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. 2020 Nov 30;10:20865. doi: 10.1038/s41598-020-77840-2

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Defense response of susceptible genotypes against CLas. In the phase 1 of this model, citrus plants receptors detect the CLas PAMPs. In phase 2, a PAMP-triggered immunity (PTI) response is initiated, resulting in the production of gibberellic acid (GA), salicylic acid (SA) and the SA-dependent gene expression activation (in blue). In phase 3, CLas deliver effectors leading in effector-triggered susceptibility (ETS). In phase 4, effectors are recognized by plants proteins, activating effector-triggered immunity (ETI). In phase 5, ETI triggers a series of genetic events (in red), including the induction of calloses synthases and pp2 expression. This exaggerated response could be considered as hypersensitive cell death (HR), since the attempt to isolate spatially the CLas leading to callose and PP2 accumulation, that cause phloem dysfunctions. The phase 6 represents the starch accumulation in the mesophyll chloroplasts(Created with BioRender.com).