown that root colonization can lead to systemic invasion and the development of classical disease symptoms on the aerial parts of the plant, and Gene-for-gene type specific disease resistance that is effective against rice blast in leaves also operates in roots.
Abstract: Pathogens have evolved different strategies to overcome the various barriers that they encounter during infection of their hosts1 The rice blast fungus Magnaporthe grisea causes one of the most damaging diseases of cultivated rice and has emerged as a paradigm system for investigation of foliar pathogenicity This fungus undergoes a series of well-defined developmental steps during leaf infection, including the formation of elaborate penetration structures (appressoria) This process has been studied in great detail2, and over thirty M grisea genes that condition leaf infection have been identified3 Here we show a new facet of the M grisea life cycle: this fungus can undergo a different (and previously uncharacterized) set of programmed developmental events that are typical of root-infecting pathogens We also show that root colonization can lead to systemic invasion and the development of classical disease symptoms on the aerial parts of the plant Gene-for-gene type specific disease resistance that is effective against rice blast in leaves also operates in roots These findings have significant implications for fungal development, epidemiology, plant breeding and disease control

346 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023377
2022756
2021410
2020438
2019526
2018640