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Cell Mol Life Sci. 2019 Jan 23. doi: 10.1007/s00018-019-03015-6. [Epub ahead of print]

The SEACIT complex is involved in the maintenance of vacuole-mitochondria contact sites and controls mitophagy.

Author information

1
CNRS, UMR 8126, Université Paris-Sud 11, Institut Gustave Roussy, 114, rue Edouard Vaillant, 94805, Villejuif, France.
2
CNRS, IBGC, UMR 5095, 1, rue Camille Saint-Saens, 33000, Bordeaux, France.
3
Université de Bordeaux, IBGC, 1, rue Camille Saint-Saens, 33000, Bordeaux, France.
4
CNRS, UMR 8126, Université Paris-Sud 11, Institut Gustave Roussy, 114, rue Edouard Vaillant, 94805, Villejuif, France. svetlana.dokudovskaya@igr.fr.

Abstract

The major signaling pathway that regulates cell growth and metabolism is under the control of the target of rapamycin complex 1 (TORC1). In Saccharomyces cerevisiae the SEA complex is one of the TORC1 upstream regulators involved in amino acid sensing and autophagy. Here, we performed analysis of the expression, interactions and localization of SEA complex proteins under different conditions, varying parameters such as sugar source, nitrogen availability and growth phase. Our results show that the SEA complex promotes mitochondria degradation either by mitophagy or by general autophagy. In addition, the SEACIT subcomplex is involved in the maintenance of the vacuole-mitochondria contact sites. Thus, the SEA complex appears to be an important link between the TORC1 pathway and regulation of mitochondria quality control.

KEYWORDS:

Autophagy; Membrane contact sites; Mitochondria; Mitophagy; SEA complex; TORC1; Vacuole

PMID:
30673821
DOI:
10.1007/s00018-019-03015-6

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