Publication | Open Access
Biochemical and physiological responses to long‐term <i>Citrus tristeza virus</i> infection in Mexican lime plants
15
Citations
25
References
2017
Year
BotanyPlant PathologyPlant-pathogen InteractionPlant HealthPhysiological Plant PathologyPlant-virus InteractionSuperoxide DismutaseMexican Lime PlantsPlant VirusVirologyPhytotoxicityBiologyCtv InfectionNatural SciencesPathogenesisCitrus Tristeza VirusPhysiological ResponsesMicrobiologyMedicinePlant Physiology
Reactions that occur when a plant is subjected to Citrus tristeza virus ( CTV ) infection often result in triggering of numerous defence mechanisms to fight the infection. The reactions vary according to virus strain, host genotype, time of exposure to the infection and environmental conditions. To date, no study has examined in detail the consequences of 10‐year exposure to CTV infection on the biochemical and physiological status of susceptible Mexican lime plants ( Citrus aurantifolia ). To understand the reaction of such plants, changes in nutrient status, total proteins, enzyme activity involved in scavenging of reactive oxygen species, photosynthetic and transpiration rates, chlorophyll content, membrane permeability and water content were analysed in plants infected with different CTV isolates and in healthy plants. The activity of superoxide dismutase and polyphenol oxidase significantly decreased in the infected leaves, and membrane permeability was lower in the infected plants. Macro‐ and micronutrient elements were significantly changed: concentrations of leaf nitrogen, zinc, magnesium and iron were elevated but potassium concentration depressed in comparison to noninfected control leaves. Levels of other analysed nutrient elements, enzymes, photosynthesis and stomatal conductance, chlorophyll content and relative water content were unchanged. Clear physiological changes were found among infected and noninfected control plants but none between plants infected with different CTV isolates. The data suggest that some of the defence mechanisms investigated here were suppressed due to the continuous and long‐term pressure of biotic stress.
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