Carbonic anhydrases CA1 and CA4 attenuate plant immunity and can contribute to altered disease resistance levels in response to changing atmospheric CO conditions. β-Carbonic anhydrases (CAs) play an important role in CO metabolism and plant development, but have also been implicated in plant immunity. Here we show that the bacterial pathogen Pseudomonas syringae and application of the microbe-associated molecular pattern (MAMP) flg22 repress CA1 and CA4 gene expression in Arabidopsis thaliana. Using the CA double-mutant ca1ca4, we provide evidence that CA1 and CA4 play an attenuating role in pathogen- and flg22-triggered immune responses. In line with this, ca1ca4 plants exhibited enhanced resistance against P. syringae, which was accompanied by an increased expression of the defense-related genes FRK1 and ICS1. Under low atmospheric CO conditions (150 ppm), when CA activity is typically low, the levels of CA1 transcription and resistance to P. syringae in wild-type Col-0 were similar to those observed in ca1ca4. However, under ambient (400 ppm) and elevated (800 ppm) atmospheric CO conditions, CA1 transcription was enhanced and resistance to P. syringae reduced. Together, these results suggest that CA1 and CA4 attenuate plant immunity and that differential CA gene expression in response to changing atmospheric CO conditions contribute to altered disease resistance levels.
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http://dx.doi.org/10.1007/s00425-020-03370-w | DOI Listing |
Biomedicines
December 2024
Department of Neurosurgery, Freiburg University Medical Center, Breisacher Str. 64, 79106 Freiburg, Germany.
Background: Temporal lobe epilepsy (TLE) is the most common form of drug-resistant epilepsy, often associated with hippocampal sclerosis (HS), which involves selective neuronal loss in the Cornu Ammonis subregion 1 CA1 and CA4 regions of the hippocampus. Granule cells show migration and mossy fiber sprouting, though the mechanisms remain unclear. Microglia play a role in neurogenesis and synaptic modulation, suggesting they may contribute to epilepsy.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Pathology, Molecular, and Cell-Based Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Introduction: Alzheimer's disease (AD), primary age-related tauopathy (PART), and chronic traumatic encephalopathy (CTE) all feature hyperphosphorylated tau (p-tau)-immunoreactive neurofibrillary degeneration, but differ in neuroanatomical distribution and progression of neurofibrillary degeneration and amyloid beta (Aβ) deposition.
Methods: We used Nanostring GeoMx Digital Spatial Profiling to compare the expression of 70 proteins in neurofibrillary tangle (NFT)-bearing and non-NFT-bearing neurons in hippocampal CA1, CA2, and CA4 subregions and entorhinal cortex of cases with autopsy-confirmed AD (n = 8), PART (n = 7), and CTE (n = 5).
Results: There were numerous subregion-specific differences related to Aβ processing, autophagy/proteostasis, inflammation, gliosis, oxidative stress, neuronal/synaptic integrity, and p-tau epitopes among these different disorders.
Scand J Gastroenterol
December 2024
Department of Medical Parasitology, Faculty of Medicine, Faculty of Medicine, Elazig, Turkey.
Objective: Colorectal cancer (CRC) is a type of digestive system cancer. At the molecular level, some factors, including genetic and epigenetic factors, as well as various signaling pathways such as oxidative stress and inflammation, play an active role in the onset of CRC. Genetic and epigenetic mutations, particularly in oncogenes and tumor suppressor genes, occur during colorectal adenocarcinoma development as a result of a change in gastrointestinal epithelial cell proliferation and self-renewal rates.
View Article and Find Full Text PDFSchizophr Res
November 2024
Department of Psychiatry, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larisa, Greece.
Background: Recent evidence brings autophagy, and specifically the RB1CC1 gene into sharp focus as aetiologically relevant to Schizophrenia. Our understanding of whether and how these genetic signatures translate to cellular functions remains limited.
Material And Methods: Post-mortem study of 10 individuals with Schizophrenia and 18 individuals without any neurological/psychiatric disorder, matched for age, sex, post-mortem-interval, pH and BRAAK score.
Mol Psychiatry
November 2024
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, USA.
Background: Previous studies have implicated hippocampal abnormalities in the neuropathology of psychosis spectrum disorders. Reduced hippocampal volume has been reported across all illness stages, and this atrophy has been hypothesized to be the result of glutamatergic excess. To test this hypothesis, we measured hippocampal subfield volumes and hippocampal glutamate levels in antipsychotic naïve first episode psychosis patients (FEP) and the progression of volume decline and changes in glutamate levels over a 16-week antipsychotic drug (APD) trial.
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