Article

Plant Molecular Biology

, Volume 62, Issue 1, pp 29-42

First online:

Loss of NECROTIC SPOTTED LESIONS 1 associates with cell death and defense responses in Arabidopsis thaliana

  • Yoshiteru NoutoshiAffiliated withPlant Molecular Biology, RIKEN Tsukuba InstituteThe Sainsbury Laboratory, John Innes Centre
  • , Takashi KuromoriAffiliated withGenomic Sciences Center, RIKEN Yokohama Institute
  • , Takuji WadaAffiliated withPlant Science Center, RIKEN Yokohama Institute
  • , Takashi HirayamaAffiliated withGenomic Sciences Center, RIKEN Yokohama InstituteInternational Graduate School of Arts and Science, Yokohama City Univ.
  • , Asako KamiyaAffiliated withGenomic Sciences Center, RIKEN Yokohama Institute
  • , Yuko ImuraAffiliated withGenomic Sciences Center, RIKEN Yokohama Institute
  • , Michiko YasudaAffiliated withPlant Functions Laboratory, RIKEN Institute
  • , Hideo NakashitaAffiliated withPlant Functions Laboratory, RIKEN Institute
  • , Ken ShirasuAffiliated withPlant Science Center, RIKEN Yokohama InstituteThe Sainsbury Laboratory, John Innes Centre
    • , Kazuo ShinozakiAffiliated withPlant Molecular Biology, RIKEN Tsukuba InstituteGenomic Sciences Center, RIKEN Yokohama InstitutePlant Science Center, RIKEN Yokohama Institute Email author 

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Abstract

We isolated a lesion mimic mutant, n ecrotic s potted l esions 1 (nsl1), from Ds-tagged Arabidopsis thaliana accession No-0. The nsl1 mutant exhibits a growth retardation phenotype and develops spotted necrotic lesions on its rosette and cauline leaves. These phenotypes occur in the absence of pathogens indicating that nsl1 mutants may constitutively express defense responses. Consistent with this idea, nsl1 accumulates high levels of callose and autofluorescent phenolic compounds localized to the necrotic lesions. Furthermore RNA gel blot analysis revealed that genes associated with disease resistance activation are upregulated in the nsl1 mutants and these plants contain elevated levels of salicylic acid (SA). Crossing nsl1 with an SA deficient mutant, eds16-1, revealed that the nsl1 lesions and growth retardation are dependent upon SA. The nsl1 phenotypes are not suppressed under either the rar1-10 or sgt1b-1 genetic background. NSL1 encodes a novel 612aa protein which contains a membrane-attack complex/perforin (MACPF) domain, which is conserved in bacteria, fungi, mammals and plants. The possible modes of action of NSL1 protein in negative regulation of cell death programs and defense responses are discussed.

Keywords

Cell death Defense responses Salicylic acid MACPF domain