132 research outputs found
Interaction of methyl viologen-induced chloroplast and mitochondrial signalling in Arabidopsis
Reactive oxygen species (ROS) are key signalling intermediates in plant
metabolism, defence, and stress adaptation. In plants, both the
chloroplast and mitochondria are centres of metabolic control and ROS
production, which coordinate stress responses in other cell
compartments. The herbicide and experimental tool, methyl viologen (MV)
induces ROS generation in the chloroplast under illumination, but is
also toxic in non-photosynthetic organisms. We used MV to probe plant
ROS signalling in compartments other than the chloroplast. Taking a
genetic approach in the model plant Arabidopsis (Arabidopsis thaliana),
we used natural variation, QTL mapping, and mutant studies with MV in
the light, but also under dark conditions, when the chloroplast electron
transport is inactive. These studies revealed a light-independent
MV-induced ROS-signalling pathway, suggesting mitochondrial involvement.
Mitochondrial Mn SUPEROXIDE DISMUTASE was required for ROS-tolerance
and the effect of MV was enhanced by exogenous sugar, providing further
evidence for the role of mitochondria. Mutant and hormone feeding assays
revealed roles for stress hormones in organellar ROS-responses. The
radical-induced cell death1 mutant, which is tolerant to MV-induced ROS
and exhibits altered mitochondrial signalling, was used to probe
interactions between organelles. Our studies suggest that mitochondria
are involved in the response to ROS induced by MV in plants.</p
PROTEIN PHOSPHATASE 2A-B 'gamma Controls Botrytis cinerea Resistance and Developmental Leaf Senescence
Plants optimize their growth and survival through highly integrated regulatory networks that coordinate defensive measures and developmental transitions in response to environmental cues. Protein phosphatase 2A (PP2A) is a key signaling component that controls stress reactions and growth at different stages of plant development, and the PP2A regulatory subunit PP2A-B'gamma is required for negative regulation of pathogenesis responses and for maintenance of cell homeostasis in short-day conditions. Here, we report molecular mechanisms by which PP2A-B'gamma regulates Botrytis cinerea resistance and leaf senescence in Arabidopsis (Arabidopsis thaliana). We extend the molecular functionality of PP2A-B'gamma to a protein kinase-phosphatase interaction with the defense-associated calcium-dependent protein kinase CPK1 and present indications this interaction may function to control CPK1 activity. In presenescent leaf tissues, PP2A-B'gamma is also required to negatively control the expression of salicylic acid-related defense genes, which have recently proven vital in plant resistance to necrotrophic fungal pathogens. In addition, we find the premature leaf yellowing of pp2a-b'gamma depends on salicylic acid biosynthesis via SALICYLIC ACID INDUCTION DEFICIENT2 and bears the hallmarks of developmental leaf senescence. We propose PP2A-B'gamma age-dependently controls salicylic acid-related signaling in plant immunity and developmental leaf senescence.Peer reviewe
Arabidopsis RCD1 coordinates chloroplast and mitochondrial functions through interaction with ANAC transcription factors
Reactive oxygen species (ROS)-dependent signaling pathways from chloroplasts and mitochondria merge at the nuclear protein RADICAL-INDUCED CELL DEATH1 (RCD1). RCD1 interacts in vivo and suppresses the activity of the transcription factors ANAC013 and ANAC017, which mediate a ROS-related retrograde signal originating from mitochondrial complex III. Inactivation of RCD1 leads to increased expression of mitochondrial dysfunction stimulon (MDS) genes regulated by ANAC013 and ANAC017. Accumulating MDS gene products, including alternative oxidases (AOXs), affect redox status of the chloroplasts, leading to changes in chloroplast ROS processing and increased protection of photosynthetic apparatus. ROS alter the abundance, thiol redox state and oligomerization of the RCD1 protein in vivo, providing feedback control on its function. RCD1-dependent regulation is linked to chloroplast signaling by 3'-phosphoadenosine 5'-phosphate (PAP). Thus, RCD1 integrates organellar signaling from chloroplasts and mitochondria to establish transcriptional control over the metabolic processes in both organelles.Peer reviewe
Evolutionary conservation and post-translational control of S-adenosyl-L-homocysteine hydrolase in land plants
Trans-methylation reactions are intrinsic to cellular metabolism in all living organisms. In land plants, a range of substrate-specific methyltransferases catalyze the methylation of DNA, RNA, proteins, cell wall components and numerous species-specific metabolites, thereby providing means for growth and acclimation in various terrestrial habitats. Trans-methylation reactions consume vast amounts of S-adenosyl-L-methionine (SAM) as a methyl donor in several cellular compartments. The inhibitory reaction by-product, S-adenosyl-L-homocysteine (SAH), is continuously removed by SAH hydrolase (SAHH), which essentially maintains trans-methylation reactions in all living cells. Here we report on the evolutionary conservation and post-translational control of SAHH in land plants. We provide evidence suggesting that SAHH forms oligomeric protein complexes in phylogenetically divergent land plants and that the predominant protein complex is composed by a tetramer of the enzyme. Analysis of light-stress-induced adjustments of SAHH inArabidopsis thalianaandPhyscomitrella patensfurther suggests that regulatory actions may take place on the levels of protein complex formation and phosphorylation of this metabolically central enzyme. Collectively, these data suggest that plant adaptation to terrestrial environments involved evolution of regulatory mechanisms that adjust the trans-methylation machinery in response to environmental cues
PROTEIN PHOSPHATASE 2A-B'γ controls Botrytis cinerea resistance and developmental leaf senescence
Plants optimize their growth and survival through highly integrated regulatory networks that coordinate defensive measures and developmental transitions in response to environmental cues. Protein phosphatase 2A (PP2A) is a key signaling component that controls stress reactions and growth at different stages of plant development, and the PP2A regulatory subunit PP2A-B'γ is required for negative regulation of pathogenesis responses and for maintenance of cell homeostasis in short day conditions. Here, we report molecular mechanisms by which PP2A-B'γ regulates Botrytis cinerea resistance and leaf senescence in Arabidopsis (Arabidopsis thaliana). We extend the molecular functionality of PP2A-B'γ to a protein kinase-phosphatase interaction with the defense-associated calcium-dependent protein kinase CPK1 and present indications this interaction may function to control CPK1 activity. In pre-senescent leaf tissues, PP2A-B'γ is also required to negatively control the expression of salicylic acid-related defense genes, which have recently proven vital in plant resistance to necrotrophic fungal pathogens. In addition, we find the premature leaf yellowing of pp2a-b'γ depends on salicylic acid biosynthesis via SALICYLIC ACID INDUCTION DEFICIENT2 and bears the hallmarks of developmental leaf senescence. We propose PP2A-B'γ age-dependently controls salicylic acid-related signaling in plant immunity and developmental leaf senescence.</p
Stomatal CO2/bicarbonate sensor consists of two interacting protein kinases, Raf-like HT1 and nonkinase-activity activity requiring MPK12/MPK4
Publisher Copyright: © 2022 The Authors.The continuing rise in the atmospheric carbon dioxide (CO2) concentration causes stomatal closing, thus critically affecting transpirational water loss, photosynthesis, and plant growth. However, the primary CO2 sensor remains unknown. Here, we show that elevated CO2 triggers interaction of the MAP kinases MPK4/MPK12 with the HT1 protein kinase, thus inhibiting HT1 kinase activity. At low CO2, HT1 phosphorylates and activates the downstream negatively regulating CBC1 kinase. Physiologically relevant HT1-mediated phosphorylation sites in CBC1 are identified. In a genetic screen, we identify dominant active HT1 mutants that cause insensitivity to elevated CO2. Dominant HT1 mutants abrogate the CO2/bicarbonate-induced MPK4/12-HT1 interaction and HT1 inhibition, which may be explained by a structural AlphaFold2- and Gaussian-accelerated dynamics-generated model. Unexpectedly, MAP kinase activity is not required for CO2 sensor function and CO2-triggered HT1 inhibition and stomatal closing. The presented findings reveal that MPK4/12 and HT1 together constitute the long-sought primary stomatal CO2/bicarbonate sensor upstream of the CBC1 kinase in plants.Peer reviewe
Natural Variation in Arabidopsis Cvi-0 Accession Reveals an Important Role of MPK12 in Guard Cell CO2 Signaling
Plant gas exchange is regulated by guard cells that form stomatal pores.
Stomatal adjustments are crucial for plant survival; they regulate
uptake of CO2 for photosynthesis, loss of water, and entrance of air
pollutants such as ozone. We mapped ozone hypersensitivity, more open
stomata, and stomatal CO2-insensitivity phenotypes of the Arabidopsis
thaliana accession Cvi-0 to a single amino acid substitution in
MITOGEN-ACTIVATED PROTEIN (MAP) KINASE 12 (MPK12). In parallel, we
showed that stomatal CO2-insensitivity phenotypes of a mutant cis
(CO2-insensitive) were caused by a deletion of MPK12. Lack of MPK12
impaired bicarbonate-induced activation of S-type anion channels. We
demonstrated that MPK12 interacted with the protein kinase HIGH LEAF
TEMPERATURE 1 (HT1)-a central node in guard cell CO2 signaling-and that
MPK12 functions as an inhibitor of HT1. These data provide a new
function for plant MPKs as protein kinase inhibitors and suggest a
mechanism through which guard cell CO2 signaling controls plant water
management.</p
Genome sequencing and population genomic analyses provide insights into the adaptive landscape of silver birch
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