The TOR complex controls ATP levels to regulate actin cytoskeleton dynamics in Arabidopsis
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Energy is essential for all cellular functions in a living organism. How cells coordinate their physiological processes with energy status and availability is thus an important question. The turnover of actin cytoskeleton between its monomeric and filamentous forms is a major energy drain in eukaryotic cells. However, how actin dynamics are regulated by ATP levels remain largely unknown in plant cells. Here, we observed that seedlings with impaired functions of target of rapamycin complex 1 (TORC1), either by mutation of the key component, RAPTOR1B, or inhibition of TOR activity by specific inhibitors, displayed reduced sensitivity to actin cytoskeleton disruptors compared to their controls. Consistently, actin filament dynamics, but not organization, were suppressed in TORC1-impaired cells. Subcellular localization analysis and quantification of ATP concentration demonstrated that RAPTOR1B localized at cytoplasm and mitochondria and that ATP levels were significantly reduced in TORC1-impaired plants. Further pharmacologic experiments showed that the inhibition of mitochondrial functions led to phenotypes mimicking those observed in raptor1b mutants at the level of both plant growth and actin dynamics. Exogenous feeding of adenine could partially restore ATP levels and actin dynamics in TORC1-deficient plants. Thus, these data support an important role for TORC1 in coordinating ATP homeostasis and actin dynamics in plant cells.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | e2122969119 |
| Tidsskrift | Proceedings of the National Academy of Sciences of the United States of America |
| Vol/bind | 119 |
| Udgave nummer | 38 |
| Antal sider | 12 |
| ISSN | 0027-8424 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:
We acknowledge the Experimental Technology Center for Life Sciences, Beijing Normal University, and are grateful to Dr. Xiaoyan Zhang for technical support. We thank Prof. Markus Schwarzlander (University of M€unster) for the ATeam1.03-nD/nA line, Prof. Yan Xiong (Fujian Agriculture and Forestry University) for the tor-es lines and the anti-S6K antibody, and Prof. Yuling Jiao (Peking University) for support in the protoplast transformation experiment. This work was supported by the National Natural Science Foundation of China (32070194 and 31870174 to Y.Z., and 32100279 to T.W.). S.P. acknowledges the financial aid from ARC Discovery (DP19001941), Villum Investigator (Project ID: 25915), DNRF Chair (DNRF155), and Novo Nordisk Laureate (NNF19OC0056076) grants. H.E.M. acknowledges funding from the Canada Research Chairs program (Canada Research Chair in Plant Cell Biology) and a Canadian Natural Sciences and Engineering Council Discovery Grant (NSERC DG 2020-05959).
Funding Information:
ACKNOWLEDGMENTS. We acknowledge the Experimental Technology Center for Life Sciences, Beijing Normal University, and are grateful to Dr. Xiaoyan Zhang for technical support. We thank Prof. Markus Schwarzlander (University of M€unster) for the ATeam1.03-nD/nA line, Prof. Yan Xiong (Fujian Agriculture and Forestry University) for the tor-es lines and the anti-S6K antibody, and Prof. Yuling Jiao (Peking University) for support in the protoplast transformation experiment. This work was supported by the National Natural Science Foundation of China (32070194 and 31870174 to Y.Z., and 32100279 to T.W.). S.P. acknowledges the financial aid from ARC Discovery (DP19001941), Villum Investigator (Project ID: 25915), DNRF Chair (DNRF155), and Novo Nordisk Laureate (NNF19OC0056076) grants. H.E.M. acknowledges funding from the Canada Research Chairs program (Canada Research Chair in Plant Cell Biology) and a Canadian Natural Sciences and Engineering Council Discovery Grant (NSERC DG 2020-05959).
Publisher Copyright:
Copyright © 2022 the Author(s). Published by PNAS.
ID: 333307694