Involvement of salicylic acid signal transduction in aluminum-responsive oxidative burst in Arabidopsis thaliana cell suspension culture

To date, a number of studies have documented the toxic impacts of Al ions in plant cells. One of the key factors required for Al cytotoxicity is the generation of reactive oxygen species (ROS). Here we observed that Al treatments of suspension-cultured Arabidopsis thaliana cells resulted in biphasic superoxide generation monitored with chemiluminescence. Among six respiratory burst oxidase homologs (Atrbohs) coding for plant NADPH oxidase, AtrbohD was shown to be the only gene responsive to Al. As the expression of AtrbohD was rapid and long-lasting (1 min to 24 h). Al-induced superoxide generation, AtrbohD expression and cell death were all inhibited by NADPH oxidase inhibitor and superoxide dismutase. Interestingly, Al-induced AtrbohD expression and cell death were inhibited in the mutant and transgenic cell lines lacking salicylic acid biosyhthesis and accumulation (sid2 and NahG). Involvements of salicylic acid signaling in Al-induced AtrbohD expression and cell death development were also confirmed by the use of npr1 mutant cells and NPR1-overexpressing cells. Taken together, there would be a loop of SA signaling and SA-dependent expression of AtrbohD gene leading to prolonged ROS production and cell death development in the Al-exposed Arabidopsis cells

Suppression of reactive oxygen species accumulation in chloroplasts prevents leaf damage but not growth arrest in salt-stressed tobacco plants

Crop yield reduction due to salinity is a growing agronomical concern in many regions. Increased production of reactive oxygen species (ROS) in plant cells accompanies many abiotic stresses including salinity, acting as toxic and signaling molecules during plant stress responses. While ROS are generated in various cellular compartments, chloroplasts represent a main source in the light, and plastid ROS synthesis and/or elimination have been manipulated to improve stress tolerance. Transgenic tobacco plants expressing a plastid-targeted cyanobacterial flavodoxin, a flavoprotein that prevents ROS accumulation specifically in chloroplasts, displayed increased tolerance to many environmental stresses, including drought, excess irradiation, extreme temperatures and iron starvation. Surprisingly, flavodoxin expression failed to protect transgenic plants against NaCl toxicity. However, when high salt was directly applied to leaf discs, flavodoxin did increase tolerance, as reflected by preservation of chlorophylls, carotenoids and photosynthetic activities. Flavodoxin decreased salt-dependent ROS accumulation in leaf tissue from discs and whole plants, but this decline did not improve tolerance at the whole plant level. NaCl accumulation in roots, as well as increased osmotic pressure and salt-induced root damage, were not prevented by flavodoxin expression. The results indicate that ROS formed in chloroplasts have a marginal effect on plant responses during salt stress, and that sensitive targets are present in roots which are not protected by flavodoxin.Para citar este articulo: Lodeyro AF, Giró M, Poli HO, Bettucci G, Cortadi A, Ferri AM, et al. (2016) Suppression of Reactive Oxygen Species Accumulation in Chloroplasts Prevents Leaf Damage but Not Growth Arrest in Salt-Stressed Tobacco Plants. PLoS ONE 11(7): e0159588. doi:10.1371/journal.pone.0159588Fil: Lodeyro, Anabella F. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Giró, Mariana. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Poli, Hugo O. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina.Fil: Bettucci, Gabriel. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Departamento de Ciencias Biológicas; Argentina.Fil: Cortadi, Adriana. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Departamento de Ciencias Biológicas; Argentina.Fil: Ferri, Alejandro M. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Departamento de Química Analítica; Argentina.Fil: Carrillo, Néstor. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario (IBR -CONICET); Argentina