Involvement of the Electrophilic Isothiocyanate Sulforaphane in Arabidopsis Local Defense Responses

Andersson, M.X., Nilsson, A.K., Johansson, O.N., Boztas, Gulin, Adolfsson, L.E., Pinosa, F., Garcia, C., Arronsson, H., Mackey, D., Tör, M. ORCID: https://orcid.org/0000-0002-4416-5048, Hamberg, M. and Ellerström, M. (2015) Involvement of the Electrophilic Isothiocyanate Sulforaphane in Arabidopsis Local Defense Responses. Plant Physiology, 167 (1). pp. 251-261. ISSN Print 0032-0889 Online 1532-2548

Abstract

Plants defend themselves against microbial pathogens through a range of highly sophisticated and integrated molecular systems. Recognition of pathogen-secreted effector proteins often triggers the hypersensitive response (HR), a complex multicellular defense reaction where programmed cell death (PCD) of cells surrounding the primary site of infection is a prominent feature. Even though the HR was described almost a century ago, cell to cell factors acting at the local level generating the full defense reaction has remained obscure. In this study, we sought to identify diffusible molecules produced during the HR that could induce cell death in naïve tissue. We found that 4-methylsulfinylbutyl isothiocyanate (sulforaphane) is released by Arabidopsis thaliana leaf tissue undergoing HR, and that this compound induces cell death as well as prime defense in naïve tissue. Two different mutants impaired in the pathogen-induced accumulation of sulforaphane displayed attenuated PCD upon bacterial and oomycete effector recognition as well as decreased resistance to several isolates of the plant pathogen Hyaloperonospora arabidopsidis. Treatment with sulforaphane provided protection against a virulent H. arabidopsidis isolate. Glucosinolate breakdown products are recognized as antifeeding compounds towards insects and recently also as intracellular signaling and bacteriostatic molecules in Arabidopsis. The data presented herein indicate that these compounds also trigger local defense responses in Arabidopsis tissue.

Actions (login required)

View Item