A genetic framework for @entity5568 induced cell death in XXXX .

@entity5568 @entity15019 @entity19041 @entity71163 @entity3785 @entity7214 @entity958 @entity6266 @entity26 @entity960 @entity19046 @entity19061 @entity15020 @entity21108 @entity44888 @entity19057 @entity29261
BACKGROUND: To survive in a changing environment plants constantly monitor their surroundings. In response to several stresses and during photorespiration plants use reactive @entity26 species as signaling molecules. The @entity958 @entity44888 ( @entity44888 ) mutant lacks a peroxisomal catalase and under photorespiratory conditions accumulates @entity5568 , which leads to activation of cell death. METHODS: A @entity44888 double mutant collection was generated through crossing and scored for cell death in different assays. Selected double mutants were further analyzed for photosynthetic performance and @entity5568 accumulation. RESULTS: We used a targeted mutant analysis with more than 50 @entity44888 double mutants to investigate the role of stress hormones and other defense regulators in @entity5568 -mediated cell death. Several transcription factors ( @entity6266 , @entity960 , @entity15020 , @entity15019 ), cell death regulators ( @entity29261 , @entity21108 ) and hormone regulators ( @entity19041 , @entity71163 , @entity19061 , @entity19057 , @entity19046 ) were essential for execution of cell death in @entity44888 . Genetic loci required for cell death in @entity44888 was compared with regulators of cell death in spontaneous lesion mimic mutants and led to the identification of a core set of plant cell death regulators. Analysis of gene expression data from @entity44888 and plants undergoing cell death revealed similar gene expression profiles, further supporting the existence of a common program for regulation of plant cell death. CONCLUSIONS: Our results provide a genetic framework for further study on the role of @entity5568 in regulation of cell death. The hormones @entity3785 , @entity7214 and auxin, as well as their interaction, are crucial determinants of cell death regulation.
