4.6 Article

Caenorhabditis elegans development requires mitochondrial function in the nervous system

Journal

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 319, Issue 4, Pages 1307-1313

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2004.05.108

Keywords

Caenorhabditis elegans; complex 1; mitochondrial disease; dauer; larval arrest; cell non-autonomous; tissue specificity

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The mitochondrial respiratory chain (MRC) supplies the majority of the energy requirements of most eucaryotic cells. A null mutation in the Caenorhabditis elegans nuo-1 gene encoding a subunit of complex I (NADH-ubiquinone oxidoreductase) is lethal, leading to a developmental arrest at the third larval stage. To identify the tissues that regulate development in response to mitochondrial dysfunction, we restored nuo-1 expression with tissue-specific promoters. Only expression of nuo-1 ubiquitously or in the nervous system supported development to the adult stage. Pharyngeal expression of nuo-1 allowed development to proceed to the fourth larval stage. Expression of nuo-1 in the body muscles or in the germline had no effect. Furthermore, only ubiquitous or nervous system expression of nuo-1 allowed exit from the dauer state. Our results indicate that MRC function in the nervous system is needed to send and receive signals that control larval development and exit from dauer. (C) 2004 Elsevier Inc. All rights reserved.

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