Chaperone AIP couples mTORC1 activation and catabolic metabolism during neonatal development
Authors list
Márta Korbonits Xian Wang Sayka Barry Chung Thong Lim Oniz Suleyman Stefano De Tito Nazia Uddin Maria Lillina Vignola Charlotte Hall Laura Perna J Paul Chapple Gabor Czibik Sian M Henson Valle Morales Katiuscia Bianchi Viðar Örn Eðvarðsson Kristján Ari Ragnarsson Viktoría Eir Kristinsdóttir Anne Debeer Yoeri Sleyp Rena Zinchenko Glenn Anderson Michael Duchen Kritarth Singh Chih Yao Chung Yu Yuan Sandip Patel Artem O Borovikov Hans Tómas Björnsson Hilde Van Esch Sharon Tooze Ezra Aksoy Caroline Brennan Oliver Haworth
Toggle all authors (34)
This article is a preprint. Preprints have not been peer-reviewed.
You can read more about preprints.
Abstract
To grow and divide cells must tightly coordinate anabolic programs with the availability of nutrients and growth factors. This balance is especially critical during postnatal development, when biosynthetic and energetic demands are high, and nutrient supply and neonates have to adapt to periods of fasting. These conditions place acute stress on the proteostasis network, making autophagy essential for nutrient recycling. We found that the chaperone aryl hydrocarbon receptor-interacting protein (AIP) supports both arms of this metabolic balance: promoting anabolic PI3K-AKT signaling for mTORC1 activation and enabling catabolic processes such as proteasomal degradation and autophagy. Loss of AIP causes a severe neonatal metabolic disorder, where affected infants fail to thrive postnatally. Our findings establish AIP as a central regulator of neonatal metabolic adaptation and cellular homeostasis.
Details
Archive
bioRxiv
Available online
Publication date
Keywords
Type of publication
