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Review
. 2018 Jul 4;9(7):339.
doi: 10.3390/genes9070339.

Disease Resistance Mechanisms in Plants

Affiliations
Review

Disease Resistance Mechanisms in Plants

Ethan J Andersen et al. Genes (Basel). .

Abstract

Plants have developed a complex defense system against diverse pests and pathogens. Once pathogens overcome mechanical barriers to infection, plant receptors initiate signaling pathways driving the expression of defense response genes. Plant immune systems rely on their ability to recognize enemy molecules, carry out signal transduction, and respond defensively through pathways involving many genes and their products. Pathogens actively attempt to evade and interfere with response pathways, selecting for a decentralized, multicomponent immune system. Recent advances in molecular techniques have greatly expanded our understanding of plant immunity, largely driven by potential application to agricultural systems. Here, we review the major plant immune system components, state of the art knowledge, and future direction of research on plant⁻pathogen interactions. In our review, we will discuss how the decentralization of plant immune systems have provided both increased evolutionary opportunity for pathogen resistance, as well as additional mechanisms for pathogen inhibition of such defense responses. We conclude that the rapid advances in bioinformatics and molecular biology are driving an explosion of information that will advance agricultural production and illustrate how complex molecular interactions evolve.

Keywords: coevolution; defense response; disease resistance; nucleotide-binding leucine-rich repeat; pathogenesis; pattern recognition receptor; phytopathology; plant immunity; plant-pest interaction; resistance gene.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Components of plant disease resistance mechanisms involved in pathogen detection, signal transduction, and defense response (detection in the upper center and progressing around clockwise, ending in defense response in the upper left). Pathogenic elicitors (cell components or effectors) produced by bacteria, fungi, insects, nematodes, or viruses trigger plant receptors to initiate signaling cascades. Activated receptors (blue) then initiate one of many signal transduction pathways or directly act as transcription factors (TFs). Signal transduction pathways (yellow) include mitogen-activated protein kinase (MAPK) cascades, calcium ion signaling, hormone production, TF activity, and epigenetic regulation. These factors trigger the expression of genes associated with defense responses, such as those regulating the production of reactive oxygen species (ROS), antimicrobial enzymes, defensins, and phytoalexins. These defense-related compounds (red) actively inhibit pathogen reproduction or make further infection more difficult. Breakdown of pathogenic cell components by defense compounds leads to further release of receptor-triggering elicitors, increasing the resistance response. Multiple organelles are involved in defense response, including chloroplasts and peroxisomes for hormone production as well as the nucleus, endoplasmic reticulum, and Golgi apparatus for antimicrobial protein production. PRR: Pattern recognition receptors; WAK: wall-associated kinases; NLR: nucleotide-binding domains and leucine-rich repeats; PDR: pathogen-derived resistance; HR: hypersensitive response; TIR: N-terminal Toll/interleukin-1 receptor-like; CC: coiled-coil; SA: salicylic acid; JA: jasmonic acid; ET: ethylene.

References

    1. Whetzel H.H. An Outline of the History of Phytopathology. WB Saunders; Philadelphia, PA, USA: 1918.
    1. Moutinho-Pereira J., Magalhaes N., Torres de Castro L., Manuela Chaves M., Torres-Pereira J. Physiological responses of grapevine leaves to bordeaux mixture under light. Vitis. 2001;40:117–121.
    1. Kutschera U., Hossfeld U. Physiological phytopathology: Origin and evolution of a scientific discipline. J. Appl. Bot. Food Qual. 2012;85:1–5.
    1. Rhoades V.H. The location of a gene for disease resistance in maize. Proc. Natl. Acad. Sci. USA. 1935;21:243–246. doi: 10.1073/pnas.21.5.243. - DOI - PMC - PubMed
    1. Bushnell W. The Cereal Rusts: Origins, Specificity, Structure, and Physiology. Volume 1 Elsevier; Amsterdam, The Netherlands: 2012.

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