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. 2020 Jun 30;8(3):349. doi: 10.3390/vaccines8030349

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Deciphering SCN resistance mechanism in Peking-type. Cross-talk between SCN resistant genes, defense genes, and phytohormones is shown as described earlier (Lakhssassi et al., 2020). Dashed lines represent unknown possible intermediary steps. The possible binding of a nematode effector (E) may interrupt the autoregulation of GmSNAP18, causing an increase in the transcription of GmSNAP18, consequently causing an induction of GmSHMT08. Next, the multi-protein complex may modulate the activity of the GmSHMT08 in single carbon metabolism, methionine synthesis, and maintenance of redox homeostasis within the root cells. Induction of the apoptosis, necrosis, and degeneration observed in the cells surrounding the syncytia may occur. Metabolite abbreviations are as follows—(SAH) S-adenosylhomocysteine; (SAM) S-adenosylmethionine; (hCyst) homocysteine; (Met) methionine; (THF) tetrahydrofolate; (GSH) reduced glutathione; (GSSG) oxidized glutathione.