Long-distance turgor pressure changes induce local activation of plant glutamate receptor-like channels. Grenzi, M., Buratti, S., Parmagnani, A. S., Abdel Aziz, I., Bernacka-Wojcik, I., Resentini, F., Šimura, J., Doccula, F. G., Alfieri, A., Luoni, L., Ljung, K., Bonza, M. C., Stavrinidou, E., & Costa, A. Current Biology, February, 2023. ![Long-distance turgor pressure changes induce local activation of plant glutamate receptor-like channels [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex In Arabidopsis thaliana, local wounding and herbivore feeding provoke leaf-to-leaf propagating Ca2+ waves that are dependent on the activity of members of the glutamate receptor-like channels (GLRs). In systemic tissues, GLRs are needed to sustain the synthesis of jasmonic acid (JA) with the subsequent activation of JA-dependent signaling response required for the plant acclimation to the perceived stress. Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. Here, we report that in vivo, the amino-acid-dependent activation of the AtGLR3.3 channel and systemic responses require a functional ligand-binding domain. By combining imaging and genetics, we show that leaf mechanical injury, such as wounds and burns, as well as hypo-osmotic stress in root cells, induces the systemic apoplastic increase of L-glutamate (L-Glu), which is largely independent of AtGLR3.3 that is instead required for systemic cytosolic Ca2+ elevation. Moreover, by using a bioelectronic approach, we show that the local release of minute concentrations of L-Glu in the leaf lamina fails to induce any long-distance Ca2+ waves.
@article{grenzi_long-distance_2023,
title = {Long-distance turgor pressure changes induce local activation of plant glutamate receptor-like channels},
issn = {0960-9822},
url = {https://www.sciencedirect.com/science/article/pii/S0960982223000763},
doi = {10.1016/j.cub.2023.01.042},
abstract = {In Arabidopsis thaliana, local wounding and herbivore feeding provoke leaf-to-leaf propagating Ca2+ waves that are dependent on the activity of members of the glutamate receptor-like channels (GLRs). In systemic tissues, GLRs are needed to sustain the synthesis of jasmonic acid (JA) with the subsequent activation of JA-dependent signaling response required for the plant acclimation to the perceived stress. Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. Here, we report that in vivo, the amino-acid-dependent activation of the AtGLR3.3 channel and systemic responses require a functional ligand-binding domain. By combining imaging and genetics, we show that leaf mechanical injury, such as wounds and burns, as well as hypo-osmotic stress in root cells, induces the systemic apoplastic increase of L-glutamate (L-Glu), which is largely independent of AtGLR3.3 that is instead required for systemic cytosolic Ca2+ elevation. Moreover, by using a bioelectronic approach, we show that the local release of minute concentrations of L-Glu in the leaf lamina fails to induce any long-distance Ca2+ waves.},
language = {en},
urldate = {2023-03-23},
journal = {Current Biology},
author = {Grenzi, Matteo and Buratti, Stefano and Parmagnani, Ambra Selene and Abdel Aziz, Ilaria and Bernacka-Wojcik, Iwona and Resentini, Francesca and Šimura, Jan and Doccula, Fabrizio Gandolfo and Alfieri, Andrea and Luoni, Laura and Ljung, Karin and Bonza, Maria Cristina and Stavrinidou, Eleni and Costa, Alex},
month = feb,
year = {2023},
keywords = {glutamate receptor-like channels, implantable bioelectronic device, ligand-binding domain, long-distance Ca signaling},
}
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In systemic tissues, GLRs are needed to sustain the synthesis of jasmonic acid (JA) with the subsequent activation of JA-dependent signaling response required for the plant acclimation to the perceived stress. Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. Here, we report that in vivo, the amino-acid-dependent activation of the AtGLR3.3 channel and systemic responses require a functional ligand-binding domain. By combining imaging and genetics, we show that leaf mechanical injury, such as wounds and burns, as well as hypo-osmotic stress in root cells, induces the systemic apoplastic increase of L-glutamate (L-Glu), which is largely independent of AtGLR3.3 that is instead required for systemic cytosolic Ca2+ elevation. 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In systemic tissues, GLRs are needed to sustain the synthesis of jasmonic acid (JA) with the subsequent activation of JA-dependent signaling response required for the plant acclimation to the perceived stress. Even though the role of GLRs is well established, the mechanism through which they are activated remains unclear. Here, we report that in vivo, the amino-acid-dependent activation of the AtGLR3.3 channel and systemic responses require a functional ligand-binding domain. By combining imaging and genetics, we show that leaf mechanical injury, such as wounds and burns, as well as hypo-osmotic stress in root cells, induces the systemic apoplastic increase of L-glutamate (L-Glu), which is largely independent of AtGLR3.3 that is instead required for systemic cytosolic Ca2+ elevation. Moreover, by using a bioelectronic approach, we show that the local release of minute concentrations of L-Glu in the leaf lamina fails to induce any long-distance Ca2+ waves.},\n\tlanguage = {en},\n\turldate = {2023-03-23},\n\tjournal = {Current Biology},\n\tauthor = {Grenzi, Matteo and Buratti, Stefano and Parmagnani, Ambra Selene and Abdel Aziz, Ilaria and Bernacka-Wojcik, Iwona and Resentini, Francesca and Šimura, Jan and Doccula, Fabrizio Gandolfo and Alfieri, Andrea and Luoni, Laura and Ljung, Karin and Bonza, Maria Cristina and Stavrinidou, Eleni and Costa, Alex},\n\tmonth = feb,\n\tyear = {2023},\n\tkeywords = {glutamate receptor-like channels, implantable bioelectronic device, ligand-binding domain, long-distance Ca signaling},\n}\n\n","author_short":["Grenzi, M.","Buratti, S.","Parmagnani, A. S.","Abdel Aziz, I.","Bernacka-Wojcik, I.","Resentini, F.","Šimura, J.","Doccula, F. G.","Alfieri, A.","Luoni, L.","Ljung, K.","Bonza, M. 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