The truncated TNL receptor TN2-mediated immune responses require ADR1 function.

Area of Science:

• Plant immunity
• Molecular genetics
• Plant pathology

Background:

• Loss of function in the exocyst subunit EXO70B1 triggers autoimmunity dependent on the truncated nucleotide-binding and leucine-rich repeat receptor (NLR) TN2.
• The precise mechanisms by which TN2 activates plant immunity and the necessity of typical NLRs in TN2-mediated resistance are not fully understood.

Purpose of the Study:

• To elucidate the signaling pathways and NLRs involved in TN2-triggered plant immunity.
• To investigate the role of helper NLRs, specifically ADR1 and NRG1 families, in EXO70B1-mediated autoimmunity.

Main Methods:

• CRISPR/Cas9 gene editing system was employed to create knockout mutants.
• Analysis of spontaneous cell death, enhanced resistance, and chilling sensitivity in various mutant lines.
• Gene expression analysis to determine transcript levels of TN2.

Main Results:

• Autoimmunity and enhanced resistance in exo70B1-3 mutants were independent of full-length NLRs SOC3 and SOC3-L1.
• Knockout of SOC3-L1 or TN2 did not affect chilling sensitivity in chs1-2 mutants.
• Exo70B1-3-induced autoimmunity critically depended on ACTIVATED DISEASE RESISTANCE 1 (ADR1) family members, but not N REQUIREMENT GENE 1 (NRG1) family members.
• ADR1s positively regulated TN2 transcript levels in exo70B1-3 mutants.
• Overexpression of TN2 also induced ADR1-dependent autoimmune responses.

Conclusions:

• The truncated TNL protein TN2 triggers plant immune responses that necessitate ADR1s acting as helper NLRs for downstream signaling activation.
• ADR1s play a crucial and complex role in regulating plant immunity, particularly in response to truncated NLR signaling.