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Review
. 2013 Aug 16;341(6147):746-51.
doi: 10.1126/science.1236011.

Pivoting the plant immune system from dissection to deployment

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Review

Pivoting the plant immune system from dissection to deployment

Jeffery L Dangl et al. Science. .

Erratum in

  • Science. 2013 Sep 13;341(6151):1175

Abstract

Diverse and rapidly evolving pathogens cause plant diseases and epidemics that threaten crop yield and food security around the world. Research over the last 25 years has led to an increasingly clear conceptual understanding of the molecular components of the plant immune system. Combined with ever-cheaper DNA-sequencing technology and the rich diversity of germ plasm manipulated for over a century by plant breeders, we now have the means to begin development of durable (long-lasting) disease resistance beyond the limits imposed by conventional breeding and in a manner that will replace costly and unsustainable chemical controls.

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Figures

Fig. 1
Fig. 1. Schematic of the plant immune system
Pathogens of all lifestyle classes (color coded and labeled) express PAMPs and MAMPs as they colonize plants (shapes are color coded to the pathogens). Plants perceive these via extracellular PRRs and initiate PRR-mediated immunity (PTI; step 1). Pathogens deliver virulence effectors to both the plant cell apoplast to block PAMP/MAMP perception (not shown) and to the plant cell interior (step 2). These effectors are addressed to specific subcellular locations where they can suppress PTI and facilitate virulence (step 3). Intracellular NLR receptors can sense effectors in three principal ways: first, by direct receptor ligand interaction (step 4a); second, by sensing effector-mediated alteration in a decoy protein that structurally mimics an effector target, but has no other function in the plant cell (step 4b); and third, by sensing effector-mediated alteration of a host virulence target, like the cytosolic domain of a PRR (step 4c). It is not yet clear whether each of these activation modes proceeds by the same molecular mechanism, nor is it clear how, or where, each results in NLR-dependent effector-triggered immunity (ETI). [Modified from (17) by Sarah R. Grant]
Fig. 2
Fig. 2. Hawaiian papaya plot in 2011
Hawaiian papaya plot showing diseased, devastated, non-transformed trees in the foreground and healthy transgenic trees behind. [Photo courtesy of Dennis Gonsalves, Agricultural Research Service, U.S. Department of Agriculture, Hawaii]

References

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