Abscisic acid is a central stress hormone in Arabidopsis which mediates rapid Ca2+-induced cellular responses, down regulates cell proliferation and inhibits growth. Early signal transduction mechanisms that down regulate cell proliferation are of central importance for controlling mitogenesis and their mis-regulation is linked to many human diseases. Abscisic acid (ABA)-triggered Ca2+ signaling will be analyzed in Arabidopsis guard cells, which provide a powerful system for quantitative and time- resolved dissection of mechanisms mediating specificity in Ca2+ signaling. How the universal second messenger Ca2+ mediates specific responses in eukaryotic cells, is a central question in cell signaling research. Data from several lines of our investigations point to a novel hypothesis for specificity in Ca2+ signal transduction, in which the physiological stimulus, ABA, """"""""primes"""""""" (de-inactivates) specific Ca2+ sensors, switching them from an inactivated Ca2+-insensitive state to a Ca2+-sensitive """"""""primed"""""""" state, thus tightly controlling Ca2+ responsiveness. Calcium sensitivity priming could provide a key mechanism contributing to specificity in eukaryotic Ca2+ signal transduction. We have recently discovered major signaling mechanisms and genes that form this ABA-regulated-cytosolic Ca2+ signaling module, including Ca2+ channel genes, Ca2+ sensors (CDPKs) and major downstream targets of Ca2+: a long-sought membrane protein, RCD3, required for Ca2+-activated anion channel activity, which is essential for the ABA-Ca2+ response, and an ABC transmembrane channel regulator (AtMRP5). We will investigate the mechanisms mediating Ca2+ signaling specificity by pursuing the following specific aims: (1) We will dissect the mechanisms by which ABA activates newly identified Ca2+ channel genes and determine their functions in generating guard cell Ca2+ oscillations. (2) Characterize possible Ca2+ specificity signaling mechanisms by analyzing ABA-dependent cellular localization and modulation of the CDPK Ca2+ sensors and associated proteins. (3) We will systematically dissect the protein- protein interaction network through which these newly isolated major Ca2+ signaling mechanisms interact, thus enabling ABA-directed specificity in Ca2+ signaling. (4) We have developed a powerful chemical genetics screen for ABA/Ca2+ signaling, using a compound that inhibits Ca2+-induced stomatal closing, and that can address genetic redundancy and signaling robustness. This has enabled us to isolate new early ABA signaling mutants that will be functionally characterized within the ABA-Ca2+ signaling network. These studies should advance a mechanistic understanding of specificity in Ca2+ signaling, which is fundamental to numerous cell signaling processes, and will reveal novel mechanisms by which a newly recognized early signaling pathway controls ABA signal transduction. Project Narrative How the universal second messenger Ca2+ mediates specific responses in eukaryotic cells, is a key question in cell signaling research. This research will reveal major mechanisms by which the early abscisic acid-directed calcium signal transduction pathway mediates stress hormone signaling. These studies should substantially advance an understanding of the mechanisms mediating specificity in Ca2+ signaling in a highly developed model cell system, a basic process that is fundamental to numerous cell signaling pathways and is mis-regulated in human diseases.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM060396-11
Application #
7821396
Study Section
Development - 1 Study Section (DEV1)
Program Officer
Chin, Jean
Project Start
2000-02-01
Project End
2012-04-30
Budget Start
2010-05-01
Budget End
2011-04-30
Support Year
11
Fiscal Year
2010
Total Cost
$305,910
Indirect Cost
Name
University of California San Diego
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Wang, Cun; Zhang, Jingbo; Schroeder, Julian I (2017) Two-electrode Voltage-clamp Recordings in Xenopus laevis Oocytes: Reconstitution of Abscisic Acid Activation of SLAC1 Anion Channel via PYL9 ABA Receptor. Bio Protoc 7:
Park, Jiyoung; Lee, Youngsook; Martinoia, Enrico et al. (2017) Plant hormone transporters: what we know and what we would like to know. BMC Biol 15:93
Pornsiriwong, Wannarat; Estavillo, Gonzalo M; Chan, Kai Xun et al. (2017) A chloroplast retrograde signal, 3'-phosphoadenosine 5'-phosphate, acts as a secondary messenger in abscisic acid signaling in stomatal closure and germination. Elife 6:
Kunz, Hans-Henning; Park, Jiyoung; Mevers, Emily et al. (2016) Small Molecule DFPM Derivative-Activated Plant Resistance Protein Signaling in Roots Is Unaffected by EDS1 Subcellular Targeting Signal and Chemical Genetic Isolation of victr R-Protein Mutants. PLoS One 11:e0155937
Wang, Cun; Hu, Honghong; Qin, Xue et al. (2016) Reconstitution of CO2 Regulation of SLAC1 Anion Channel and Function of CO2-Permeable PIP2;1 Aquaporin as CARBONIC ANHYDRASE4 Interactor. Plant Cell 28:568-82
Azoulay-Shemer, Tamar; Bagheri, Andisheh; Wang, Cun et al. (2016) Starch Biosynthesis in Guard Cells But Not in Mesophyll Cells Is Involved in CO2-Induced Stomatal Closing. Plant Physiol 171:788-98
Stephan, Aaron B; Kunz, Hans-Henning; Yang, Eric et al. (2016) Rapid hyperosmotic-induced Ca2+ responses in Arabidopsis thaliana exhibit sensory potentiation and involvement of plastidial KEA transporters. Proc Natl Acad Sci U S A 113:E5242-9
Li, Zixing; Waadt, Rainer; Schroeder, Julian I (2016) Release of GTP Exchange Factor Mediated Down-Regulation of Abscisic Acid Signal Transduction through ABA-Induced Rapid Degradation of RopGEFs. PLoS Biol 14:e1002461
Engineer, Cawas B; Hashimoto-Sugimoto, Mimi; Negi, Juntaro et al. (2016) CO2 Sensing and CO2 Regulation of Stomatal Conductance: Advances and Open Questions. Trends Plant Sci 21:16-30
Hõrak, Hanna; Sierla, Maija; Tõldsepp, Kadri et al. (2016) A Dominant Mutation in the HT1 Kinase Uncovers Roles of MAP Kinases and GHR1 in CO2-Induced Stomatal Closure. Plant Cell 28:2493-2509

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