TY - JOUR
T1 - KAR2, a karyogamy gene, is the yeast homolog of the mammalian BiP/GRP78 gene
AU - Rose, Mark D.
AU - Misra, Leanne M.
AU - Vogel, Joseph P.
N1 - Funding Information:
We thank K. Normington, M.-J. Gething, and J. Sambrook for sharing DNA sequence data prior to publication. We thank R. Schekman, R. Deshaies, and C. Kaiser for strains and helpful discussions. This research was supported by grants from the National Institutes of Health (GM3779), National Science Foundation (DCB8657497) and McDonell Foundation.
PY - 1989/6/30
Y1 - 1989/6/30
N2 - The yeast KAR2 gene was isolated by complementation of a mutation that blocks nuclear fusion. The predicted KAR2 protein sequence is most homologous to mammalian BiP/GRP78 and has several structural features in common with it: a functional secretory signal sequence, a yeast endoplasmic reticulum retention signal (HDEL) at the carboxyl terminus, and the absence of potential N-linked glycosylation sites. Moreover KAR2 is regulated like BiP/GRP78: the level of mRNA is increased by drug treatments and mutations that cause accumulation of secretory precursors in the endoplasmic reticulum. However, unlike BiP/GRP78, KAR2 is also regulated by heat shock. Deletion of the KAR2 gene generated a recessive lethal mutation, showing that BiP/GRP78 function is required for cell viability.
AB - The yeast KAR2 gene was isolated by complementation of a mutation that blocks nuclear fusion. The predicted KAR2 protein sequence is most homologous to mammalian BiP/GRP78 and has several structural features in common with it: a functional secretory signal sequence, a yeast endoplasmic reticulum retention signal (HDEL) at the carboxyl terminus, and the absence of potential N-linked glycosylation sites. Moreover KAR2 is regulated like BiP/GRP78: the level of mRNA is increased by drug treatments and mutations that cause accumulation of secretory precursors in the endoplasmic reticulum. However, unlike BiP/GRP78, KAR2 is also regulated by heat shock. Deletion of the KAR2 gene generated a recessive lethal mutation, showing that BiP/GRP78 function is required for cell viability.
UR - http://www.scopus.com/inward/record.url?scp=0024338964&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(89)90058-5
DO - 10.1016/0092-8674(89)90058-5
M3 - Article
C2 - 2661018
AN - SCOPUS:0024338964
SN - 0092-8674
VL - 57
SP - 1211
EP - 1221
JO - Cell
JF - Cell
IS - 7
ER -