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Review
. 2018 May 21;28(10):R619-R634.
doi: 10.1016/j.cub.2018.03.054.

Plant-Pathogen Warfare under Changing Climate Conditions

André C Velásquez  1 , Christian Danve M Castroverde  2 , Sheng Yang He  3
Affiliations
Review

Plant-Pathogen Warfare under Changing Climate Conditions

André C Velásquez et al. Curr Biol. .

Abstract

Global environmental changes caused by natural and human activities have accelerated in the past 200 years. The increase in greenhouse gases is predicted to continue to raise global temperature and change water availability in the 21st century. In this Review, we explore the profound effect the environment has on plant diseases - a susceptible host will not be infected by a virulent pathogen if the environmental conditions are not conducive for disease. The change in CO2 concentrations, temperature, and water availability can have positive, neutral, or negative effects on disease development, as each disease may respond differently to these variations. However, the concept of disease optima could potentially apply to all pathosystems. Plant resistance pathways, including pattern-triggered immunity to effector-triggered immunity, RNA interference, and defense hormone networks, are all affected by environmental factors. On the pathogen side, virulence mechanisms, such as the production of toxins and virulence proteins, as well as pathogen reproduction and survival are influenced by temperature and humidity. For practical reasons, most laboratory investigations into plant-pathogen interactions at the molecular level focus on well-established pathosystems and use a few static environmental conditions that capture only a fraction of the dynamic plant-pathogen-environment interactions that occur in nature. There is great need for future research to increasingly use dynamic environmental conditions in order to fully understand the multidimensional nature of plant-pathogen interactions and produce disease-resistant crop plants that are resilient to climate change.

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Conflict of interest statement

DECLARATION OF INTERESTS

The authors declare no competing interests.

Figures

Figure 1
Figure 1. Impact of environmental conditions on plant pathogen interactions
The environment-host-pathogen tripartite interaction operates within a continuum, from interactions fully conducive for disease (disease optima) to those that maintain healthy plants. Environmental conditions can have profound effects on a host plant’s physiological state, including its growth, immune signaling and abiotic stress response, as well as a pathogen’s survival, germination, and expression and delivery of virulence factors. These variable environmental conditions can render the same plant being fully susceptible to being fully resistant, while the pathogen could range from being able to cause severe disease to being only weakly pathogenic. The three most important environmental variables predicted to change in this century are atmospheric CO2 concentration, temperature, and water availability.
Figure 2
Figure 2. Environmental impact on the molecular mechanisms influencing disease
(A) A diagram depicting examples of plant-pathogen-environment triangular interactions. High temperature (left half of plant cell) increases the production of bacterial plant cell wall-degrading enzymes by soft-rotting bacteria, while it decreases transfer DNA (T-DNA) delivery by Agrobacterium spp. Viral accumulation can be positively or negatively influenced by elevated temperature, however, the plant antiviral RNA interference (RNAi) mechanisms are generally increased by warm temperatures. Abscisic acid (ABA) accumulation is increased, whereas effector-triggered immunity (ETI) can be unaffected, heightened, or rendered ineffective at high temperatures. High humidity (left half of cell) increases sporulation by fungal and oomycete pathogens, and allows bacterial effectors to establish an aqueous apoplast in infected leaves. In tomato, ETI is negatively affected by high humidity. Abbreviation: RISC, RNA-induced silencing complex. (B) A diagram depicting the current knowledge of the Arabidopsis-Pseudomonas-environment triangular interaction. Elevated temperature increases effector translocation into plant cells and decreases production of the toxin coronatine from P. syringae. On the other hand, elevated temperature increases ABA and decreases salicylic acid (SA) hormone concentrations in Arabidopsis. A decrease in ETI and an increase in PAMP-triggered immunity (PTI) at elevated temperature have been reported. Higher air humidity conditions favor P. syringae, which produce effectors that establish an aqueous apoplast in the infected leaves to favor disease. Also, higher humidity affects some aspects of the ETI response.
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