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Frank Van Breusegem

Publications and source records attributed to Frank Van Breusegem.

5 recordsLinked to original sources

A redox-regulated RCC1-like protein controls catalase activity in Arabidopsis.

Reactive oxygen species (ROS) regulate plant growth and stress responses. Catalases play a central role in detoxifying hydrogen peroxide, predominantly within peroxisomes, yet key aspects of catalase regulation remain incompletely understood. Using affinity purification of the UV-B photoreceptor UVR8 coupled with mass spectrometry, we identified CATALASE-INTERACTING RCC1-LIKE 1 (CAIR1), which interacts with all three Arabidopsis catalases and their chaperone NO CATALASE ACTIVITY 1. Loss of CAIR1 reduces catalase activity and causes oxidative stress sensitivity, impaired root growth, and alkaline sensitivity, resembling cat2 and nca1 mutants. CAIR1 promotes peroxisomal import and proper localization of CAT2, preventing CAT2 aggregation and maintaining its activity. CAIR1 undergoes reversible redox-dependent oligomerization that enhances catalase binding, whereas mutation of Cys-356 and Cys-545 compromises this interaction and fails to rescue the oxidative stress sensitivity of cair1 mutants. UV-B weakens CAIR1-catalase interactions and suppresses catalase activity, linking light signalling with redox homeostasis. These findings identify CAIR1 as a redox-responsive regulator of catalase localization and activity.

Arabidopsis↗

Changes in hydrogen peroxide homeostasis trigger an active cell death process in tobacco.

In transgenic tobacco plants with reduced catalase activity, high levels of hydrogen peroxide (H2O2) can accumulate under photorespiratory conditions. Such a perturbation in H2O2 homeostasis induced cell death in clusters of palisade parenchyma cells, primarily along the veins. Ultrastructural alterations, such as chromatin condensation and disruption of mitochondrial integrity, took place before cell death. Furthermore, enhanced transcript levels of mitochondrial defense genes accompanied these mitochondrial changes. Pharmacological data indicated that the initiation and execution of cell death require de novo protein synthesis and that the signal transduction pathway leading to cell death involved changes in ion homeostasis, (de)phosphorylation events and an oxidative burst, as observed during hypersensitive responses. This oxidase-dependent oxidative burst is essential for cell death, but it is not required for the accumulation of defense proteins, suggesting a more prominent role for the oxidative burst in abiotic stress-induced cell death.

Apoptosis↗

Transcriptome analysis during cell division in plants.

Using synchronized tobacco Bright Yellow-2 cells and cDNA-amplified fragment length polymorphism-based genomewide expression analysis, we built a comprehensive collection of plant cell cycle-modulated genes. Approximately 1,340 periodically expressed genes were identified, including known cell cycle control genes as well as numerous unique candidate regulatory genes. A number of plant-specific genes were found to be cell cycle modulated. Other transcript tags were derived from unknown plant genes showing homology to cell cycle-regulatory genes of other organisms. Many of the genes encode novel or uncharacterized proteins, indicating that several processes underlying cell division are still largely unknown.

Cell Cycle↗

Double antisense plants lacking ascorbate peroxidase and catalase are less sensitive to oxidative stress than single antisense plants lacking ascorbate peroxidase or catalase.

The plant genome is a highly redundant and dynamic genome. Here, we show that double antisense plants lacking the two major hydrogen peroxide-detoxifying enzymes, ascorbate peroxidase (APX) and catalase (CAT), activate an alternative/redundant defense mechanism that compensates for the lack of APX and CAT. A similar mechanism was not activated in single antisense plants that lacked APX or CAT, paradoxically rendering these plants more sensitive to oxidative stress compared to double antisense plants. The reduced susceptibility of double antisense plants to oxidative stress correlated with suppressed photosynthetic activity, the induction of metabolic genes belonging to the pentose phosphate pathway, the induction of monodehydroascorbate reductase, and the induction of IMMUTANS, a chloroplastic homologue of mitochondrial alternative oxidase. Our results suggest that a co-ordinated induction of metabolic and defense genes, coupled with the suppression of photosynthetic activity, can compensate for the lack of APX and CAT. In addition, our findings demonstrate that the plant genome has a high degree of plasticity and will respond differently to different stressful conditions, namely, lack of APX, lack of CAT, or lack of both APX and CAT.

Antisense Elements (Genetics)↗

Signal transduction during oxidative stress.

As an unfortunate consequence of aerobic life, active oxygen species (AOS) are formed by partial reduction of molecular oxygen. Plants possess a complex battery of enzymatic and non-enzymatic antioxidants that can protect cells from oxidative damage by scavenging AOS. It is becoming evident that AOS, which are generated during pathogen attack and abiotic stress situations, are recognized by plants as a signal for triggering defence responses. An overview of the literature is presented on the signalling role of AOS in plant defence responses, cell death, and development. Special attention is given to AOS and redox-regulated gene expression and the role of kinases and phosphatases in redox signal transduction.

Aerobiosis↗