Year: 2016
Type: article
Abstract: Industrial activities have caused tropospheric CO2 concentrations to increase over the last two centuries, a trend that is predicted to continue for at least the next several decades. Here, we report that growth of plants in a CO2-enriched environment activates responses that are central to defense against pathogenic attack. Salicylic acid accumulation was triggered by high-growth CO2 in Arabidopsis (Arabidopsis thaliana) and other plants such as bean (Phaseolus vulgaris). A detailed analysis in Arabidopsis revealed that elevated CO2 primes multiple defense pathways, leading to increased resistance to bacterial and fungal challenge. Analysis of gene-specific mutants provided no evidence that activation of plant defense pathways by high CO2 was caused by stomatal closure. Rather, the activation is partly linked to metabolic effects involving redox signaling. In support of this, genetic modification of redox components (glutathione contents and NADPH-generating enzymes) prevents full priming of the salicylic acid pathway and associated resistance by high CO2. The data point to a particularly influential role for the nonphosphorylating glyceraldehyde-3-phosphate dehydrogenase, a cytosolic enzyme whose role in plants remains unclear. Our observations add new information on relationships between high CO2 and oxidative signaling and provide novel insight into plant stress responses in conditions of increased CO2.
Source: PLANT PHYSIOLOGY
DOI: 10.1104/pp.16.01129
Authors: Amna Mhamdi, Graham Noctor
Institutions: Université Paris-Sud, Centre National de la Recherche Scientifique, Université Paris-Saclay, Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement, Institut des Sciences des Plantes de Paris Saclay, Institut National de la Recherche Agronomique, Sorbonne Paris Cité
Language: English
Subfield: Plant Science
Domain: Life Sciences
SDG: Climate action
Open Access status: hybrid
Estimated APC paid: $3,851
Funder: Agence Nationale de la Recherche
OpenAlex ID: W2510031254
