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Phytohormones integrate external environmental and developmental signals with internal cellular responses for plant survival and multiplication in changing surroundings. Jasmonate (JA), which might originate from prokaryotes and benefit plant terrestrial adaptation, is a vital phytohormone that regulates diverse developmental processes and defense responses against various environmental stresses. In this review, we first provide an overview of ligand-receptor binding techniques used for the characterization of phytohormone-receptor interactions, then introduce the identification of the receptor COI1 and active JA molecules, and finally summarize recent advances on the regulation of JA perception and its evolution., (Copyright © 2022 The Author. Published by Elsevier Inc. All rights reserved.)

Main Conclusion: The N-myristoylation is required for BSK1 proper plasma membrane targeting and protein turnover. Brassinosteroid (BR) signaling kinase 1 (BSK1), with a myristoylation site at its N-terminus to anchor at plasma membrane (PM), is involved in BR-regulated plant growth and flg22-triggered immunity responses. However, little is known about the role of N-myristoylation in BSK1 protein homeostasis. Here, we revealed that N-myristoylation is critical to the PM targeting and protein stability of BSK1. The N-myristoylation-deficient mutant BSK1 G2A mainly distributed in the cytoplasm and retained in the endoplasmic reticulum. We further found that the BSK1 G2A proteins were unstable and degraded through ATG8e-labled autophagic pathway. This study provides a new insight into the regulation of plant protein homeostasis., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

In animals, endocytosis of a seven-transmembrane GPCR is mediated by arrestins to propagate or arrest cytoplasmic G protein-mediated signaling, depending on the bias of the receptor or ligand, which determines how much one transduction pathway is used compared to another. In Arabidopsis thaliana , GPCRs are not required for G protein-coupled signaling because the heterotrimeric G protein complex spontaneously exchanges nucleotide. Instead, the seven-transmembrane protein AtRGS1 modulates G protein signaling through ligand-dependent endocytosis, which initiates derepression of signaling without the involvement of canonical arrestins. Here, we found that endocytosis of AtRGS1 initiated from two separate pools of plasma membrane: sterol-dependent domains and a clathrin-accessible neighborhood, each with a select set of discriminators, activators, and candidate arrestin-like adaptors. Ligand identity (either the pathogen-associated molecular pattern flg22 or the sugar glucose) determined the origin of AtRGS1 endocytosis. Different trafficking origins and trajectories led to different cellular outcomes. Thus, in this system, compartmentation with its associated signalosome architecture drives biased signaling., (Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Arabidopsis heterotrimeric G proteins regulate diverse plant growth and defense processes by coupling to 7TM AtRGS1 proteins. Although G protein mutants display alterations in response to multiple plant hormones, the underlying mechanism by which G proteins participate in the regulation of hormone responses remains elusive. Here, we show that genetic disruption of Gα and Gβ subunits results in reduced sensitivity to JA treatment. Furthermore, using confocal microscopy, VA-TIRFM, and FRET-FLIM, we provide evidence that stimulation by JA induces phosphorylation- and C-terminus-dependent endocytosis of AtRGS1, which then promotes dissociation of AtRGS1 from AtGPA1. In addition, SPT analysis reveals that JA treatment affects the diffusion dynamics of AtRGS1 and AtRGS1-ΔCt. Taken together, these findings suggest that the JA signal activates heterotrimeric G proteins through the endocytosis of AtRGS1 and dissociation of AtRGS1 from AtGPA1, thus providing valuable insight into the mechanisms of how the G protein system perceives and transduces phytohormone signals.

The chloroplast, as the photosynthetic organelle of plants, plays a crucial role in plant development. Extensive studies have been conducted on chloroplast development; however, the related regulatory mechanism still remains elusive. Here, we characterized a mutant with defective chloroplasts in Arabidopsis, termed pigment-defective mutant3 (pdm3), which exhibits a distinct albino phenotype in leaves, eventually leading to pdm3 seedling lethality under autotrophic growth conditions. Electron microscopy demonstrated that the number of thylakoids was reduced and the structure of those thylakoids was disrupted in the pdm3 mutant, which eventually led to the breakdown of chloroplasts. Sequence analysis showed that PDM3 encodes a chloroplast protein consisting of 12 pentratricopeptide repeat domains that belongs to the P subgroup. Both confocal microscopic analysis and immunoblotting in the chloroplast protein fraction showed that PDM3 was located in the stroma. Furthermore, analysis of the transcript profiles of chloroplast genes revealed that plastid-encoded polymerase-dependent transcript levels were markedly reduced, while nuclear-encoded polymerase-dependent transcript levels were increased in pdm3 mutants. In addition, we found that the splicing of introns in trnA, ndhB, and clpP-1 is also affected in pdm3. Taken together, we propose that PDM3 plays an essential role in chloroplast development in Arabidopsis., (© The Author 2017. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Jasmonates (JAs) induce leaf senescence in many plant species. The Arabidopsis F-box protein coronatine insensitive 1 (COI1) is required for various JA-regulated plant responses including plant fertility, defense responses and leaf senescence. However, the molecular basis for COI1-dependent JA-induced leaf senescence remains unknown. In our Plant Physiology paper, we identified a COI1-dependent JA-repressed protein, Rubisco activase (RCA) in Arabidopsis. Further genetic and physiological analyses showed that the COI1-dependent JA repression of RCA correlated with JA-induced leaf senescence, and that loss of RCA led to typical senescence-associated features. Therefore, we suggested that the COI1-dependent JA repression of RCA played an important role in JA-induced leaf senescence. In this addendum, we made a relatively deep discussion on RCA function in JA-induced leaf senescence and JA-mediated defense responses. We also discussed the possible role of JA in plant natural senescence.

Leaf senescence, as the last stage of leaf development, is regulated by diverse developmental and environmental factors. Jasmonates (JAs) have been shown to induce leaf senescence in several plant species; however, the molecular mechanism for JA-induced leaf senescence remains unknown. In this study, proteomic, genetic, and physiological approaches were used to reveal the molecular basis of JA-induced leaf senescence in Arabidopsis (Arabidopsis thaliana). We identified 35 coronatine-insensitive 1 (COI1)-dependent JA-regulated proteins using two-dimensional difference gel electrophoresis in Arabidopsis. Among these 35 proteins, Rubisco activase (RCA) was a COI1-dependent JA-repressed protein. We found that RCA was down-regulated at the levels of transcript and protein abundance by JA in a COI1-dependent manner. We further found that loss of RCA led to typical senescence-associated features and that the COI1-dependent JA repression of RCA played an important role in JA-induced leaf senescence.

Jasmonates (JAs) are a new class of plant hormone that regulate expression of diverse genes to mediate various plant responses. The Arabidopsis F-box protein COI1 is required for plant defense and male fertility in JA signal pathway. To further investigate the regulatory role of COI1 in male fertility, we compared the proteomics profiles of Arabidopsis wild type (WT) flowers with coi1-1 mutant male-sterile flowers using two-dimensional difference gel electrophoresis coupled with matrix-assisted laser desoption/ionization-time-of-flight mass spectrometry. Sixteen proteins with potential function in specific biological processes such as metabolism processes and defense/stress responses were differentially expressed in WT and coi1-1 mutant flowers. Verification on a phi class glutathione transferase AtGSTF9, one out of these 16 identified proteins, revealed that the expression of AtGSTF9 was severely downregulated in flowers of coi1-1 mutant compared with that of WT. Further function analyses of these genes would provide new insights into the molecular basis of COI1-regulated male fertility.

Anthocyanins are important plant pigments that fulfil many physiological and ecological functions. Anthocyanin biosynthesis is controlled by numerous regulatory factors at the transcriptional level. Jasmonates (JAs) has been shown to induce anthocyanin accumulation in several plant species, however, the molecular mechanism for JA-regulated anthocyanin accumulation remains unknown. In this study, genetic, molecular, and physiological approaches were used to reveal the molecular basis of JA-regulated pigmentation in Arabidopsis. It was found that the F-box protein COI1 was required for JA-specific induced expression of the 'late' anthocyanin biosynthetic genes DFR, LDOX, and UF3GT. It is further demonstrated that COI1 was essential for JA-induction of transcription factors PAP1, PAP2, and GL3. It is speculated that COI1 regulates the expression of the transcription factors, including PAP1, PAP2, and GL3, which mediates the 'late' anthocyanin biosynthetic genes DFR, LDOX, and UF3GT, thereby modulating JA-induced anthocyanin biosynthesis in Arabidopsis.