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Abstract BackgroundAlternative splicing of precursor mRNAs serves as a crucial mechanism to enhance gene expression plasticity for organismal adaptation. However, the precise regulation and function of alternative splicing in plant immune gene regulation remain elusive. ResultsHere, by deploying in-depth transcriptome profiling with deep genome coverage coupled with differential expression, differential alternative splicing, and differential transcript usage analysis, we reveal profound and dynamic changes in alternative splicing following treatment with microbial pattern flg22 peptides inArabidopsis. Our findings highlight RNA polymerase II C-terminal domain phosphatase-like 3 (CPL3) as a key regulator of alternative splicing, preferentially influencing the splicing patterns of defense genes rather than their expression levels. CPL3 mediates the production of a flg22-induced alternative splicing variant, diacylglycerol kinase 5α (DGK5α), which differs from the canonical DGK5β in its interaction with the upstream kinase BIK1 and subsequent phosphorylation, resulting in reduced flg22-triggered production of phosphatidic acid and reactive oxygen species. Furthermore, our functional analysis suggests that DGK5β, but not DGK5α, contributes to plant resistance against virulent and avirulent bacterial infections. ConclusionsThese findings underscore the role of CPL3 in modulating alternative splicing dynamics of defense genes and DGK5 isoform-mediated phosphatidic acid homeostasis, shedding light on the intricate mechanisms underlying plant immune gene regulation. 

Abstract Processing bodies (PBs) and stress granules (SGs) are membrane-less cellular compartments consisting of ribonucleoprotein complexes. Whereas PBs are more ubiquitous, SGs are assembled mainly in response to stress. PBs and SGs are known to physically interact and molecules exchange between the two have been documented in mammals. However, the molecular mechanisms underpinning these processes are virtually unknown in plants. We have reported recently that tandem CCCH zinc finger 1 (TZF1) protein can recruit MAPK signaling components to SGs. Here we have found that TZF1-MPK3/6-MKK4/5 form a protein-protein interacting network in SGs. The mRNA decapping factor 1 (DCP1) is a core component of PBs. MAPK signaling mediated phosphorylation triggers a rapid reduction of DCP1 partition into PBs, concomitantly associated with an increase of DCP1 assembly into SGs. Furthermore, we have found that plant SG marker protein UBP1b (oligouridylate binding protein 1b) plays a role in maintaining DCP1 in PBs by suppressing the accumulation of MAPK signaling components. Together, we propose that MAPK signaling and UBP1b mediate the dynamics of PBs and SGs in plant cells. 

Embedded in the plasma membrane of plant cells, receptor kinases (RKs) and receptor proteins (RPs) act as key sentinels, responsible for detecting potential pathogenic invaders. These proteins were originally characterized more than three decades ago as disease resistance (R) proteins, a concept that was formulated based on Harold Flor's gene-for-gene theory. This theory implies genetic interaction between specific plant R proteins and corresponding pathogenic effectors, eliciting effector-triggered immunity (ETI). Over the years, extensive research has unraveled their intricate roles in pathogen sensing and immune response modulation. RKs and RPs recognize molecular patterns from microbes as well as dangers from plant cells in initiating pattern-triggered immunity (PTI) and danger-triggered immunity (DTI), which have intricate connections with ETI. Moreover, these proteins are involved in maintaining immune homeostasis and preventing autoimmunity. This review showcases seminal studies in discovering RKs and RPs as R proteins and discusses the recent advances in understanding their functions in sensing pathogen signals and the plant cell integrity and in preventing autoimmunity, ultimately contributing to a robust and balanced plant defense response. [Formula: see text] The author(s) have dedicated the work to the public domain under the Creative Commons CC0 “No Rights Reserved” license by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law, 2024. 

6:2 Fluorotelomer sulfonic acid (6:2 FTSA) is a dominant per- and poly-fluoroalkyl substance (PFAS) in aqueous film-forming foam (AFFF)-impacted soil. While its biotransformation mechanisms have been studied, the complex effects of plants, nutrients, and soil microbiome interactions on the fate and removal of 6:2 FTSA are poorly understood. This study systematically investigated the potential of phytoremediation for 6:2 FTSA by Arabidopsis thaliana coupled with bioaugmentation of Rhodococcus jostiiRHA1 (designated as RHA1 hereafter) under different nutrient and microbiome conditions. Hyperaccumulation of 6:2 FTSA, defined as tissue/soil concentration > 10 and high translocation factor > 3, was observed in plants. However, biotransformation of 6:2 FTSA only occurred under sulfur-limited conditions. Spiking RHA1 not only enhanced the biotransformation of 6:2 FTSA in soil but also promoted plant growth. Soil microbiome analysis uncovered Rhodococcus as one of the dominant species in all RHA1-spiked soil. Different nutrients such as sulfur and carbon, bioaugmentation, and amendment of 6:2 FTSA caused significant changes in - the microbial community structure. This study revealed the synergistic effects of phytoremediation and bioaugmentation on 6:2 FTSA removal. and highlighted that the fate of 6:2 FTSA was highly influenced by the complex interactions of plants, nutrients, and soil microbiome.