The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease

Rachel K. Pilloff, Sendil K. Devadas, Alexander Enyedi, Ramesh Raina

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

We describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion+ leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that significant overlap exist between the signalling pathways leading to resistance- and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.

Original languageEnglish (US)
Pages (from-to)61-70
Number of pages10
JournalPlant Journal
Volume30
Issue number1
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

lesions (plant)
Arabidopsis
cell death
Cell Death
mutants
pathogens
Pseudomonas syringae
foliar diseases
epistasis
hypersensitive response
salicylic acid
ethylene production
biomarkers
virulence
Growth
genetic markers
Transfer Factor
Disease Resistance
Salicylic Acid
Plant Cells

Keywords

  • Arabidopsis
  • Cell death
  • Compatible interactions
  • Disease
  • Dll1
  • PR genes

ASJC Scopus subject areas

  • Plant Science

Cite this

The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease. / Pilloff, Rachel K.; Devadas, Sendil K.; Enyedi, Alexander; Raina, Ramesh.

In: Plant Journal, Vol. 30, No. 1, 2002, p. 61-70.

Research output: Contribution to journalArticle

Pilloff, Rachel K. ; Devadas, Sendil K. ; Enyedi, Alexander ; Raina, Ramesh. / The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease. In: Plant Journal. 2002 ; Vol. 30, No. 1. pp. 61-70.
@article{f01f7fe6f83c4253bdead428a3e8ea1c,
title = "The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease",
abstract = "We describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion+ leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that significant overlap exist between the signalling pathways leading to resistance- and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.",
keywords = "Arabidopsis, Cell death, Compatible interactions, Disease, Dll1, PR genes",
author = "Pilloff, {Rachel K.} and Devadas, {Sendil K.} and Alexander Enyedi and Ramesh Raina",
year = "2002",
doi = "10.1046/j.1365-313X.2002.01265.x",
language = "English (US)",
volume = "30",
pages = "61--70",
journal = "Plant Journal",
issn = "0960-7412",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - The Arabidopsis gain-of-function mutant dll1 spontaneously develops lesions mimicking cell death associated with disease

AU - Pilloff, Rachel K.

AU - Devadas, Sendil K.

AU - Enyedi, Alexander

AU - Raina, Ramesh

PY - 2002

Y1 - 2002

N2 - We describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion+ leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that significant overlap exist between the signalling pathways leading to resistance- and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.

AB - We describe the characterization of a novel gain-of-function Arabidopsis mutant, dll1 (disease-like lesions1), which spontaneously develops lesions mimicking bacterial speck disease and constitutively expresses biochemical and molecular markers associated with pathogen infection. Despite the constitutive expression of defense-related responses, dll1 is unable to suppress the growth of virulent pathogens. However, dll1 elicits normal hypersensitive response in response to avirulent pathogens, thus indicating that dll1 is not defective in the induction of normal resistance responses. The lesion+ leaves of dll1 support the growth of hrcC mutant of Pseudomonas syringae, which is defective in the transfer of virulence factors into the plant cells, and therefore non-pathogenic to wild-type Col-0 plants. This suggests that dll1 intrinsically expresses many of the cellular processes that are required for pathogen growth during disease. Epistasis analyses reveal that salicylic acid and NPR1 are required for lesion formation, while ethylene modulates lesion development in dll1, suggesting that significant overlap exist between the signalling pathways leading to resistance- and disease-associated cell death. Our results suggest that host cell death during compatible interactions, at least in part, is genetically controlled by the plant and DLL1 may positively regulate this process.

KW - Arabidopsis

KW - Cell death

KW - Compatible interactions

KW - Disease

KW - Dll1

KW - PR genes

UR - http://www.scopus.com/inward/record.url?scp=0036011029&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036011029&partnerID=8YFLogxK

U2 - 10.1046/j.1365-313X.2002.01265.x

DO - 10.1046/j.1365-313X.2002.01265.x

M3 - Article

C2 - 11967093

AN - SCOPUS:0036011029

VL - 30

SP - 61

EP - 70

JO - Plant Journal

JF - Plant Journal

SN - 0960-7412

IS - 1

ER -