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

2016 ◽  
Vol 28 (9) ◽  
pp. 2026-2042 ◽  
Author(s):  
Inmaculada Couso ◽  
Bradley S. Evans ◽  
Jia Li ◽  
Yu Liu ◽  
Fangfang Ma ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Growth Control ◽  
Nutrient Sensing ◽  
Kinase Signaling ◽  
Inositol Polyphosphates ◽  
Tor Kinase

scholarly journals Homeostasis of branched-chain amino acids is critical for the activity of TOR signaling in Arabidopsis

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Pengfei Cao ◽  
Sang-Jin Kim ◽  
Anqi Xing ◽  
Craig A Schenck ◽  
Lu Liu ◽  
...  
Keyword(s):  
Amino Acids ◽  
Mammalian Cells ◽  
Branched Chain Amino Acids ◽  
Nutrient Sensing ◽  
Tor Signaling ◽  
Functional Connection ◽  
Primary Input ◽  
Tor Kinase ◽  
Arabidopsis Mutant ◽  
Branched Chain

The target of rapamycin (TOR) kinase is an evolutionarily conserved hub of nutrient sensing and metabolic signaling. In plants, a functional connection of TOR activation with glucose availability was demonstrated, while it is yet unclear whether branched-chain amino acids (BCAAs) are a primary input of TOR signaling as they are in yeast and mammalian cells. Here, we report on the characterization of an Arabidopsis mutant over-accumulating BCAAs. Through chemical interventions targeting TOR and by examining mutants of BCAA biosynthesis and TOR signaling, we found that BCAA over-accumulation leads to up-regulation of TOR activity, which causes reorganization of the actin cytoskeleton and actin-associated endomembranes. Finally, we show that activation of TOR is concomitant with alteration of cell expansion, proliferation and specialized metabolism, leading to pleiotropic effects on plant growth and development. These results demonstrate that BCAAs contribute to plant TOR activation and reveal previously uncharted downstream subcellular processes of TOR signaling.

scholarly journals Relationship between insulin sensitivity and gene expression in human skeletal muscle

2020 ◽  
Author(s):  
Hemang Parikh ◽  
Targ Elgzyri ◽  
Amra Alibegovic ◽  
Natalie Hiscock ◽  
Ola Ekström ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Insulin Sensitivity ◽  
Human Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Mammalian Target Of Rapamycin ◽  
Independent Study ◽  
Nutrient Sensing ◽  
Muscle Gene Expression

Abstract BackgroundInsulin resistance in skeletal muscle is a key feature of the pre-diabetic state, hypertension, dyslipidemia, cardiovascular diseases, and also predicts type 2 diabetes. However, the underlying molecular mechanisms are still poorly understood. MethodsTo explore these mechanisms, we related global skeletal muscle gene expression profiling of 38 non-diabetic men to physiological measures of insulin sensitivity. Results We identified 70 genes positively and 110 genes inversely correlated with insulin sensitivity in human skeletal muscle, identifying autophagy-related genes as positively correlated with insulin sensitivity. Replication in an independent study of 9 non-diabetic men resulted in 10 overlapping genes that strongly correlated with insulin sensitivity, including CPT1B and SIRT2 , involved in lipid metabolism, and FBXW5 that regulates mammalian target-of-rapamycin (mTOR) and autophagy. The expression of CPT1B , SIRT2 and FBXW5 was also positively correlated with the expression of key genes promoting the phenotype of an insulin sensitive myocyte e.g. PPARGC1A . ConclusionsThese data suggest that activation of genes involved in lipid metabolism, e.g. CPT1B and SIRT2 , and genes regulating autophagy and mTOR signaling, e.g. FBXW5 , are associated with increased insulin sensitivity in human skeletal muscle, reflecting a highly flexible nutrient sensing.

scholarly journals Protein Kinase A and Sch9 Cooperatively Regulate Induction of Autophagy in Saccharomyces cerevisiae

2007 ◽  
Vol 18 (10) ◽  
pp. 4180-4189 ◽  
Author(s):  
Tomohiro Yorimitsu ◽  
Shadia Zaman ◽  
James R. Broach ◽  
Daniel J. Klionsky
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Transcription Factors ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Signaling Pathways ◽  
Nutrient Sensing ◽  
Regulatory Mechanisms ◽  
Eukaryotic Cells ◽  
Tor Kinase ◽  
Kinase A

Autophagy is a highly conserved, degradative process in eukaryotic cells. The rapamycin-sensitive Tor kinase complex 1 (TORC1) has a major role in regulating induction of autophagy; however, the regulatory mechanisms are not fully understood. Here, we find that the protein kinase A (PKA) and Sch9 signaling pathways regulate autophagy cooperatively in yeast. Autophagy is induced in cells when PKA and Sch9 are simultaneously inactivated. Mutant alleles of these kinases bearing a mutation that confers sensitivity to the ATP-analogue inhibitor C3-1′-naphthyl-methyl PP1 revealed that autophagy was induced independently of effects on Tor kinase. The PKA–Sch9-mediated autophagy depends on the autophagy-related 1 kinase complex, which is also essential for TORC1-regulated autophagy, the transcription factors Msn2/4, and the Rim15 kinase. The present results suggest that autophagy is controlled by the signals from at least three partly separate nutrient-sensing pathways that include PKA, Sch9, and TORC1.

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