Synergism between Inositol Polyphosphates and TOR Kinase Signaling in Nutrient Sensing, Growth Control, and Lipid Metabolism in Chlamydomonas

被引：69

作者：

Couso, Inmaculada ^{[1
,4
]}

Evans, Bradley S. ^{[1
]}

Li, Jia ^{[1
]}

Liu, Yu ^{[1
]}

Ma, Fangfang ^{[1
,5
]}

Diamond, Spencer ^{[2
]}

Allen, Doug K. ^{[1
,3
]}

Umen, James G. ^{[1
]}

机构：

[1] Donald Danforth Plant Sci Ctr, St Louis, MO 63132 USA

[2] Univ Calif Berkeley, Earth & Planetary Sci, Berkeley, CA 94720 USA

[3] USDA, Agr Res Serv, St Louis, MO 63132 USA

[4] Inst Bioquim Vegetal & Fotosintesis, Seville 41092, Spain

[5] Univ Florida, Gainesville, FL 32611 USA

来源：

PLANT CELL | 2016年 / 28卷 / 09期

基金：

美国国家科学基金会;

关键词：

FLUX BALANCE ANALYSIS; CYCLIC ELECTRON FLOW; GREEN-ALGA; TRIACYLGLYCEROL ACCUMULATION; NITROGEN DEPRIVATION; PLANT-GROWTH; INSERTIONAL MUTAGENESIS; MAMMALIAN PROTEIN; CARBON METABOLISM; RAPAMYCIN KINASE;

D O I：

10.1105/tpc.16.00351

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The networks that govern carbon metabolism and control intracellular carbon partitioning in photosynthetic cells are poorly understood. Target of Rapamycin (TOR) kinase is a conserved growth regulator that integrates nutrient signals and modulates cell growth in eukaryotes, though the TOR signaling pathway in plants and algae has yet to be completely elucidated. We screened the unicellular green alga Chlamydomonas reinhardtii using insertional mutagenesis to find mutants that conferred hypersensitivity to the TOR inhibitor rapamycin. We characterized one mutant, vip1-1, that is predicted to encode a conserved inositol hexakisphosphate kinase from the VIP family that pyrophosphorylates phytic acid (InsP(6)) to produce the low abundance signaling molecules InsP(7) and InsP(8). Unexpectedly, the rapamycin hypersensitive growth arrest of vip1-1 cells was dependent on the presence of external acetate, which normally has a growth-stimulatory effect on Chlamydomonas. vip1-1 mutants also constitutively overaccumulated triacylglycerols (TAGs) in a manner that was synergistic with other TAG inducing stimuli such as starvation. vip1-1 cells had reduced InsP(7) and InsP(8), both of which are dynamically modulated in wild-type cells by TOR kinase activity and the presence of acetate. Our data uncover an interaction between the TOR kinase and inositol polyphosphate signaling systems that we propose governs carbon metabolism and intracellular pathways that lead to storage lipid accumulation.

引用

页码：2026 / 2042

页数：17