Salicylic Acid Regulates Systemic Defense Signaling in Chickpea During Fusarium oxysporum f. sp. ciceri Race 1 Infection
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Annual loss of productivity of the important crop legume chickpea has received prime scientific concern at recent times. Vascular wilt caused by fungal pathogen Fusarium oxysporum f. sp. ciceris race 1 (Foc1) accounts for major share of yield loss of chickpea. Control of this disease remains a challenge due to the lack of appropriate breeding programs to manage fast pathogen mutability. Previous studies with this pathogen have highlighted the role of reactive oxygen species (ROS) as chemical signal in enkindling downstream systemic resistance response instead of activating site specific defense. But the role of salicylic acid in modulating resistance is still unexplored. Present study explains the probable function of salicylic acid (SA) in coordination with ROS. The external SA application reveals the restoration of relative water content of infected susceptible chickpea plants. The qRT-PCR based expression study of key SA biosynthetic genes indicate that the SA biogenesis takes place by the activity of phenylalanine ammonia lyase (PAL) that activates other SA responsive genes and TGA transcription factors to induce an active defense against Foc1. Finally, detection of SA by LC MS/MS along with the accumulation of transcripts of SA marker genes, PR1 and PR5, strengthens the involvement of SA in translocation of distant systemic signals in chickpea-Foc1 interaction.
KeywordsBiotic stress Cicer arietinum Fusarium oxysporum f. sp. ciceri race 1 Systemic response Salicylic acid Wilt disease
Authors thank Dr. S.C. Pande (ICRISAT, Patancheru) for providing fungal culture and Dr. S.K. Chaturvedi (IIPR, Kanpur) for providing chickpea seeds. Authors are also thankful to Dr. Kaushik Bannerjee, National Research Centre for Grapes, Solapur, Pune, India, for performing the LC MS/MS of the sample. Unwearied assistance of Mr. Swarnava Das for physiological experiments is greatly acknowledged. Mr. Sudipta Basu is duly acknowledged for seed multiplication. Finally, authors acknowledge the Director, Bose Institute for infrastructural facilities.
This work was supported by the grant provided to A.Bhar by Council of Scientific and Industrial Research, India (09/015(0378) /2009-EMR-1) and to M.Chatterjee by Department of Biotechnology, Government of India (BT/01/COE/06/03/2006). The funding organizations had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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