Autophagy Is Enhanced and Floral Development Is Impaired in AtHVA22d RNAi Arabidopsis
Autophagy is an intracellular process in which a portion of cytoplasm is transported into vacuoles for recycling. Physiological roles of autophagy in plants include recycling nutrients during senescence, sustaining life during starvation and the formation of central digestive vacuoles. Regulation of autophagy and formation of autophagosomes, spherical double membrane structures containing cytoplasm moving towards vacuoles, are poorly understood. HVA22 is a gene originally cloned from barley, which is highly induced by abscisic acid (ABA) and environmental stress. Homologs of HVA22 include Yop1 in yeast, TB2/DP1 in humans, and AtHVA22a-e in Arabidopsis. Reverse genetics followed by a cell biology approach was employed to study the function of HVA22 homologs. The AtHVA22d RNAi Arabidopsis plants produced small siliques with reduced seed yield. This phenotype co-segregated with the RNAi transgene. Causes of the reduced seed yield include short filaments, defective carpels and dysfunctional pollen grains. Enhanced autophagy was observed in the filament cells. Number of autophagosomes in root tips of RNAi plants was also increased dramatically. The yop1 deletion mutant of Saccharomyces cerevisiae was used to verify our hypothesis that HVA22 homologs are suppressors of autophagy. Autophagy activity of this mutant during nitrogen starvation increased in five minutes and reached a plateau after two hours with about 80% of cells showing autophagy, while the wild-type cells exhibited low levels of autophagy following eight hours of nitrogen starvation. We conclude that HVA22 homologs function as suppressors of autophagy in both plants and yeast. Potential mechanisms of this suppression and the roles of ABA-induced HVA22 expression in vegetative and reproductive tissues are discussed.
N. Chen et al., "Autophagy Is Enhanced and Floral Development Is Impaired in AtHVA22d RNAi Arabidopsis," Plant Physiology, American Society of Plant Biologists, Jan 2009.
The definitive version is available at http://dx.doi.org/10.1104/pp.108.131490
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