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Quantitative Imaging Reveals Distinct Contributions of SnRK2 and ABI3 in Plasmodesmatal Permeability in Physcomitrella patens

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Title: Quantitative Imaging Reveals Distinct Contributions of SnRK2 and ABI3 in Plasmodesmatal Permeability in Physcomitrella patens
Authors: Tomoi, Takumi Browse this author
Kawade, Kensuke Browse this author
Kitagawa, Munenori Browse this author
Sakata, Yoichi Browse this author
Tsukaya, Hirokazu Browse this author
Fujita, Tomomichi Browse this author →KAKEN DB
Keywords: Abscisic acid signaling
Cell-to-cell communication
Physcomitrella patens
Quantitative imaging analysis
Salt stress tolerance
Issue Date: May-2020
Publisher: Oxford University Press
Journal Title: Plant and Cell Physiology
Volume: 61
Issue: 5
Start Page: 942
End Page: 956
Publisher DOI: 10.1093/pcp/pcaa021
Abstract: Cell-to-cell communication is tightly regulated in response to environmental stimuli in plants. We previously used a photoconvertible fluorescent protein Dendra2 as a model reporter to study this process. This experiment revealed that macromolecular trafficking between protonemal cells in Physcomitrella patens is suppressed in response to abscisic acid (ABA). However, it remains unknown which ABA signaling components contribute to this suppression and how. Here, we show that ABA signaling components SUCROSE NON-FERMENTING 1-RELATED PROTEIN KINASE 2 (PpSnRK2) and ABA INSENSITIVE 3 (PpABI3) play roles as an essential and promotive factor, respectively, in regulating ABA-induced suppression of Dendra2 diffusion between cells (ASD). Our quantitative imaging analysis revealed that disruption of PpSnRK2 resulted in defective ASD onset itself, whereas disruption of PpABI3 caused an 81-min delay in the initiation of ASD. Live-cell imaging of callose deposition using aniline blue staining showed that, despite this onset delay, callose deposition on cross walls remained constant in the PpABI3 disruptant, suggesting that PpABI3 facilitates ASD in a callose-independent manner. Given that ABA is an important phytohormone to cope with abiotic stresses, we further explored cellular physiological responses. We found that the acquisition of salt stress tolerance is promoted by PpABI3 in a quantitative manner similar to ASD. Our results suggest that PpABI3-mediated ABA signaling may effectively coordinate cell-to-cell communication during the acquisition of salt stress tolerance. This study will accelerate the quantitative study for ABA signaling mechanism and function in response to various abiotic stresses.
Rights: This is a pre-copyedited, author-produced version of an article accepted for publication in Plant and cell physiology following peer review. The version of record Plant Cell Physiol (2020) 61 (5): 942–956 is available online at:
Type: article (author version)
Appears in Collections:理学院・理学研究院 (Graduate School of Science / Faculty of Science) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 藤田 知道

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