Growth suppression, altered stomatal responses, and augmented induction of heat shock proteins in cytosolic ascorbate peroxidase (Apx1)‐deficient Arabidopsis plants

Abstract

Summary: The accumulation of hydrogen peroxide (H 2 O 2) in plants is typically associated with biotic or abiotic stresses. However, H 2 O 2 is continuously produced in cells during normal metabolism. Yet, little is known about how H 2 O 2 accumulation will affect plant metabolism in the absence of pathogens or abiotic stress. Here, we report that a deficiency in the H 2 O 2‐scavenging enzyme, cytosolic ascorbate peroxidase (APX1), results in the accumulation of H 2 O 2 in Arabidopsis plants grown under optimal conditions. Knockout‐Apx1 plants were characterized by suppressed growth and development, altered stomatal responses, and augmented induction of heat shock proteins during light stress. The inactivation of Apx1 resulted in the induction of several transcripts encoding signal transduction proteins. These were not previously linked to H 2 O 2 signaling during stress and may belong to a signal transduction pathway specifically involved in H 2 O 2 sensing during normal metabolism. Surprisingly, the expression of transcripts encoding H 2 O 2 scavenging enzymes, such as catalase or glutathione peroxidase, was not elevated in knockout‐Apx1 plants. The expression of catalase, two typical plant peroxidases, and several different heat shock proteins was however elevated in knockout‐Apx1 plants during light stress. Our results demonstrate that in planta accumulation of H 2 O 2 can suppress plant growth and development, interfere with different physiological processes, and enhance the response of plants to abiotic stress conditions. Our findings also suggest that at least part of the induction of heat shock proteins during light stress in Arabidopsis is mediated by H 2 O 2 that is scavenged by APX1.