Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. Signal., 16 April 2013
Vol. 6, Issue 271, p. ec86
[DOI: 10.1126/scisignal.2004244]

EDITORS' CHOICE

Plant Biology Transcriptional Reprogramming by TOR

Nancy R. Gough

Science Signaling, AAAS, Washington, DC 20005, USA

As seeds germinate and form their first leaves, seedlings switch from heterotrophic growth that relies on maternal nutrient stores in the seed to photoautotrophic growth that relies on photosynthesis. Meristems are the source of the stem and progenitor cells that divide and differentiate to produce roots, leaves, and flowers. Xiong et al. found that after glucose stores had been depleted during germination, root growth and S-phase entry was stimulated by providing light and increased CO2 to promote photosynthesis or by supplying exogenous glucose. Inhibition of glycolysis or mitochondrial oxidative phosphorylation prevented photosynthetic or glucose-mediated reactivation of the root meristem. The addition of rapamycin to inhibit the kinase TOR or the use of an inducible tor mutant showed that TOR activity was required for the glucose-mediated reactivation of the root meristem and root growth. Analysis of the stem cell population in the root meristem and the responsiveness to cytokinin and auxin signaling showed that rapamycin or a mitochondrial inhibitor did not compromise stem cell maintenance or activation of hormone-responsive genes, suggesting that there are distinct energy and metabolic processes supporting stem cell activation and stem cell maintenance. Transcriptional profiling of wild-type and inducible tor mutant seedlings at the photoautotrophic transition checkpoint revealed that glucose regulated more than 2000 genes in a TOR-dependent manner. In addition to the expected regulation of genes involved in translation and anabolic processes, the glucose-TOR signaling pathway also stimulated genes involved in root growth, oxidative phosphorylation, and glycolysis—and repressed genes that inhibit the root meristem or that promote germination or survival in prolonged darkness. Targeted investigation of genes implicated in regulation of the cell cycle showed that glucose-TOR signaling stimulated E2Fa target genes. E2F transcription factors are conserved proteins that promote S phase entry and DNA replication and are stimulated by the cyclin-dependent kinase (CDK)–retinoblastoma-related (RBR) pathway. In vitro kinase assays with TOR immunoprecipitated from plants showed that E2Fa was phosphorylated by TOR, and assays with truncation and point mutants suggested that there were multiple TOR phosphorylation sites in the N-terminal 80-residue regulatory domain of E2Fa. The transcriptional activity of E2Fa was abolished by deletion of this 80-residue domain, but not the domain targeted by the CDK-RBR pathway. Consistent with a key role for E2Fa in activation of the root meristem, glucose-mediated activation of root growth and root meristem expansion and cell cycle division was impaired in an e2fa mutant. This study expands the functions of TOR signaling to include transcriptional regulation and identifies the transcription factor E2Fa as a direct target of TOR in this process.

Y. Xiong, M. McCormack, L. Li, Q. Hall, C. Xiang, J. Sheen, Glucose–TOR signalling reprograms the transcriptome and activates meristems. Nature 496, 181–186 (2013). [PubMed]

Citation: N. R. Gough, Transcriptional Reprogramming by TOR. Sci. Signal. 6, ec86 (2013).


To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882