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. 2020 Feb 5;18(8):1810–1829. doi: 10.1111/pbi.13343

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© 2020 The Authors. Plant Biotechnology Journal published by Society for Experimental Biology and The Association of Applied Biologists and John Wiley & Sons Ltd.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Crosstalk between the GmSNAP18‐, GmSHMT08‐ and GmPR08‐Bet VI‐resistant genes and SA and CK phytohormones to activate defence and resistant response in Peking‐type SCN resistance. In the absence of pathogen attack, endogenous cytokinins (CKs) promote shoot growth. Infection by a biotrophic pathogen (in the case of SCN) stimulates pattern‐triggered immunity (PTI) activation, oxidative stress (ROS) and salicylic acid (SA) biosynthesis, resulting in salicylic acid‐dependent defence responses to suppress pathogen growth (blue) (Albrecht and Argueso, 2017). Endogenous and/or exogenous cytokinins can help pathogen growth, by mechanisms that include suppression of PTI and ROS (cytokinin‐induced susceptibility: red) (Albrecht and Argueso, 2017). Increased salicylic acid content/signalling induces salicylic acid component genes including GmSAMT, GmNPR and GmTGA resulting in the induction of the GmPR08‐Bet VI, potentially promoting SA defence response. QRT‐PCR analysis demonstrates that at ten days post‐SCN inoculation, the expression of GmSNAP18 returns to levels prior to nematode infection. These data point to a model in which GmSNAP18 may directly or indirectly negatively autoregulate itself. Induction of genes in response to stress is commonly associated with rapid inactivation of a negative co‐regulator. Accordingly, the possible binding of a nematode effector (E) like the HgSLP‐1, SA and/or CKs may interrupt the autoregulation of GmSNAP18, causing an increase in the transcription of GmSNAP18, consequently causing an induction of GmSHMT08. An interaction between GmPR08‐Bet VI, GmSNAP18 and the GmSHMT08 protein complex will occur and carry the complex towards the plasma membrane and modulate the activity of the GmSHMT08 in single‐carbon metabolism, methionine synthesis and maintenance of redox homeostasis within the root cells. By binding cytokinins, GmPR08‐Bet VI may hijack the increase of both exogenous and endogenous cytokinins at the feeding site and therefore suppress the cytokinin‐regulated processes (brown). Finally, induction of the reported apoptosis, cell death and necrosis that were intensified when the GmSNAP18/GmSHMT08/GmPR08‐Bet VI protein complex was present, in addition to the degeneration observed in the cells surrounding the syncytia, will occur. Abbreviations are as follows: CKs, endogenous or exogenous cytokinins; E, possible effectors; NPR, non‐inducible pathogenesis‐related; PR, pathogenesis‐related protein; SA, salicylic acid; TGA,transcription factor; SAMT,S‐adenosyl‐L‐methionine‐dependent salicylic acid methyltransferase; SHMT,serine hydroxymethyltransferase; SNAP, soluble NSF attachment protein. Arrows indicate positive interactions; blunt ends indicate negative interactions (inhibition); dashed lines represent unknown possible intermediary steps; (yellow) possibility of the presence of other intermediate(s).