RT Journal Article
SR Electronic
T1 The yeast KRE5 gene encodes a probable endoplasmic reticulum protein required for (1----6)-beta-D-glucan synthesis and normal cell growth.
JF Molecular and Cellular Biology
JO Mol. Cell. Biol.
FD American Society for Microbiology
SP 3013
OP 3019
DO 10.1128/MCB.10.6.3013
VO 10
IS 6
A1 Meaden, P
A1 Hill, K
A1 Wagner, J
A1 Slipetz, D
A1 Sommer, S S
A1 Bussey, H
YR 1990
UL http://mcb.asm.org/content/10/6/3013.abstract
AB Yeast kre mutants define a pathway of cell wall (1----6)-beta-D-glucan synthesis, and mutants in genes KRE5 and KRE6 appear to interact early in such a pathway. We have cloned KRE5, and the sequence predicts the product to be a large, hydrophilic, secretory glycoprotein which contains the COOH-terminal endoplasmic reticulum retention signal, HDEL. Deletion of the KRE5 gene resulted in cells with aberrant morphology and extremely compromised growth. Suppressors to the KRE5 deletions arose at a frequency of 1 in 10(7) to 1 in 10(8) and permitted an analysis of deletions which were found to contain no alkali-insoluble (1----6)-beta-D-glucan. These results indicate a role for (1----6)-beta-D-glucan in normal cell growth and suggest a model for sequential assembly of (1----6)-beta-D-glucan in the yeast secretory pathway.