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Biochem Biophys Res Commun. 2015 Nov 13;467(2):389-94. doi: 10.1016/j.bbrc.2015.09.143. Epub 2015 Sep 30.

Caenorhabditis elegans ATAD-3 modulates mitochondrial iron and heme homeostasis.

Author information

1
Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Heinrich-Heine-University, Moorenstr. 5, 40225 Düsseldorf, Germany.
2
Institute of Clinical Chemistry and Laboratory Diagnostic, Medical Faculty, Heinrich-Heine-University and the IUF- Leibniz Research Institute for Environmental Medicine, Auf'm Hennekamp 50, 40225 Düsseldorf, Germany.
3
Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Heinrich-Heine-University, Moorenstr. 5, 40225 Düsseldorf, Germany. Electronic address: felix.distelmaier@med.uni-duesseldorf.de.

Abstract

ATAD3 (ATPase family AAA domain-containing protein 3) is a mitochondrial protein, which is essential for cell viability and organismal development. ATAD3 has been implicated in several important cellular processes such as apoptosis regulation, respiratory chain function and steroid hormone biosynthesis. Moreover, altered expression of ATAD3 has been associated with several types of cancer. However, the exact mechanisms underlying ATAD3 effects on cellular metabolism remain largely unclear. Here, we demonstrate that Caenorhabditis elegans ATAD-3 is involved in mitochondrial iron and heme homeostasis. Knockdown of atad-3 caused mitochondrial iron- and heme accumulation. This was paralleled by changes in the expression levels of several iron- and heme-regulatory genes as well as an increased heme uptake. In conclusion, our data indicate a regulatory role of C. elegans ATAD-3 in mitochondrial iron and heme metabolism.

KEYWORDS:

Heme; Iron; Metabolism; Mitochondria; Oxidative phosphorylation

PMID:
26427876
DOI:
10.1016/j.bbrc.2015.09.143
[Indexed for MEDLINE]

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