Present address: Rufeng Xu-Friedman, Frontier Science and Technology Research Foundation 4033 Maple Rd, Amherst, NY 14226, USA.
Genome-wide analysis of the response to protein glycosylation deficiency in yeast
Article first published online: 4 JUL 2006
FEMS Yeast Research
Volume 6, Issue 8, pages 1264–1273, December 2006
How to Cite
Cullen, P. J., Xu-Friedman, R., Delrow, J. and Sprague, G. F. (2006), Genome-wide analysis of the response to protein glycosylation deficiency in yeast. FEMS Yeast Research, 6: 1264–1273. doi: 10.1111/j.1567-1364.2006.00120.x
Editor: Andrew Alspaugh
- Issue published online: 4 JUL 2006
- Article first published online: 4 JUL 2006
- Received 28 February 2006; revised 12 April 2006; accepted 13 April 2006.First published online 4 July 2006.
Vol. 10, Issue 7, 957, Article first published online: 16 SEP 2010
- MAP kinase;
- filamentous growth;
- cell wall
Protein modification by glycosylation occurs through an essential biochemical pathway that produces mannosyl side chain substrates, which are covalently attached to proteins in the endoplasmic reticulum. We used DNA microarray analysis to characterize the cellular response to a conditional defect (pmi40-101) in the protein glycosylation pathway. Expression profiles were obtained from DNA microarrays containing essentially every gene from Saccharomyces cerevisiae. We validated the microarray analysis by examining the expression patterns of induced genes using transcriptional lacZ fusions. The major class of genes differentially expressed in the glycosylation mutant overlapped significantly with that of a starvation response and included those required for gluconeogenesis, the tricarboxylic acid and glyoxylate cycles, and protein and amino acid biosynthesis. Two mitogen-activated protein (MAP) kinase pathways were also activated in the mutant, the filamentous growth and protein kinase C pathways. Taken together, our results suggest that a checkpoint is activated in response to a protein glycosylation defect, allowing the cell to mount an adaptive response by the activation of multiple MAP kinase pathways.