期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2022
卷号：119
期号：38
DOI：10.1073/pnas.2122969119
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Significance
Cells must overcome energy shortage, and the ability to do so determines their fate. The ability of cells to coordinate their cellular activities and energy status is therefore important for all living organisms. One of the major energy drains in eukaryotic cells is the constant turnover of the actin cytoskeleton, which consumes ATP during the cycle of polymerization and depolymerization. We report that the TOR complex, a master regulatory hub that integrates cellular energy information to coordinate cell growth and metabolism, controls cellular ATP levels in plant cells. We further elucidate that low ATP levels cause reduced actin dynamics in plant cells. These findings provide insight into how plant cells handle low energy situations.
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.
