Distinct Molecular Pattern-Induced Calcium Signatures Lead to Different Downstream Transcriptional Regulations via AtSR1/CAMTA3

• Main Authors: Peiguo Yuan, Jeremy B. Jewell, Smrutisanjita Behera, Kiwamu Tanaka, B. W. Poovaiah
• Format: Article
• Language: English
• Published: MDPI AG 2020-10-01
• Series: International Journal of Molecular Sciences
• Subjects: MAMPs; DAMPs; nuclear and cytoplasmic calcium signaling; plant immune response; salicylic acid; jasmonic acid
• Online Access: https://www.mdpi.com/1422-0067/21/21/8163

Plants encrypt the perception of different pathogenic stimuli into specific intracellular calcium (Ca²⁺) signatures and subsequently decrypt the signatures into appropriate downstream responses through various Ca²⁺ sensors. Two microbe-associated molecular patterns (MAMPs), bacterial flg22 and fungal chitin, and one damage-associated molecular pattern (DAMP), AtPep1, were used to study the differential Ca²⁺ signatures in <i>Arabidopsis</i> leaves. The results revealed that flg22, chitin, and AtPep1 induced distinct changes in Ca²⁺ dynamics in both the cytosol and nucleus. In addition, Flg22 and chitin upregulated the expression of salicylic acid-related genes, <i>ICS1</i> and <i>EDS1</i>, whereas AtPep1 upregulated the expression of jasmonic acid-related genes, <i>JAZ1</i> and <i>PDF1.2</i>, in addition to <i>ICS1</i> and <i>EDS1.</i> These data demonstrated that distinct Ca²⁺ signatures caused by different molecular patterns in leaf cells lead to specific downstream events. Furthermore, these changes in the expression of defense-related genes were disrupted in a knockout mutant of the <i>AtSR1/CAMTA3</i> gene, encoding a calmodulin-binding transcription factor, in which a calmodulin-binding domain on AtSR1 was required for deciphering the Ca²⁺ signatures into downstream transcription events. These observations extend our knowledge regarding unique and intrinsic roles for Ca²⁺ signaling in launching and fine-tuning plant immune response, which are mediated by the AtSR1/CAMTA3 transcription factor.