z-logo
open-access-imgOpen Access
Dominant and recessive suppressors that restore glucose transport in a yeast snf3 mutant.
Author(s) -
L Marshall-Carlson,
Lenore Neigeborn,
David M. Coons,
Linda F. Bisson,
Marian Carlson
Publication year - 1991
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1093/genetics/128.3.505
Subject(s) - snf3 , complementation , mutant , biology , glucose transporter , genetics , gene , saccharomyces cerevisiae , biochemistry , endocrinology , insulin
The SNF3 gene of Saccharomyces cerevisiae encodes a high-affinity glucose transporter that is homologous to mammalian glucose transporters. To identify genes that are functionally related to SNF3, we selected for suppressors that remedy the growth defect of snf3 mutants on low concentrations of glucose or fructose. We recovered 38 recessive mutations that fall into a single complementation group, designated rgt1 (restores glucose transport). The rgt1 mutations suppress a snf3 null mutation and are not linked to snf3. A naturally occurring rgt1 allele was identified in a laboratory strain. We also selected five dominant suppressors. At least two are tightly linked to one another and are designated RGT2. The RGT2 locus was mapped 38 cM from SNF3 on chromosome IV. Kinetic analysis of glucose uptake showed that the rgt1 and RGT2 suppressors restore glucose-repressible high-affinity glucose transport in a snf3 mutant. These mutations identify genes that may regulate or encode additional glucose transport proteins.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom