The nuclear cofactor DOR regulates autophagy in mammalian and Drosophila cells

Caroline Mauvezin, Meritxell Orpinell, Víctor A. Francis, Francisco Mansilla, Jordi Duran, Vicent Ribas, Manuel Palacín, Patricia Boya, Aurelio A. Teleman, Antonio Zorzano

Research output: Indexed journal article Articlepeer-review

60 Citations (Scopus)


The regulation of autophagy in metazoans is only partly understood, and there is a need to identify the proteins that control this process. The diabetes-and obesity-regulated gene (DOR), a recently reported nuclear cofactor of thyroid hormone receptors, is expressed abundantly in metabolically active tissues such as muscle. Here, we show that DOR shuttles between the nucleus and the cytoplasm, depending on cellular stress conditions, and re-localizes to autophagosomes on autophagy activation. We demonstrate that DOR interacts physically with autophagic proteins Golgi-associated ATPase enhancer of 16 kDa (GATE16) and microtubule-associated protein 1A/1B-light chain 3. Gain-of-function and loss-of-function studies indicate that DOR stimulates autophagosome formation and accelerates the degradation of stable proteins. CG11347, the DOR Drosophila homologue, has been predicted to interact with the Drosophila Atg8 homologues, which suggests functional conservation in autophagy. Flies lacking CG11347 show reduced autophagy in the fat body during pupal development. All together, our data indicate that DOR regulates autophagosome formation and protein degradation in mammalian and Drosophila cells.

Original languageEnglish
Pages (from-to)37-44
Number of pages8
JournalEMBO Reports
Issue number1
Publication statusPublished - Jan 2010
Externally publishedYes


  • Fat body
  • GATE16
  • LC3
  • Nuclear co-regulator
  • Protein degradation


Dive into the research topics of 'The nuclear cofactor DOR regulates autophagy in mammalian and Drosophila cells'. Together they form a unique fingerprint.

Cite this