New insights into the regulation of the SNC1 resistance gene

Combined genetic analysis of loss- and gain-of-function mutants identifies a new MPK3/MPK6-CHR5-SNC1 immune signaling module in Arabidopsis thaliana

To defend against pathogens (bacteria, fungi, etc.), plants have a complex immune system composed of two main lines of defense: Pattern-Triggered Immunity (PTI) triggered by the recognition of Pathogen-Associated Molecular Patterns (PAMPs) at the plasma membrane, and Effector-Triggered Immunity (ETI) triggered by the detection of microbial effectors within plant cells. Long considered independent, recent studies show that PTI and ETI interacts closely. For instance, the PAMP-induced Mitogen Activated Protein Kinases 3 and 6 (MPK3/6) are involved in the induction of certain immune genes, such as the SNC1 gene, coding for receptors of effectors. However, the underlying regulatory mechanisms remain largely unknown.

In a research article published in Scientific Reports, researchers from the STRESS team at IPS2 have shown through genetic approaches that the chromatin remodeling factor 5 (CHR5) acts downstream of MPK3/6 to promote the expression of SNC1. The authors also showed that, while CHR5 does not regulate the abundance or activity of MPK3/6, the combination of autoimmune gain-of-function mutants for MPK3 and SNC1 leads to a strong synergistic effect. Overall, the results obtained identify a new MPK3/6-CHR5-SNC1 signaling module and thus contribute to a better understanding of the links between PTI and ETI.

Model for the MPK3/6-CHR5-SNC1 module in Arabidopsis, further refining the connection between PTI and ETI components. Other signaling components were also included, based on literature data. Question marks indicate unidentified or poorly documented events. P in the red circles: Phosphorylation

16/06/2026