Concurrent overactivation of the cytosolic glutamine synthetase and the GABA shunt in the ABA‐deficient sitiens mutant of tomato leads to resistance against Botrytis cinerea. Issue 2 (29th April 2013)

• Record Type: Journal Article
• Authors: Seifi, Hamed Soren; Curvers, Katrien; De, David; Delaere, Ilse; Aziz, Aziz; Höfte, Monica
• Is Part Of: New phytologist. Volume 199:Issue 2(2013)
• Page Start: 490
• Page End: 504
• Publication Date: 2013-04-29
• Subjects: Botany -- Periodicals; 580
• DOI: 10.1111/nph.12283
• Languages: English
• ISSNs: 0028-646X

Abstract

<abstract abstract-type="main" id="nph12283-abs-0001"> <title>Summary</title> <p> <list id="nph12283-list-0001" list-type="bullet"> <list-item> <p>Deficiency of abscisic acid (ABA) in the <italic>sitiens</italic> mutant of tomato (<italic>Solanum lycopersicum</italic>) culminates in increased resistance to <italic>Botrytis cinerea</italic> through a rapid epidermal hypersensitive response (HR) and associated phenylpropanoid pathway‐derived cell wall fortifications. This study focused on understanding the role of primary carbon : nitrogen (C : N) metabolism in the resistance response of <italic>sitiens</italic> to <italic>B. cinerea</italic>. How alterations in C : N metabolism are linked with the HR‐mediated epidermal arrest of the pathogen has been also investigated.</p> </list-item> <list-item> <p>Temporal alterations in the γ‐aminobutyric acid (GABA) shunt, glutamine synthetase/glutamate synthase (GS/GOGAT) cycle and phenylpropanoid pathway were transcriptionally, enzymatically and metabolically monitored in both wild‐type and <italic>sitiens</italic> plants. Virus‐induced gene silencing, microscopic analyses and pharmacological assays were used to further confirm the data.</p> </list-item> <list-item> <p>Our results on the <italic>sitiens–B. cinerea</italic> interaction favor a model in which cell viability in the cells surrounding the invaded tissue is maintained by a constant replenishment of the tricarboxylic acid (TCA) cycle through overactivation of the GS/GOGAT cycle and the GABA shunt, resulting in resistance through both tightly controlling the defense‐associated HR and slowing down the pathogen‐induced senescence.</p> </list-item> <list-item> <p>Collectively, this study shows that maintaining cell viability via alterations in host C : N metabolism plays a vital role in the resistance response against necrotrophic pathogens.</p> </list-item> </list> </p> </abstract>