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As mentioned in the previous thread,
“Pattern-recognition receptors are required for NLR-mediated plant immunity” and our preprint is a back-to-back publication.
This thread is generated by Minhang Yuan from Xin lab.
(I am posting on behalf of him):
“Pattern-recognition receptors are required for NLR-mediated plant immunity” and our preprint is a back-to-back publication.
This thread is generated by Minhang Yuan from Xin lab.
(I am posting on behalf of him):
Our recent work “Pattern-recognition receptors are required for NLR-mediated plant immunity” has been posted on BioRxiv :
https://www.biorxiv.org/content/10.1101/2020.04.10.031294v1.">https://www.biorxiv.org/content/1...
https://www.biorxiv.org/content/10.1101/2020.04.10.031294v1.">https://www.biorxiv.org/content/1...
In this study, we uncovered the enigmatic relationship between PRR mediated pattern-triggered immunity (PTI) and NLR mediated effector-triggered immunity (ETI) in plants.
A thread:
A thread:
1. We first used two independent PTI receptor mutants fls2/efr/cerk1 (fec) and bak1/bkk1/cerk1 (bbc) to test ETI resistance triggered by effectors. Interestingly, the fec and bbc mutants are greatly compromised in ETI resistance and show delayed HR response.
2. Next, we want to figure out how PRR/co-receptors mediate ETI responses and mainly focused on AvrRpt2-triggered ETI for in-depth characterization. We first checked RIN4 cleavage and MAPK activation in the PRR/coreceptor mutants and found that these responses were normal.
3. We found that PTI+ETI triggers strong and sustained “second-phase” ROS burst, while ETI alone only triggered weak ROS production. bbc mutation almost completely abolished AvrRpt2-ROS burst. This indicated that PRR/coreceptors are required for ROS triggered by AvrRpt2.
4. Furthermore, we found that ETI-ROS is mainly produced in the apoplast space and mediated by RBOHD. Consistently, we found rbohd mutant showed largely compromised resistance to Pst DC3000(avrRpt2). These results suggest a critical role of RBOHD in ETI.
5. We found that the transcript&protein levels are much higher during PTI+ETI than PTI alone. Interestingly, this process was PRR/coreceptor-independent. We found that ETI-ROS burst is partially mediated by BIK1, and the ETI-S343/S347 phosphorylation of RBOHD was dependent on PTI
5. Therefore, our results suggest that two classes of immune receptors coordinate to ensure the abundance (i.e. by RPS2) and activity (i.e. by PRRs) of RBOHD for generating robust ETI-ROS.
6. We also performed RNAseq to analyze the relationship between PTI&ETI. We found that ETI can largely restore the deficiency of PTI-associated global gene expression in bbc. Similar trends were observed for genes associated with salicylic acid, jasmonate & ethylene pathways.
7. Furthermore, we found that a subset of 272 genes were differentially expressed between Col-0 and bbc infected by D36E(avrRpt2). Interestingly, the canonical marker genes including WRKY22/29 and FRK1 are down-regulated in the bbc during AvrRpt2-triggered ETI.
7. This suggests that the activation of this branch during ETI requires PRR/coreceptors.
8. Strikingly, we found that many key components of PTI signaling, including BAK1, BIK1, PCRK1/2, XLG2, MKK4/5, and MPK3, are largely up-regulated during ETI, suggesting that PTI is integrated into ETI.
9. We confirmed this interesting finding by qRT-PCR and WB. Consistent with RNAseq, the transcript and protein levels were strongly augmented by ETI, and this process is PTI independent (we propose that the “activity” of these components, similar to RBOHD, relies on PTI).
9. Therefore, we propose PTI being an essential component of ETI.
10. In addition, we found that ETI seems to “re-enforce” the PTI pathway in a SA/NHP-independent manner.
11. In conclusion, our study reveals a surprising requirement of PRR/co-receptors for effective ETI responses and supports an alternative model in which PTI is in fact an indispensable component of ETI during bacterial infection.
11. This also implies that ETI halts pathogen infection, in part, by directly co-opting the anti-pathogen mechanisms proposed for PTI.
12. Our study sheds light on a long-standing puzzle in the field of plant immunity with respect to the enigmatic similarities in many PTI- and ETI-associated cellular defense features.
12. Our model is supported by a parallel study by Ngou et al. ( https://www.biorxiv.org/content/10.1101/2020.04.10.034173v1),">https://www.biorxiv.org/content/1... who focus on AvrRps4 which is recognized by TIR-type NLRs (RPS4/RRS1), while we focus on RPS2, a CC-type NLR. Together with Ngou et al, we updated the classical “zig-zag” model.
13. I would like to thank Xiu-Fang Xin, Sheng Yang He, Jian-Min Zhou and all other co-authors’ contributions and Bruno Pok Man Ngou, Pingtao Ding, Jonathan Jones from the Sainsbury Laboratory, UK, for the helpful and insightful discussions.
13. We hope that our complementary work advances our understanding of plant immunity and can be recognized and discussed by the public. Please feel free to contact us (mhyuan@sibs.ac.cn) if you have any suggestions or comments. Thanks!
