Suppression of ETI by PTI priming to balance plant growth and defense through an MPK3/MPK6-WRKYs-PP2Cs module

Pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)are required for host defense against pathogens.Although PTI and ETI are intimately connected,the underlying molecular mechanisms remain elusive.In this study,we demonstrate that flg22 priming attenuates Pseudomonas syringae pv.tomato DC3000(Pst)AvrRpt2-induced hypersensitive cell death,resistance,and biomass reduction in Arabidopsis.Mitogen-activated protein kinases(MAPKs)are key signaling regulators of PTI and ETI.The absence of MPK3 and MPK6 significantly reduces pre-PTI-mediated ETI suppression(PES).We found that MPK3/MPK6 interact with and phosphorylate the downstream transcription factor WRKY18,which regulates the expression of AP2C1 and PP2C5,two genes encoding protein phosphatases.Furthermore,we observed that the PTI-suppressed ETI-triggered cell death,MAPK activation,and growth retardation are significantly attenuated in wrky18/40/60 and ap2c1 pp2c5 mutants.Taken together,our results suggest that the MPK3/MPK6-WRKYs-PP2Cs module underlies PES and is essential for the maintenance of plant fitness during ETI.

MYB44 regulates PTI by promoting the expression of EIN2 and MPK3/6 in Arabidopsis

The plant signaling pathway that regulates pathogen-associated molecular pattern(PAMP)-triggered immunity(PTI)involves mitogen-activated protein kinase(MAPK)cascades that comprise sequential activation of several protein kinases and the ensuing phosphorylation of MAPKs,which activate transcription factors(TFs)to promote downstream defense responses.To identify plant TFs that regulate MAPKs,we investigated TF-defective mutants of Arabidopsis thaliana and identified MYB44 as an essential constituent of the PTI pathway.MYB44 confers resistance against the bacterial pathogen Pseudomonas syringae by cooperating with MPK3 and MPK6.Under PAMP treatment,MYB44 binds to the promoters of MPK3 and MPK6 to activate their expression,leading to phosphorylation of MPK3 and MPK6 proteins.In turn,phosphorylated MPK3 and MPK6 phosphorylate MYB44 in a functionally redundant manner,thus enabling MYB44 to activate MPK3 and MPK6 expression and further activate downstream defense responses.Activation of defense responses has also been attributed to activation of EIN2 transcription by MYB44,which has previously been shown to affect PAMP recognition and PTI development.AtMYB44 thus functions as an integral component of the PTI pathway by connecting transcriptional and posttranscriptional regulation of the MPK3/6 cascade.

GoldCLIP： Gel-omitted Ligation-dependent CLIP

Protein-RNA interaction networks are essential to understand gene regulation control. Identifying binding sites of RNA-binding proteins （RBPs） by the UV-crosslinking and immunoprecipitation （CLIP） represents one of the most powerful methods to map protein RNA interactions in vivo. However, the traditional CLIP protocol is technically challenging, which requires radioactive labeling and suffers from material loss during PAGE-membrane transfer procedures. Here we introduce a super-efficient CLIP method （GoldCLIP） that omits all gel purification steps. This nonisotopic method allows us to perform highly reproducible CLIP experiments with polypyrimidine tract-binding protein （PTB）, a classical RBP in human cell lines. In principle, our method guarantees sequencing library constructions, providing the protein of interest can be successfully crosslinked to RNAs in living cells. GoldCLIP is readily applicable to diverse proteins to uncover their endogenous RNA targets.

Post-transcriptional regulation of miRNA biogenesis and functions

MicroRNAs(miRNAs)are a highly conserved class of small(18–24 nucleotides)non-coding RNAs that regulate a broad spectrum of biological processes.Aberrations or corruptions of miRNA functions may lead to deregulated cell proliferation,tumorigenesis,and ultimately,cancer.Increasing evidences suggested that a large fraction of miRNAs is regulated at the posttranscriptional stage,which impacts on the level and function of miRNAs during cell development and human diseases.Recently,several distinct mechanisms are emerging to regulate the biogenesis,stability and function of miRNAs at post-transcriptional level,such as specific binding to terminal loops of miRNA precursors(primiRNAs or pre-miRNAs)by RNA-binding proteins and 3’-terminal modifications by particular enzymes.Signaling cascades and post-translational modifications of the core components of RNA machinery also take part in the posttranscriptional regulation of miRNAs.

Advances in airborne microorganisms detection using biosensors:A critical review

Humanity has been facing the threat of a variety of ifectious diseases.Airborne microorganisms can cause airbome infectious diseases,which spread rapidly and extensively,causing huge losscs to human society on a global scale.In recent years,the detection technology for airbome microorganisms has developed rapidly;it can be roughly divided into biochemical,immune,and molecular technologies.However,these technologies still have some shortcomings;they are time consuming and have low sensitivity and poor stability.Most of them need to be used in the ideal environment of a laboratory,which limits their applications.A biosensor is a device that converts biological signals into detectable signals.As an interdisciplinary feld,biosensors have successfully introduced a variety of technologies for bio-detection.Given their fast analysis speed,high sensitivity good portability,strong specifcity,and low cost,biosensors have been widely uised in cnvironmental monitoring,medical research,food and agricultural safety,military.medicine and other fields.In recent years,the performance of biosensors has greatly improved,becoming.a promising techmology for airborne microorganism detection.This review introduces the detection principle of biosensors from the three aspects of component identification,energy conversion principle,and signal amplification.It also summarizes its research and application in airborne microorganism detection.The new progress and future development trend of the biosensor detection of airbormne microorganisms are analyzed.

Non-CG DNA methylation-deficiency mutations enhance mutagenesis rates during salt adaptation in cultured Arabidopsis cells

Much has been learned about how plants acclimate to stressful environments,but the molecular basis of stress adaptation and the potential involvement of epigenetic regulation remain poorly understood.Here,we examined if salt stress induces mutagenesis in suspension cultured plant cells and if DNA methylation affects the mutagenesis using whole genome resequencing analysis.We generated suspension cell cultures from two Arabidopsis DNA methylation-deficient mutants and wild-type plants,and subjected the cultured cells to stepwise increases in salt stress intensity over 40 culture cycles.We show that ddc(drm1 drm2 cmt3)mutant cells can adapt to grow in 175 mM NaCl-containing growth medium and exhibit higher adaptability compared to wild type Col-0 and nrpe1 cells,which can adapt to grow in only 125mM NaCl-containing growth medium.Salt treated nrpe1 and ddc cells but not wild type cells accumulate more mutations compared with their respective untreated cells.There is no enrichment of stress responsive genes in the list of mutated genes in salt treated cells compared to the list of mutated genes in untreated cells.Our results suggest that DNA methylation prevents the induction of mutagenesis by salt stress in plant cells during stress adaptation.

Publisher Correction: Non-CG DNA methylation-deficiency mutations enhance mutagenesis rates during salt adaptation in cultured Arabidopsis cells

Following publication of this article(Zhu et al.2021),it is noticed that the article contained an error.The affiliation of the author Ray A.Bressan should be below:4.Department of Horticulture and Landscape Architecture,Purdue University,West Lafayette,IN 47907,USA.The author Ray A.Bressan’s affiliation has been updated in this Correction,and the original article has been updated as well.