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Atg6 promotes organismal health by suppression of cell stress and inflammation.
Shen, James L; Doherty, Johnna; Allen, Elizabeth; Fortier, Tina M; Baehrecke, Eric H.
Afiliación
  • Shen JL; Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA.
  • Doherty J; Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA.
  • Allen E; Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA.
  • Fortier TM; Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA.
  • Baehrecke EH; Department of Molecular, Cell and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA. eric.baehrecke@umassmed.edu.
Cell Death Differ ; 29(11): 2275-2287, 2022 11.
Article en En | MEDLINE | ID: mdl-35523956
ABSTRACT
Autophagy targets cytoplasmic materials for degradation, and influences cell health. Alterations in Atg6/Beclin-1, a key regulator of autophagy, are associated with multiple diseases. While the role of Atg6 in autophagy regulation is heavily studied, the role of Atg6 in organism health and disease progression remains poorly understood. Here, we discover that loss of Atg6 in Drosophila results in various alterations to stress, metabolic and immune signaling pathways. We find that the increased levels of circulating blood cells and tumor-like masses in atg6 mutants vary depending on tissue-specific function of Atg6, with contributions from intestine and hematopoietic cells. These phenotypes are suppressed by decreased function of macrophage and inflammatory response receptors crq and drpr. Thus, these findings provide a basis for understanding how Atg6 systemically regulates cell health within multiple organs, and highlight the importance of Atg6 in inflammation to organismal health.
Asunto(s)

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Autofagia / Transducción de Señal Límite: Humans Idioma: En Revista: Cell Death Differ Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Autofagia / Transducción de Señal Límite: Humans Idioma: En Revista: Cell Death Differ Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos