Abstract
Target of Rapamycin (TOR) signaling is an important regulator in multiple organisms including yeast, plants, and animals. However, the TOR signaling in plants is much less understood as compared to that in yeast and animals. TOR kinase can be efficiently suppressed by rapamycin in the presence of functional FK506 Binding Protein 12 KD (FKBP12) in yeast and animals. In most examined higher plants rapamycin fails to inhibit TOR kinase due to the non-functional FKBP12. Here we find that tomato plants showed obvious growth inhibition when treated with rapamycin and the inhibitory phenotype is similar to suppression of TOR causing by active-site TOR inhibitors (asTORis) such as KU63794, AZD8055, and Torin1. The chemical genetic assays using TOR inhibitors and heterologous expressing SlFKBP12 in Arabidopsis indicated that the TOR signaling is functional in tomato. The protein gel shifting and TOR inhibitors combination assays showed that SlFKBP12 can mediate the interaction between rapamycin and TOR. Furthermore, comparative expression profile analysis between treatments with rapamycin and KU63794 identified highly overlapped Differentially Expressed Genes (DEGs) which are involved in many anabolic and catabolic processes, such as photosynthesis, cell wall restructuring, and senescence in tomato. These observations suggest that SlFFBP12 is functional in tomato. The results provided basic information of TOR signaling in tomato, and also some new insights into how TOR controls plant growth and development through reprogramming the transcription profiles.
Highlights
Target of Rapamycin (TOR) is a Ser/Thr protein kinase that was first discovered in budding yeast (Saccharonmyces cerevisiae) by a genetic selection for screening the mutants which are insensitive to rapamycin (Heitman et al, 1991)
We found that the growth of tomato plants was retarded by rapamycin, indicating that SlFKBP12 may be functional in tomato
The results shows that a single TOR homolog gene (Solyc01g106770) locates on chromosome 1 of tomato (Figure 1A)
Summary
Target of Rapamycin (TOR) is a Ser/Thr protein kinase that was first discovered in budding yeast (Saccharonmyces cerevisiae) by a genetic selection for screening the mutants which are insensitive to rapamycin (Heitman et al, 1991). The rapamycin-FKBP12 complex further binds to FRB domain of TOR to form rapamycin-FKBP12-TOR ternary complex, resulting in partial abolishment of TOR kinase activity (Heitman et al, 1991; Chiu et al, 1994; Sabatini et al, 1994). The accumulated documents showed that TOR is a central coordinator of energy, nutrient, and stress signaling networks from yeast to mammals and plants (Henriques et al, 2014; Rexin et al, 2015; Xiong and Sheen, 2015; Dobrenel et al, 2016). Rapamycin-sensitive TORC1 plays a major role in cell growth, development, and proliferation in a temporal manner, while rapamycin-resistant TORC2 seems to spacially regulate the development of cell cytoskeleton (Loewith et al, 2002; Wang and Proud, 2009; Takahara and Maeda, 2013; Xiong and Sheen, 2014)
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