E3 ligase SAUL1 serves as a positive regulator of PAMP‐triggered immunity and its homeostasis is monitored by immune receptor SOC3

Tong, Meixuezi; Kotur, Tanja; Liang, Wanwan; Vogelmann, Katja; Kleine, Tatjana; Leister, Dario; Brieske, Catharina; Yang, Shuhua; Lüdke, Daniel; Wiermer, Marcel; Zhang, Yuelin; Li, Xin; Hoth, Stefan

doi:10.1111/nph.14678

Cited by 56 publications

(80 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Phosphorylated BIK1 was recently demonstrated to be directly involved in regulating levels of the defense hormones JA and SA (Lal et al, 2018). When autoimmune effects are removed, the corresponding genes of some mutants, such as saul1 , have been shown to facilitate immune signaling (Tong et al, 2017). Similarly, when the high level of basal SA was removed by the expression of the SA dehydrogenase NahG, the sik1 knockout was compromised in flg22-induced bacterial growth inhibition and no longer exhibited enhanced resistance to virulent Pst .…”

Section: Discussionmentioning

confidence: 99%

The MAP4 Kinase SIK1 Ensures Robust Extracellular ROS Burst and Antibacterial Immunity in Plants

Zhang

Chiang

Toruño

et al. 2018

Cell Host & Microbe

110

107

View full text Add to dashboard Cite

Microbial patterns are recognized by cell-surface receptors to initiate pattern-triggered immunity (PTI) in plants. Receptor-like cytoplasmic kinases (RLCKs), such as BIK1, and calcium-dependent protein kinases (CPKs) are engaged during PTI to activate the NADPH oxidase RBOHD for reactive oxygen species (ROS) production. It is unknown whether protein kinases besides CPKs and RLCKs participate in RBOHD regulation. We screened mutants in all ten Arabidopsis MAP4 kinases (MAP4Ks) and identified the conserved MAP4K SIK1 as a positive regulator of PTI. sik1 mutants were compromised in their ability to elicit the ROS burst in response to microbial features and exhibited compromised PTI to bacterial infection. SIK1 directly interacts with, phosphorylates, and stabilizes BIK1 in a kinase activity-dependent manner. Furthermore, SIK1 directly interacts with and phosphorylates RBOHD upon flagellin perception. Thus, SIK1 positively regulates immunity by stabilizing BIK1 and activating RBOHD to promote the extracellular ROS burst.

show abstract

Section: Discussionmentioning

confidence: 99%

The MAP4 Kinase SIK1 Ensures Robust Extracellular ROS Burst and Antibacterial Immunity in Plants

Zhang

Chiang

Toruño

et al. 2018

Cell Host & Microbe

110

107

View full text Add to dashboard Cite

show abstract

“…We previously reported that loss of SAUL1 results in autoimmunity that is dependent on SOC3 (Tong et al ., ). From the saul1‐1 suppressor screen, we did not isolate any chs1 or tn2 alleles.…”

Section: Resultsmentioning

confidence: 97%

“…As reported before, the TNL SOC3 is required for autoimmunity of both saul1‐1 and the 35S::SAUL1 transgenic line (Tong et al ., ). Based on the data mentioned above, the truncated TN protein CHS1, but not TN2, is required for the saul1‐ mediated autoimmune phenotype.…”

Section: Resultsmentioning

confidence: 97%

“…We recently reported that the TNL SOC3 monitors the homeostasis of SAUL1 (Tong et al ., ). Here, through genetic analysis, we found that knocking out CHS1 alone is sufficient to suppress the autoimmunity of saul1‐1 (Fig.…”

Section: Discussionmentioning

confidence: 97%

“…This autoimmunity is dependent on the signaling components Enhanced Disease Susceptibility 1 (EDS1), Phytoalexin Deficient 4 (PAD4) and Suppressor of the G2 Allele of SKP1b (SGT1B) (Vogelmann et al, 2012;Lee et al, 2016). From saul1-1 suppressor screens, the TNL protein SOC3 was identified and was proposed to guard SAUL1, a positive regulator of PTI (Tong et al, 2017). As no alleles of chs1 or tn2 were found in the saul1-1 suppressor screens, the head-to-head tandem arrangement of SOC3, CHS1 and TN2 on chromosome 1 prompted us to test whether the two TN proteins, CHS1 and TN2, could redundantly pair with SOC3 in saul1-mediated autoimmunity.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2018

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Ubiquitin/Proteasome System in Plant Pathogen Responses

Sorel

Mooney

Marchi

et al. 2019

Annual Plant Reviews Online

View full text Add to dashboard Cite

In eukaryotes, the ubiquitin/proteasome system plays crucial roles in the regulation of protein stability. These functions are largely mediated through the covalent attachment of ubiquitin to substrate proteins and their targeting to the 26S proteasome, a large multi‐subunit protease. In the last three decades, the ubiquitin system has been shown to regulate essentially all processes in eukaryotes. In plants, it appears to play particularly important roles, perhaps as a result of the plants' sessile lifestyle and their need to adapt to rapidly changing environmental conditions. In particular, the ubiquitin system is key to the regulation of plant responses to pathogens, not only during interaction with a pathogen but also in the absence of infection to prevent the constitutive activation of defence responses that would have detrimental effects. In this article, we discuss the roles of the ubiquitin system in the regulation of different cellular pathways involved in plant defence responses, including the regulation of transmembrane and intracellular receptors, and the control of the signalling pathways that are activated downstream of pathogen detection. We also review how pathogens hijack the ubiquitin system to increase their virulence. Finally, we briefly discuss the emerging roles of autophagy in the regulation of plant/pathogen interactions.

show abstract

E3 ligase SAUL1 serves as a positive regulator of PAMP‐triggered immunity and its homeostasis is monitored by immune receptor SOC3

Cited by 56 publications

References 72 publications

The MAP4 Kinase SIK1 Ensures Robust Extracellular ROS Burst and Antibacterial Immunity in Plants

The MAP4 Kinase SIK1 Ensures Robust Extracellular ROS Burst and Antibacterial Immunity in Plants

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

Ubiquitin/Proteasome System in Plant Pathogen Responses

Contact Info

Product

Resources

About