TIR‐NB‐LRR immune receptor SOC3 pairs with truncated TIR‐NB protein CHS1 or TN2 to monitor the homeostasis of E3 ligase SAUL1

Abstract

Summary Intracellular nucleotide binding (NB) and leucine‐rich repeat (NLR) proteins function as immune receptors to recognize effectors from pathogens. They often guard host proteins that are the direct targets of those effectors. Recent findings have revealed that a typical NLR sometimes cooperates with another atypical NLR for effector recognition. Here, by using the CRISPR/Cas9 gene editing method, knockout analysis and biochemical assays, we uncovered differential pairings of typical Toll Interleukin1 receptor (TIR) type NLR (TNL) receptor SOC3 with atypical truncated TIR‐NB (TN) proteins CHS1 or TN2 to guard the homeostasis of the E3 ligase SAUL1. Overaccumulation of SAUL1 is monitored by the SOC3−TN2 pair, while SAUL1's disappearance is guarded by the SOC3−CHS1 pair. SOC3 forms a head‐to‐head genomic arrangement with CHS1 and TN2, indicative of transcriptional co‐regulation. Such intricate cooperative interactions can probably enlarge the recognition spectrum and increase the functional flexibility of NLRs, which can partly explain the overwhelming occurrence of NLR gene clustering in higher plants.

Help wanted: helper NLRs and plant immune responses

“…SOC3 can partner with either of the genetically linked CHS1 or TN2 to monitor the homeostasis of E3 ligase SAUL1. SOC3 appears to be the executor module [18,19].…”

CRISPR technology is revolutionizing the improvement of tomato and other fruit crops

“…At present, CRISPR-Cas has multiplex editing capability, that is, it edits more than one gene at a time 38 . In addition, CRISPR-Cas can target not only the open reading frame (ORF) 39 and untranslated region 40 of one coding gene but also non-coding RNAs (ncRNAs) including long ncRNA 41 and microRNA 42 , as well as promoter regions 43 . Single-base substitutions at genomic targets without requiring DSBs have also been achieved 44 .…”

Soybean GmSAUL1, a Bona Fide U-Box E3 Ligase, Negatively Regulates Immunity Likely through Repressing the Activation of GmMPK3

“…Arabidopsis senescence-associated E3 ubiquitin ligase 1 (SAUL1) was initially identified as a U-box E3 ubiquitin ligase required for the suppression of premature senescence [ 19 ]. Recently, it has been shown that a loss-of-function mutation in SAUL1 results in enhanced disease resistance against multiple biotrophic pathogens [ 20 , 21 , 22 , 23 , 24 ]. This autoimmunity is totally dependent on Enhanced Disease Susceptibility 1 (EDS1), Phytoalexin Deficient 4 (PAD4), and Suppressor of the G2 Allele of SKP1b (SGT1B) [ 20 , 21 , 22 ].…”

“…A level of SAUL1 exceeding a certain threshold range will lead to the activation of immunity. Liang et al recently uncovered SOC3 pairs with different truncated TIR-NB (TN) proteins to monitor either the absence or overexpression of SAUL1, respectively [ 24 ].…”