Cell Signalling and Ageing

May 20th, 2015
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Yeast, C. elegans, Drosophila, mammals increase their lifespan when they have mutations that lower glucose or Insulin/IGF signalling. Calorie restriction (not malnutrition) improves life span, nutrient excess causes obesity and metabolic problems that can shorten life.

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SCRA.21 AB.04 AGEING BIOLOGY 04 Cell Signalling and AgeingKey objectives - Understand the conserved nature of much of the Insulin/Igf1 signalling pathway and its role in nutrient-sensing- Describe Calorie Restriction as an inducer of increased lifespan - Explain the possible mechanisms of DR/CR including TOR, SIRTs and mitochondrial biologyYeast, C. elegans, Drosophila, mammals increase their lifespan when they have mutations that lower glucose or Insulin/IGF signalling. Calorie restriction (not malnutrition) improves life span, nutrient excess causes obesity and metabolic problems that can shorten life. CR may reduce metabolism thereby reducing damage load and so cells live longer. CR upregulates stress responses that produce more ROS scavengers making the cells more stress resistant. Is there a cellular nutrient sensor that regulates ageing? CELL SIGNALLINGNUTRIENT SENSING Glucose sensing in yeast GPR1 is a transmembrane G-coupled receptor that when bound to glucose initiates a signalling cascade that produces transcription factors that changes the cells gene expression profile. GPR1 signalling indicates that there is glucose available. MNS2/MNS4 are TFs that downregulate some gene activity and upregulates stress resistance. It may be that IGF signalling delays ageings deleterious effects instead of necessarily increasing lifespan. PKA is a kinase that when activated phosphorylates and inactivates transcription factors. Mutation

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