CALCIUM AND CALMODULIN-MEDIATED SIGNALING REGULATES BIOTIC STRESS RESPONSES IN PLANTS

YONGJIAN QIU

Calcium (Ca2+) is a ubiquitous second messenger that plays a vital role in numerous signaling pathways in plants. The change of cytosolic free Ca2+ concentration can be triggered by a variety of environmental and developmental stimuli. The encrypted Ca2+ signaling information is decoded by a variety of Ca2+-binding proteins which transduce the message to downstream targets involved in signal-specific responses. Our data reveal the novel roles of two Ca2+-sensors, calmodulin (CaM) and calreticulin (CRT), in plant defense against biotic stresses. CRT is an endoplasmic reticulum (ER)-resident Ca2+-binding protein that is highly conserved in multi-cellular eukaryotes. Our experiments suggest that AtCRT2 is a crucial modulator of plant innate immunity. Despite significantly elevated salicylic acid (SA) levels and constitutive expression of defense-related marker genes, transgenic plants overexpressing AtCRT2 display a reduced resistance to virulent Pseudomonas syringae pv tomato DC3000 (Pst DC3000). A 45Ca2+-overlay assay and a domain-swapping experiment further demonstrate that the negatively charged C-terminal tail of AtCRT2 is responsible for its high Ca2+-binding capacity and function in regulating SA biosynthesis. In addition, overexpression of the His173 mutant of AtCRT2 greatly enhances plant defense against Pst DC3000, supporting a self-inhibition mechanism that can counteract the effects of SA-dependent immune responses. Ca2+/CaM has long been considered a crucial component in wound signaling pathways. However, no functional significance of Ca2+/CaM-binding proteins has been identified in plant responses to herbivore attack/wounding stress. We have reported earlier that a family of Ca2+/CaM-binding transcription factors designated as AtSRs can respond differentially to wounding stress. We further determine that Ca2+/CaM-binding is critical for AtSR1-mediated herbivore-induced wound response. Interestingly, atsr1 mutant plants are more susceptible to herbivore attack than wild-type plants. Complementation of atsr1 mutant plants by overexpressing wild-type AtSR1 protein can effectively restore plant resistance to herbivore attack, whereas overexpression of AtSR1 mutants with impaired CaM-binding ability fails to, suggesting a key role for Ca2+/CaM-binding in wound signaling. Furthermore, elevated SA level in atsr1 mutant plants has a negative impact on both basal and induced biosynthesis of jasmonates (JA). These results reveal that Ca2+/CaM-mediated signaling regulates plant response to herbivore attack/wounding by modulating SA-JA cross-talk through AtSR1.

CALCIUM AND CALMODULIN-MEDIATED SIGNALING REGULATES BIOTIC STRESS RESPONSES IN PLANTS

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