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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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Model of interaction between CLas and Citrus plants. Susceptible plants, the downregulation of signaling receptors promotes a late recognition of CLas infection and consequently, no proper signaling is activated. Auxin-related genes positively modulate the gibberellin synthesis, which activates response mechanisms to CLas infection, such as callose and PP2 deposition and impaired substances transport. Interference on substance transport along with callose deposition causes phloem dysfunction resulting in starch accumulation on photosynthetic tissues. Starch accumulation promotes thylakoid rupture and chlorophyll degradation culminating in HLB classical symptoms. Tolerant plants, the induction of signaling receptors causes a fast and efficient defense response modulated by suppression of auxin pathway and induction of GA degradation. The suppression of these pathways prevents the events that lead to the phloem dysfunction (callose deposition, starch accumulation and transport alteration) and activates defense response through the synthesis of phenylpropanoids and cell wall-strengthened related genes. This transcriptional reprograming is efficient to impair the development of symptoms. Resistant genotypes, a possibly early and fast defense may occur in response to CLas, since low numbers of the genes are modulated after 240 days post inoculation. Nonetheless, this response is related to induction of signaling receptors and upregulation of Endochitinase B, which might be associated with bacterial cell lysis (Created with BioRender.com).