Volume 253, Issue 2 pp. 207-213

Mitochondrial dysfunction enhances Gal4-dependent transcription

Branka Jeličić

Branka Jeličić

Department of Molecular Biology, Ru?er Bošković Institute, Bijenička 54, 10000 Zagreb, Croatia

These authors contributed equally to this work.

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Ana Traven

Ana Traven

Department of Molecular Biology, Ru?er Bošković Institute, Bijenička 54, 10000 Zagreb, Croatia

These authors contributed equally to this work.

St. Vincent's Institute, 9 Princes Street, Fitzroy, Vic. 3065, Australia.

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Vedrana Filić

Vedrana Filić

Department of Molecular Biology, Ru?er Bošković Institute, Bijenička 54, 10000 Zagreb, Croatia

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Mary Sopta

Corresponding Author

Mary Sopta

Department of Molecular Biology, Ru?er Bošković Institute, Bijenička 54, 10000 Zagreb, Croatia

*Corresponding author. Tel.: +385 1 4560 948; fax: +385 1 4561 177., E-mail address: [email protected]Search for more papers by this author
First published: 09 January 2006

St. Vincent's Institute, 9 Princes Street, Fitzroy, Vic. 3065, Australia.

Edited by M. Jacquet

Abstract

Mitochondrial dysfunction has been shown to elicit broad effects on nuclear gene expression. We show here that transcription dependent on the prototypical acidic activator Gal4 is responsive to mitochondrial dysfunction. In cells with no mitochondrial DNA, Gal4-dependent gene expression is elevated. A minimal Gal4 activator containing the DNA binding and activation domain is sufficient for this response. Transcription dependent on a fusion of Gal4 to a heterologous DNA binding domain is similarly elevated in a mitochondrial mutant. Analysis of different Gal4-dependent promoters and gel mobility shift assays suggest that the effect of mitochondrial dysfunction on Gal4 activity is related to increased DNA binding to the cognate Gal4 element. Given that fermentation is the only means to obtain energy in respiratory deficient cells, it is possible that higher Gal4 activity in cells with dysfunctional mitochondria works to promote more efficient fermentation of galactose.

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