Regulation und physiologische Integration von Salzstresssignalwegen und deren Anpassung in Arabidopsis
Pflanzenphysiologie
Zusammenfassung der Projektergebnisse
Collectively, the insights emanating from this project revealed several paradigm changing findings, which dramatically advanced our understanding of plant salt tolerance. One general advance overarching all aspects of this project is that we were able to integrate cellular salt stress mechanisms into a high-resolution picture that delineates salt stress signaling and salt tolerance regulation at the organ scale. Our Ca2+ bioimaging revealed several surprising and most significant findings: Firstly, we unambiguously established that the ionic component of NaCl stress can specifically induce Ca2+ signal. Secondly, we discovered a spatially defined sodium sensing niche (NaSN) that is defined by an oligo-cellular primary Ca2+ signal. Thirdly, we established that the intensity of Na+ stress quantitatively determines the amplitude of the PCS and that thereby the PCS provides quantitative information about stress intensity. Lastly, we also discovered that stress intensity determines the speed of the resulting systemic Ca2+ wave. An intriguing question for future research will be which factors or mechanisms determine (prime) the sensitivity and spatial pattern of PCS formation in the NaSN. Moreover, we delineate a Ca2+ sensing mechanisms the stress intensity in order to mount appropriate salt detoxification responses. This is mediated by a Ca2+ sensor switch mechanism in which the sensors CBL4 and CBL8 are activated by distinct Ca2+ signal amplitudes. Furthermore, we corroborated the existence of a secondary oligo-cellular Ca2+ signal that is formed three hours after onset of stress exposure and exhibits characteristics of systemic expansion via the vasculature. This finding reveals a surprising complexity of plant Ca2+ signaling that deserves further investigation in the future. Moreover, this project revealed a novel sophisticated mechanism that allows plants to protect their sensitive stem cells in the meristem. By directly interconnecting peptide-triggered RLK signaling with the CIPK24-SOS1 module and cell type specific modulation of GSO1 and CIPK24 expression, the plant simultaneously achieves protection of its root vasculature and its stem cells from the toxic effects of NaCl exposition. An intriguing question arising from these findings is which peptides are activating this signaling axis and how salt stress triggers peptide accumulation/activation. In the course of this work, we also discovered and characterized a negative feedback loop in which components of the SOS pathway feedback on ANN4 activity to fine-tune Ca2+ signal formation and optimize plant salt tolerance. However, loss of ANN4 function reduced but did not abolish NaCl induced PCS formation indicating that other Ca2+ channels contribute to salt induced Ca2+ signal formation. This finding suggests that multiple channels may contribute to PCS formation and that an “individual Ca2+ signal” may actually represent a composition of multiple singular Ca2+ signals within one cell. Such a mechanism would obviously further complicate the clarification of the mechanisms underlying Ca2+ signal formation. Lastly, this project provided important insights into the direct interconnection of Ca2+ signaling and proton fluxes in salt stress responses. A surprising finding was that the Ca2+ sensor CBL7 can exert a regulatory function on AHA2 by direct interaction with this proton pump instead of requiring interaction with a CIPK to convey target regulation. This facet of CBL/CIPK signaling is not unprecedented since it for example has been reported that CBL10 can directly regulate the potassium channel AKT1 through protein-protein interaction. Nevertheless, this finding underscores that deviations from a “classical” CBL-CIPK-target phosphorylation concept should be considered when exploring the function of the CBL/CIPK network in plants.
Projektbezogene Publikationen (Auswahl)
-
The Ca2+ Sensor SCaBP3/CBL7 Modulates Plasma Membrane H+-ATPase Activity and Promotes Alkali Tolerance in Arabidopsis. The Plant Cell, 31(6), 1367-1384.
Yang, Yongqing; Wu, Yujiao; Ma, Liang; Yang, Zhijia; Dong, Qiuyan; Li, Qinpei; Ni, Xuping; Kudla, Jörg; Song, ChunPeng & Guo, Yan
-
The SOS2-SCaBP8 Complex Generates and Fine-Tunes an AtANN4-Dependent Calcium Signature under Salt Stress. Developmental Cell, 48(5), 697-709.e5.
Ma, Liang; Ye, Jiamin; Yang, Yongqing; Lin, Huixin; Yue, Lili; Luo, Jin; Long, Yu; Fu, Haiqi; Liu, Xiangning; Zhang, Yulin; Wang, Yi; Chen, Liangyi; Kudla, Joerg; Wang, Youjun; Han, Shengcheng; Song, Chun-Peng & Guo, Yan
-
A Ca2+-sensor switch for tolerance to elevated salt stress in Arabidopsis. Developmental Cell, 57(17), 2081-2094.e7.
Steinhorst, Leonie; He, Gefeng; Moore, Lena K.; Schültke, Stefanie; Schmitz-Thom, Ina; Cao, Yibo; Hashimoto, Kenji; Andrés, Zaida; Piepenburg, Katrin; Ragel, Paula; Behera, Smrutisanjita; Almutairi, Bader O.; Batistič, Oliver; Wyganowski, Thomas; Köster, Philipp; Edel, Kai H.; Zhang, Chunxia; Krebs, Melanie; Jiang, Caifu ... & Kudla, Jörg
-
A salt stress‐activated GSO1‐SOS2‐SOS1 module protects the Arabidopsis root stem cell niche by enhancing sodium ion extrusion. The EMBO Journal, 42(13).
Chen, Changxi; He, Gefeng; Li, Jianfang; Perez‐Hormaeche, Javier; Becker, Tobias; Luo, Manqing; Wallrad, Lukas; Gao, Junping; Li, Jia; Pardo, José M.; Kudla, Jörg & Guo, Yan
