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Reactive Oxygen Species Alleviate Cell Death Induced by Thaxtomin A in Arabidopsis thaliana Cell Cultures

Thaxtomin A (TA) is a cellulose biosynthesis inhibitor synthesized by the soil actinobacterium Streptomyces scabies, which is the main causal agent of potato common scab. TA is essential for the induction of scab lesions on potato tubers. When added to Arabidopsis thaliana cell cultures, TA induces...

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Detalles Bibliográficos
Autores principales: Awwad, Fatima, Bertrand, Guillaume, Grandbois, Michel, Beaudoin, Nathalie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6784117/
https://www.ncbi.nlm.nih.gov/pubmed/31489878
http://dx.doi.org/10.3390/plants8090332
Descripción
Sumario:Thaxtomin A (TA) is a cellulose biosynthesis inhibitor synthesized by the soil actinobacterium Streptomyces scabies, which is the main causal agent of potato common scab. TA is essential for the induction of scab lesions on potato tubers. When added to Arabidopsis thaliana cell cultures, TA induces an atypical programmed cell death (PCD). Although production of reactive oxygen species (ROS) often correlates with the induction of PCD, we observed a decrease in ROS levels following TA treatment. We show that this decrease in ROS accumulation in TA-treated cells is not due to the activation of antioxidant enzymes. Moreover, Arabidopsis cell cultures treated with hydrogen peroxide (H(2)O(2)) prior to TA treatment had significantly fewer dead cells than cultures treated with TA alone. This suggests that H(2)O(2) induces biochemical or molecular changes in cell cultures that alleviate the activation of PCD by TA. Investigation of the cell wall mechanics using atomic force microscopy showed that H(2)O(2) treatment can prevent the decrease in cell wall rigidity observed after TA exposure. While we cannot exclude the possibility that H(2)O(2) may promote cell survival by altering the cellular redox environment or signaling pathways, our results suggest that H(2)O(2) may inhibit cell death, at least partially, by reinforcing the cell wall to prevent or compensate for damages induced by TA.