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vip1-1 vip1-1 TAP TAP AU 15 * * Plant Cell Advance Publication. Published on September 7, 2016, doi:10.1105/tpc.16.00702 * AU 0.01 5 0 0 Carbon metabolism in Chlamydomonas: inositol polyphosphates and TORInsP signaling center IP6 stage IP3 3 InsP IP4take IP5 4 InsP5 InsP 6 TOR (TARGET OF RAPAMYCIN) kinase is a conserved regulator of cell growth that directs protein synthesis, metabolic outputs, and other growth-related processes in response to developmental and external nutrient cues (reviewed in Rexin et al., 2015). In Arabidopsis, glucose activates TOR and stimulates cell division in root meristems (Xiong et al., 2013); however, little is known about the downstream targets of TOR and how TOR signaling integrates with other metabolic pathways to control carbon allocation and growth in photosynthetic organisms. In a Breakthrough Report, Couso et al. (2016) reveal a link between TOR signaling and inositol polyphosphates in the model unicellular green alga Chlamydomonas reinhardtii, which toggles between phototrophic (obtaining energy from light sources), heterotrophic (obtaining energy from carbon sources), and mixotrophic (obtaining energy from light and carbon sources) modes of growth. To decipher the TOR signaling network in Chlamydomonas, the authors screened for mutants that were hypersensitive to the antibiotic rapamycin (RAP), an established inhibitor of TOR in this organism and others. They identified the vip1-1 mutant, which harbors a mutation in a gene predicted to encode a diphosphoinositol phosphate kinase that pyrophosphorylates phytic acid to produce the inositol phosphate (InsP)7 and InsP8 signaling molecules. To test if the vip11 mutant has defects in InsP7 and InsP8 accumulation, the authors developed a sensitive liquid chromatography and mass spectrometry (LC-MS/MS)-based method for detecting these molecules, which are present in eukaryotic cells at such low concentrations that they are difficult to detect. The vip1-1 mutant indeed had reduced levels of InsP7 and InsP8, accumulating just 20-30% of wildtype levels. Therefore, VIP1 appears to function in InsP7 and InsP8 biosynthesis, linking TOR signaling to InsPs. To investigate the relationship between TOR and InsPs, the authors next examined the effect of inhibiting TOR signaling. Growth of both wild-type and vip1-1 cells was blocked soon after RAP treatment, and wild-type, but not vip1-1, cells acclimated to RAP by 12 h 0.03 0.02 10 IN BRIEF 7 IP7 InsP 7 IP8 InsP 8 IP8 InsP8 after treatment. Interestingly, InsP7 and InsP8 nutrients B levels dipped in both wild-type and vip1-1 cells acetate after treatment with RAP and gradually increased in the wild-type cells as they VIP1 ? acclimated to the treatment. These findings show that inhibiting TOR signaling alters InsP7 and InsP8 levels and suggest that the InsPs TOR InsPs function downstream of TOR signaling. In a surprising twist, the authors found ? that RAP completely blocked growth under mixotrophic conditions (in the presence of light and acetate), but that phototrophic conditions relieved RAP hypersensitivity. This prompted the authors to examine whether the two main cell growth TAGs carbon pools present in Chlamydomonas, TCA cycle starch and neutral lipids, are affected by the vip1-1 mutation. No Figure differences in InsP starch 8. TOR and interact to control cell growth, acetate metabolism and neutral lipid accumu of intracellular InsP levels by carbon source. Graphs labeled as in Fig. 3 showing Model linking carbon source (acetate) with InsP levels fr content were observedModulation between vip1-1 and (WT) and vip1-1 growing in the presence or absence of acetate (TAP and TP, respectively). B. Summary fi TOR kinase and inositol phosphates. InsPs wild-type cells. However, in contrast to wildproposed relationships between carbon source (acetate), TOR, and InsPs produced by VIP1. Black arrows interactions shown in this work (TOR signalingby andVIP1 carbon source levels) while dashed gray act withinfluence TOR toInsP block TAG type cells, which typically only exhibit lipid produced question marks are possibilities that were not directly tested. TOR and the InsPs produced by VIP1 synerg accumulation and stimulate cell growth. Black TAG accumulation (repression bar) and promote cell growth (arrow). bodies under nitrogen-starvation conditions, vip1-1 cells contained lipids in both the lines show interactions deduced from this presence and absence of nitrogen, and the study and gray dashed lines show interactions that remain to be confirmed. [Adapted from mutant contained higher levels of total lipids Couso et al. (2016), Figure 8B.] than the wild type. Further analysis showed that vip1-1 constitutively accumulated triacylglycerols. In addition, the mutant had REFERENCES reduced levels of some Krebs cycle metabolites (citrate, aconitate, and malate) Couso, I., Evans, B.S., Li, J., Liu, Y., Ma, F., under mixotrophic conditions, and elevated Diamond, S., Allen, D.K., and Umen, J.G. levels of others (succinate, fumarate, and (2016). Synergism between Inositol aconitate) under phototrophic conditions, Polyphosphates and TOR Kinase Signaling further linking VIP1 with metabolic flux. in Nutrient Sensing, Growth Control and Finally, the authors showed that InsP7 and Lipid Metabolism in Chlamydomonas. Plant InsP8 profiles change dramatically in cell 10.1105/tpc.15.00351. response to acetate, supporting the notion Rexin, D., Meyer, C., Robaglia, C., and Veit, that InsP7 and InsP8 are signals that respond B. (2015). TOR signalling in plants. to and/or control carbon metabolism. Biochem. J. 470: 1–14. This work (summarized in figure) is likely Xiong, Y., McCormack, M., Li, L., Hall, Q., to open new research frontiers in carbon Xiang, C., and Sheen, J. (2013). Glucosemetabolism and partitioning in photosynthetic TOR signalling reprograms the cells, and could have exciting applications in transcriptome and activates meristems. the field of biofuel production. Nature 496: 181–6. Kathleen L. Farquharson Science Editor [email protected] http://orcid.org/0000-0002-8032-0041 ©2016 American Society of Plant Biologists. All Rights Reserved Carbon metabolism in Chlamydomonas: inositol polyphosphates and TOR signaling take center stage Kathleen L Farquharson Plant Cell; originally published online September 7, 2016; DOI 10.1105/tpc.16.00702 This information is current as of June 17, 2017 Supplemental Data /content/suppl/2016/09/09/tpc.16.00702.DC1.html Permissions https://www.copyright.com/ccc/openurl.do?sid=pd_hw1532298X&issn=1532298X&WT.mc_id=pd_hw1532298X eTOCs Sign up for eTOCs at: http://www.plantcell.org/cgi/alerts/ctmain CiteTrack Alerts Sign up for CiteTrack Alerts at: http://www.plantcell.org/cgi/alerts/ctmain Subscription Information Subscription Information for The Plant Cell and Plant Physiology is available at: http://www.aspb.org/publications/subscriptions.cfm © American Society of Plant Biologists ADVANCING THE SCIENCE OF PLANT BIOLOGY