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The plasma membrane (PM) is at the interface of plant-pathogen interactions and, thus, many bacterial type-III effector (T3E) proteins target membrane-associated processes to interfere with immunity. The Pseudomonas syringae T3E HopZ1a is a host cell PM-localized effector protein that has several immunity-associated host targets but also activates effector-triggered immunity in resistant backgrounds. Although HopZ1a has been shown to interfere with early defense signaling at the PM, no dedicated PM-associated HopZ1a target protein has been identified until now. Here, we show that HopZ1a interacts with the PM-associated remorin protein NbREM4 from Nicotiana benthamiana in several independent assays. NbREM4 relocalizes to membrane nanodomains after treatment with the bacterial elicitor flg22 and transient overexpression of NbREM4 in N. benthamiana induces the expression of a subset of defense-related genes. We can further show that NbREM4 interacts with the immune-related receptor-like cytoplasmic kinase avrPphB-susceptible 1 (PBS1) and is phosphorylated by PBS1 on several residues in vitro. Thus, we conclude that NbREM4 is associated with early defense signaling at the PM. The possible relevance of the HopZ1a-NbREM4 interaction for HopZ1a virulence and avirulence functions is discussed.
Modern plant cultivars often possess superior growth characteristics, but within a limited range of environmental conditions. Due to climate change, crops will be exposed to distressing abiotic conditions more often in the future, out of which heat stress is used as example for this study. To support identification of tolerant germplasm and advance screening techniques by a novel multivariate evaluation method, a diversity panel of 14 tomato genotypes, comprising Mediterranean landraces of Solanum lycopersicum, the cultivar "Moneymaker" and Solanum pennellii LA0716, which served as internal references, was assessed toward their tolerance against long-term heat stress. After 5 weeks of growth, young tomato plants were exposed to either control (22/18 degrees C) or heat stress (35/25 degrees C) conditions for 2 weeks. Within this period, water consumption, leaf angles and leaf color were determined. Additionally, gas exchange and leaf temperature were investigated. Finally, biomass traits were recorded. The resulting multivariate dataset on phenotypic plasticity was evaluated to test the hypothesis, that more tolerant genotypes have less affected phenotypes upon stress adaptation. For this, a cluster-analysis-based approach was developed that involved a principal component analysis (PCA), dimension reduction and determination of Euclidean distances. These distances served as measure for the phenotypic plasticity upon heat stress. Statistical evaluation allowed the identification and classification of homogeneous groups consisting each of four putative more or less heat stress tolerant genotypes. The resulting classification of the internal references as "tolerant" highlights the applicability of our proposed tolerance assessment model. PCA factor analysis on principal components 1-3 which covered 76.7% of variance within the phenotypic data, suggested that some laborious measure such as the gas exchange might be replaced with the determination of leaf temperature in larger heat stress screenings. Hence, the overall advantage of the presented method is rooted in its suitability of both, planning and executing screenings for abiotic stress tolerance using multivariate phenotypic data to overcome the challenge of identifying abiotic stress tolerant plants from existing germplasms and promote sustainable agriculture for the future.
Thigmomorphogenesis
(2018)
Controlled regulation of plant growth is a general prerequisite for the production of marketable ornamental plants. Consumers as well as retailers prefer stronger, more compact plants with greener leaves as these not only better meet a certain desired visual quality but also allow for a maximization of production per unit area as well as facilitation of packaging and transport. The same applies for the production of young vegetable plants. Special attention is paid to solid, compact and resilient plants that survive transport and planting without any problems. During the last decades plant growth control has mainly been achieved through the application of chemical plant growth regulators that generally interfere with the function of growth regulating hormones. However, there is an increasing demand to replace chemical treatments by other means such as the modulation of growth conditions, including temperature, light and fertilization. Alternatively, the application of mechanical stimulation has been shown to induce plant responses that yield some of the commercially relevant phenotypes including increased compactness, higher girth, darker leaves and a delay in flowering. The ability of plants to sense and respond to mechanical stimuli is an adaptive trait associated with increased fitness in many environmental settings. Mechanical stimulation in nature occurs e.g. through wind, rain, neighboring plants or predatory animals and induces a range of morphogenic responses that have been summarized under the term thigmomorphogenesis. We are only just about to begin to understand the molecular mechanisms underlying mechanosensing and the associated morphogenic changes in plants. However, a number of examples suggest that mechanical stimulation applied in a greenhouse setting can be used to alter plant growth in order to produce marketable plants. In this review will briefly summarize the current knowledge concerning the biological principles of thigmomorphogenesis and discuss the potential of mechanical growth regulation in commercial plant production especially with respect to organic horticulture.
Sucrose nonfermenting related kinase1 (SnRK1) is a conserved energy sensor kinase that regulates cellular adaptation to energy deficit in plants. Activation of SnRK1 leads to the down-regulation of ATP-consuming biosynthetic processes and the stimulation of energy-generating catabolic reactions by transcriptional reprogramming and posttranslational modifications. Although considerable progress has been made during the last years in understanding the SnRK1 signaling pathway, many of its components remain unidentified. Here, we show that the catalytic alpha-subunits KIN10 and KIN11 of the Arabidopsis (Arabidopsis thaliana) SnRK1 complex interact with the STOREKEEPER RELATED1/G-Element Binding Protein (STKR1) inside the plant cell nucleus. Overexpression of STKR1 in transgenic Arabidopsis plants led to reduced growth, a delay in flowering, and strongly attenuated senescence. Metabolite profiling revealed that the transgenic lines exhausted their carbohydrates during the dark period to a greater extent than the wild type and accumulated a range of amino acids. At the global transcriptome level, genes affected by STKR1 overexpression were broadly associated with systemic acquired resistance, and transgenic plants showed enhanced resistance toward a virulent strain of the biotrophic oomycete pathogen Hyaloperonospora arabidopsidis Noco2. We discuss a possible connection of STKR1 function, SnRK1 signaling, and plant immunity.
In plants, SNF1-related kinase (SnRK1) responds to the availability of carbohydrates as well as to environmental stresses by down-regulating ATP consuming biosynthetic processes, while stimulating energy-generating catabolic reactions through gene expression and post-transcriptional regulation. The functional SnRK1 complex is a heterotrimer where the catalytic alpha subunit associates with a regulatory beta subunit and an activating gamma subunit. Several different metabolites as well as the hormone abscisic acid (ABA) have been shown to modulate SnRK1 activity in a cell- and stimulus-type specific manner. It has been proposed that tissue- or stimulus-specific expression of adapter proteins mediating SnRK1 regulation can at least partly explain the differences observed in SnRK1 signaling. By using yeast two-hybrid and in planta bi-molecular fluorescence complementation assays we were able to demonstrate that proteins containing the domain of unknown function (DUF) 581 could interact with both isoforms of the SnRK1 alpha subunit (AKIN10/11) of Arabidopsis. A structure/function analysis suggests that the DUF581 is a generic SnRK1 interaction module and co-expression with DUF581 proteins in plant cells leads to reallocation of the kinase to specific regions within the nucleus. Yeast two-hybrid analyses suggest that SnRK1 and DUF581 proteins share common interaction partners inside the nucleus. The analysis of available microarray data implies that expression of the 19 members of the DUF581 encoding gene family in Arabidopsis is differentially regulated by hormones and environmental cues, indicating specialized functions of individual family members. We hypothesize that DUF581 proteins could act as mediators conferring tissue- and stimulus-type specific differences in SnRK1 regulation.
Since years, research on SnRK1, the major cellular energy sensor in plants, has tried to define its role in energy signalling. However, these attempts were notoriously hampered by the lethality of a complete knockout of SnRK1. Therefore, we generated an inducible amiRNA:: SnRK1 alpha 2 in a snrk1 alpha 1 knock out background (snrk1 alpha 1/alpha 2) to abolish SnRK1 activity to understand major systemic functions of SnRK1 signalling under energy deprivation triggered by extended night treatment. We analysed the in vivo phosphoproteome, proteome and metabolome and found that activation of SnRK1 is essential for repression of high energy demanding cell processes such as protein synthesis. The most abundant effect was the constitutively high phosphorylation of ribosomal protein S6 (RPS6) in the snrk1 alpha 1/alpha 2 mutant. RPS6 is a major target of TOR signalling and its phosphorylation correlates with translation. Further evidence for an antagonistic SnRK1 and TOR crosstalk comparable to the animal system was demonstrated by the in vivo interaction of SnRK1 alpha 1 and RAPTOR1B in the cytosol and by phosphorylation of RAPTOR1B by SnRK1 alpha 1 in kinase assays. Moreover, changed levels of phosphorylation states of several chloroplastic proteins in the snrk1 alpha 1/alpha 2 mutant indicated an unexpected link to regulation of photosynthesis, the main energy source in plants.
As a critical part of plant immunity, cells that are attacked by pathogens undergo rapid transcriptional reprogramming to minimize virulence. Many bacterial phytopathogens use type III effector (T3E) proteins to interfere with plant defense responses, including this transcriptional reprogramming. Here, we show that Xanthomonas outer protein S (XopS), a T3E of Xanthomonas campestris pv. vesicatoria (Xcv), interacts with and inhibits proteasomal degradation of WRKY40, a transcriptional regulator of defense gene expression. Virus-induced gene silencing of WRKY40 in pepper (Capsicum annuum) enhanced plant tolerance to Xcv infection, indicating that WRKY40 represses immunity. Stabilization of WRKY40 by XopS reduces the expression of its targets, which include salicylic acid-responsive genes and the jasmonic acid signaling repressor JAZ8. Xcv bacteria lacking XopS display significantly reduced virulence when surface inoculated onto susceptible pepper leaves. XopS delivery by Xcv, as well as ectopic expression of XopS in Arabidopsis thaliana or Nicotiana benthamiana, prevented stomatal closure in response to bacteria and biotic elicitors. Silencing WRKY40 in pepper or N. benthamiana abolished XopS's ability to prevent stomatal closure. This suggests that XopS interferes with both preinvasion and apoplastic defense by manipulating WRKY40 stability and downstream gene expression, eventually altering phytohormone crosstalk to promote pathogen proliferation.
In eukaryotes, regulated protein turnover is required during many cellular processes, including defense against pathogens. Ubiquitination and degradation of ubiquitinated proteins via the ubiquitin proteasome system (UPS) is the main pathway for the turnover of intracellular proteins in eukaryotes. The extensive utilization of the UPS in host cells makes it an ideal pivot for the manipulation of cellular processes by pathogens. Like many other Gram-negative bacteria, Xanthomonas species secrete a suite of type-III effector proteins (T3Es) into their host cells to promote virulence. Some of these T3Es exploit the plant UPS to interfere with immunity. This review summarizes T3E examples from the genus Xanthomonas with a proven or suggested interaction with the host UPS or UPS-like systems and also discusses the apparent paradox that arises from the presence of T3Es that inhibit the UPS in general while others rely on its activity for their function.
Redox modulation of protein activity by thioredoxins (TRXs) plays a key role in cellular regulation. Thioredoxin z (TRX z) and its interaction partner fructokinase-like protein 1 (FLN1) represent subunits of the plastid-encoded RNA polymerase (PEP), suggesting a role of both proteins in redox regulation of chloroplast gene expression. Loss of TRX z or FLN1 expression generates a PEP-deficient phenotype and renders the plants incapable to grow autotrophically. This study shows that PEP function in trx z and fln1 plants can be restored by complementation with redox-inactive TRX z C106S and FLN1 C(105/106)A protein variants, respectively. The complemented plants showed wild-type levels of chloroplast gene expression and were restored in photosynthetic capacity, indicating that redox regulation of PEP through TRX z/FLN1 per se is not essential for autotrophic growth. Promoter-reporter gene studies indicate that TRX z and FLN1 are expressed during early phases of leaf development while expression ceases at maturation. Taken together, our data support a model in which TRX z and FLN1 are essential structural components of the PEP complex and their redox activity might only play a role in the fine tuning of PEP function.