Degradation of arouser by endosomal microautophagy is essential for adaptation to starvation in Drosophila.
Anne-Claire JacominRaksha GohelZunoon HussainAgnes VargaTamas MaruzsMark EddisonMargaux SicaAshish JainKevin G MoffatTerje JohansenAndreas JennyGábor JuhászIoannis P NezisPublished in: Life science alliance (2020)
Hunger drives food-seeking behaviour and controls adaptation of organisms to nutrient availability and energy stores. Lipids constitute an essential source of energy in the cell that can be mobilised during fasting by autophagy. Selective degradation of proteins by autophagy is made possible essentially by the presence of LIR and KFERQ-like motifs. Using in silico screening of Drosophila proteins that contain KFERQ-like motifs, we identified and characterized the adaptor protein Arouser, which functions to regulate fat storage and mobilisation and is essential during periods of food deprivation. We show that hypomorphic arouser mutants are not satiated, are more sensitive to food deprivation, and are more aggressive, suggesting an essential role for Arouser in the coordination of metabolism and food-related behaviour. Our analysis shows that Arouser functions in the fat body through nutrient-related signalling pathways and is degraded by endosomal microautophagy. Arouser degradation occurs during feeding conditions, whereas its stabilisation during non-feeding periods is essential for resistance to starvation and survival. In summary, our data describe a novel role for endosomal microautophagy in energy homeostasis, by the degradation of the signalling regulatory protein Arouser.
Keyphrases
- cell death
- adipose tissue
- human health
- oxidative stress
- endoplasmic reticulum stress
- signaling pathway
- fatty acid
- single cell
- transcription factor
- mental health
- electronic health record
- protein protein
- insulin resistance
- risk assessment
- molecular docking
- big data
- machine learning
- binding protein
- metabolic syndrome
- artificial intelligence
- weight loss
- gram negative
- drug induced