A Role of the FZL gene in regulating cell death and defense in Arabidopsis
H. LU (1), A. Tremblay (1), S. Seabolt (1), H. Zeng (2), S. Boeckler (3), D. Tate (1), T. Dong (1), N. Yao (2), B. Westermann (3) (1) University of Maryland Baltimore County, U.S.A.; (2) School of Life Sciences, Sun Yat-sen University, China; (3) Institut für Zellbiologie, Universität Bayreuth, Germany

Programmed cell death (PCD) is critical for development and responses to environmental stimuli in many organisms. The FUZZY ONIONS (FZO) genes in yeast, flies, and mammals are known to affect mitochondrial fusion, disruption of which could lead to PCD and disease. The FZO-like (FZL) gene of Arabidopsis was previously shown to encode a chloroplast protein that regulates cell death and chloroplast morphology. We cloned the FZL gene based on the lesion mimic phenotype conferred by a fzl mutation, which was in the background of another mutant. Our protein co-localization studies failed to detect the FZL protein in the mitochondrion of Arabidopsis cells. Neither FZL nor a truncated FZL without the chloroplast transit peptide rescued the yeast strain lacking the FZO gene. Thus Arabidopsis FZL may have evolved new function from its homologs in yeast, flies, and mammals. We found that cell death conferred by a fzl mutation was associated with increased accumulation of reactive oxygen species and activation of the autophagy pathway. Such cell death was largely dependent on the key defense signaling mediated by salicylic acid (SA) and affected by genetic background. Exogenous SA treatment also exacerbated cell death formation in fzl mutants. We further showed that fzl mutations conferred enhanced disease resistance to the bacterial pathogen Pseudomonas syringae and the oomycete pathogen Hyaloperonospora arabidopsidis. Together these data suggest that the Arabidopsis FZL gene is a negative regulator of cell death and disease resistance, possibly through affecting function of the chloroplast and involving ROS and autophagy pathways.

Abstract Number: P18-681
Session Type: Poster