|QIU, YONGJIAN - Washington State University|
|XI, JING - Washington State University|
|DU, LIQUN - Washington State University|
|POOVAIAH, B - Washington State University|
Submitted to: Plant Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/13/2012
Publication Date: 6/11/2012
Citation: Qiu, Y., Xi, J., Du, L., Suttle, J.C., Poovaiah, B.W. 2012. Coupling calcium/calmodulin-mediated signaling and herbivore-induced plant response calmodulin-binding transcription factor AtSR1/CAMTA3. Plant Molecular Biology. 79:89-99.
Interpretive Summary: Wounding or herbivore (insect) attack initiates a wide-range of plant biochemical defense responses to repair the wounded tissue and deter future herbivore attack. Calcium and calcium binding proteins have been shown to be involved in inducing plant defense responses but their actual mechanism of action is currently unknown. In this paper, the role of a calcium-binding protein was investigated. The results obtained demonstrate that this protein plays a key role in mediating wound-induced gene expression and the synthesis of a wound hormone that is critical for long-distance signaling within the damaged plant. The loss of this protein renders test plants more susceptible to insect damage.
Technical Abstract: Calcium/calmodulin (Ca2+/CaM) has long been considered a crucial component in wound signaling pathway. 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 (also known as AtCAMTAs) can respond differentially to wounding stress. Further studies showed that AtSR1/CAMTA3 is a negative regulator of plant defense, and Ca2+/CaM-binding to AtSR1 is indispensable for suppression of salicylic acid (SA) accumulation and disease resistance. Here we report that Ca2+/CaM-binding is also 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. However, when mutants of AtSR1 with impaired calmodulin-binding ability were overexpressed in atsr1 mutants, plant resistance to herbivore attack was not restored, suggesting a key role for Ca2+/CaM-binding in wound signaling. Furthermore, it was observed that elevated SA level in atsr1 mutant plants has a negative impact on both basal and induced biosynthesis of jasmonates (JA). These results revealed that Ca2+/CaM-mediated signaling regulates plant response to herbivore attack/wounding by modulating SA-JA crosstalk through AtSR1.