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,
Paola Catanuto,1,
Flavia Fontanesi,2,3
Carmen Rios,1
Natalie Sanchez,1
Antoni Barrientos,2,3 and
Fulvia Verde1*
Department of Molecular and Cellular Pharmacology,1 Department of Neurology and Department of Biochemistry and Molecular Biology,2 The John T. MacDonald Center for Medical Genetics, University of Miami School of Medicine, P.O. Box 016129, Miami, Florida 33101-61293
Received 19 February 2007/ Accepted 12 December 2007
Maintenance of cell morphology is essential for normal cell function. For eukaryotic cells, a growing body of recent evidence highlights a close interdependence between mitochondrial function, the cytoskeleton, and cell cycle control mechanisms; however, the molecular details of this interconnection are still not completely understood. We have identified a novel protein, Bot1p, in the fission yeast Schizosaccharomyces pombe. The bot1 gene is essential for cell viability. bot1
mutant cells expressing lower levels of Bot1p display altered cell size and cell morphology and a disrupted actin cytoskeleton. Bot1p localizes to the mitochondria in live cells and cofractionates with purified mitochondrial ribosomes. Reduced levels of Bot1p lead to mitochondrial fragmentation, decreased mitochondrial protein translation, and a corresponding decrease in cell respiration. Overexpression of Bot1p results in cell cycle delay, with increased cell size and cell length and enhanced cell respiration rate. Our results show that Bot1p has a novel function in the control of cell respiration by acting on the mitochondrial protein synthesis machinery. Our observations also indicate that in fission yeast, alterations of mitochondrial function are linked to changes in cell cycle and cell morphology control mechanisms.
Published ahead of print on 1 February 2008.
Supplemental material for this article may be found at http://ec.asm.org/.
These authors contributed equally.
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