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Article|23 Aug 2017|OPEN
Molecular mechanisms behind the accumulation of ATP and H2O2 in citrus plants in response to ‘Candidatus Liberibacter asiaticus’ infection
Marco Pitino1 , Cheryl M Armstrong1 and Yongping Duan,1 ,
1USDA-ARS, US Horticultural Research Laboratory, 2001 S. Rock Road, Fort Pierce, FL 34945, USA
*Corresponding author. E-mail: Yongping.Duan@ars.usda.gov

Horticulture Research 4,
Article number: 40 (2017)
doi: https://doi.org/10.1038/hortres.2017.40
Views: 922

Received: 03 May 2017
Revised: 29 Jun 2017
Accepted: 05 Jul 2017
Published online: 23 Aug 2017

Abstract

Candidatus Liberibacter asiaticus (Las) is a fastidious, phloem-restricted pathogen with a significantly reduced genome, and attacks all citrus species with no immune cultivars documented to date. Like other plant bacterial pathogens, Las deploys effector proteins into the organelles of plant cells, such as mitochondria and chloroplasts to manipulate host immunity and physiology. These organelles are responsible for the synthesis of adenosine triphosphate (ATP) and have a critical role in plant immune signaling during hydrogen peroxide (H2O2) production. In this study, we investigated H2O2 and ATP accumulation in relation to citrus huanglongbing (HLB) in addition to revealing the expression profiles of genes critical for the production and detoxification of H2O2 and ATP synthesis. We also found that as ATP and H2O2 concentrations increased in the leaf, so did the severity of the HLB symptoms, a trend that remained consistent among the four different citrus varieties tested. Furthermore, the upregulation of ATP synthase, a key enzyme for energy conversion, may contribute to the accumulation of ATP in infected tissues, whereas downregulation of the H2O2 detoxification system may cause oxidative damage to plant macromolecules and cell structures. This may explain the cause of some of the HLB symptoms such as chlorosis or leaf discoloration. The findings in this study highlight important molecular and physiological mechanisms involved in the host plants’ response to Las infection and provide new targets for interrupting the disease cycle.