Present addresses: James J. Ritch, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, 114 16th St., Charlestown, MA 02129, USA. Jared J. Sheehan, Cancer Immunology & AIDS, Dana-Farber Cancer Institute, 44 Binney St., JFB 703, Boston, MA 02115, USA.
The Saccharomyces SUN gene, UTH1, is involved in cell wall biogenesis
Article first published online: 18 DEC 2009
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Yeast Research
Volume 10, Issue 2, pages 168–176, March 2010
How to Cite
Ritch, J. J., Davidson, S. M., Sheehan, J. J. and Austriaco, O.P., N. (2010), The Saccharomyces SUN gene, UTH1, is involved in cell wall biogenesis. FEMS Yeast Research, 10: 168–176. doi: 10.1111/j.1567-1364.2009.00601.x
Editor: Ian Dawes
- Issue published online: 4 FEB 2010
- Article first published online: 18 DEC 2009
- Received 9 August 2009; revised 6 December 2009; accepted 13 December 2009.Final version published online 12 January 2010.
- SUN genes;
- cell wall biogenesis;
Deletion of the Saccharomyces gene, UTH1, a founding member of the SUN family of fungal genes, has pleiotropic effects. Several phenotypes of Δuth1 cells including their decreased levels of mitochondrial proteins, their impaired autophagic degradation of mitochondria, and their increased viability in the presence of mammalian BAX, a proapoptotic regulator localized to the mitochondria, have prompted others to propose that the Uth1p functions primarily at the mitochondria. In this report, we show that cells lacking UTH1 have more robust cell walls with higher levels of β-d-glucan that allows them to grow in the presence of calcofluor white or sodium dodecyl sulfate, two reagents known to perturb the yeast cell wall. Moreover, these Δuth1 cells are also significantly more resistant to spheroplast formation induced by zymolyase treatment than their wild-type counterparts. Surprisingly, our data suggest that several of the enhanced growth phenotypes of Δuth1 cells, including their resistance to BAX-mediated toxicity, arise from a strengthened cell wall. Therefore, we propose that Uth1p's role at the cell wall and not at the mitochondria may better explain many of its effects on yeast physiology and programmed cell death.