Poster: Oxidative stress

Abs # 97: Calcium and Calcium Dependent Protein Kinases (CDPK) are involved in ROS generation during Mercury stress

Presenter:	Gouthu, Satyanarayana , sgouthu@postman.riken.go.jp
Authors	Gouthu, Satyanarayana  (A)   Yokomizo, Satoko  (A)   Kamada, Hiroshi  (B)   Yamaguchi, Isamu  (A)   Hamamoto, Hiroshi  (A)
Affiliations:	(A): RIKEN Yokohama Institute, Plant Science Center, Laboratory for Adaptation and Resistance (B): Institute of Biological Sciences, University of Tsukuba

The common consequence of most abiotic and biotic stresses is formation of "reactive oxygen species" (ROS). Besides ROS, elevation of cytosolic free calcium ([Ca²⁺]_cyt), often termed as Ca²⁺ signal, has also been demonstrated to be indispensable in most of the stresses. Both, ROS and Ca²⁺ act as secondary messengers and, in many instances, presumed to facilitate adaptation. A close relation between stress-induced Ca²⁺ influx and ROS production is becoming clear from studies in both plant and animal cells. Several heavy metals induce oxidative burst through ROS generation, which (in case of cadmium) was thought to be the result of depletion of GSH and antioxidant enzymes. In our experiments, mercury treatment to cultured tobacco (Nicotiana tobacum Xanthi nc) cells induced rapid and sustained increase in cytoplasmic Ca²⁺ followed by ROS generation. Treatment with cadmium resulted in ROS formation, but not the Ca²⁺ elevation. The mercury-induced [Ca²⁺]_cyt-increase was from extracellular Ca²⁺ sources and gated through La³⁺ and Gd³⁺-responsive plasmamembrane calcium channels. Further, mercury treatment also resulted in the increased expression of calcium dependent protein kinases (CDPKs). Pharmacological approach suggests that ROS formation was NADPH oxidase-mediated and was dependent on both Ca²⁺ influx and CDPK. Role of anion channels before Ca²⁺ influx and phosphorylation events essential for ROS generation were also identified. These observations suggest that signaling mechanism involving Ca²⁺, CDPKs and ROS, similar to pathogen or abiotic stresses is activated during mercury stress.