Transcriptional regulation of Annexin A2 promotes starvation-induced autophagy

Kevin Moreau, Ghita Ghislat, Warren Hochfeld, Maurizio Renna, Eszter Zavodszky, Gautam Runwal, Claudia Puri, Shirley Lee, Farah Siddiqi, Fiona M. Menzies, Brinda Ravikumar and David C. Rubinsztein ()
Additional contact information
Kevin Moreau: Cambridge Institute for Medical Research
Ghita Ghislat: Cambridge Institute for Medical Research
Warren Hochfeld: Cambridge Institute for Medical Research
Maurizio Renna: Cambridge Institute for Medical Research
Eszter Zavodszky: Cambridge Institute for Medical Research
Gautam Runwal: Cambridge Institute for Medical Research
Claudia Puri: Cambridge Institute for Medical Research
Shirley Lee: Cambridge Institute for Medical Research
Farah Siddiqi: Cambridge Institute for Medical Research
Fiona M. Menzies: Cambridge Institute for Medical Research
Brinda Ravikumar: Cambridge Institute for Medical Research
David C. Rubinsztein: Cambridge Institute for Medical Research

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract Autophagy is an important degradation pathway, which is induced after starvation, where it buffers nutrient deprivation by recycling macromolecules in organisms from yeast to man. While the classical pathway mediating this response is via mTOR inhibition, there are likely to be additional pathways that support the process. Here, we identify Annexin A2 as an autophagy modulator that regulates autophagosome formation by enabling appropriate ATG9A trafficking from endosomes to autophagosomes via actin. This process is dependent on the Annexin A2 effectors ARP2 and Spire1. Annexin A2 expression increases after starvation in cells in an mTOR-independent fashion. This is mediated via Jun N-terminal kinase activation of c-Jun, which, in turn, enhances the trans-activation of the Annexin A2 promoter. Annexin A2 knockdown abrogates starvation-induced autophagy, while its overexpression induces autophagy. Hence, c-Jun-mediated transcriptional responses support starvation-induced autophagy by regulating Annexin A2 expression levels.

Date: 2015
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/ncomms9045 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9045

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms9045

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().