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Glucose Transporter (HXT) Homeostasis in Saccharomyces cerevisiae
Author(s) -
Swain Evelyn
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.950.11
Subject(s) - endocytosis , saccharomyces cerevisiae , glucose transporter , endocytic cycle , transporter , biology , yeast , glucose homeostasis , snf3 , microbiology and biotechnology , function (biology) , biochemistry , membrane transport protein , cell , gene , insulin , insulin resistance , endocrinology
The proposed research explores the regulation of glucose metabolism in Saccharomyces cerevisiae. Specifically, the focus is on how the loss of endocytic function results in aberrant glucose homeostasis through the deregulation of glucose transporter localization/function. By combining methods of yeast genetics, molecular biology, and cell biology, novel features regulating transporter function and localization will be studied to uncover mechanisms for maintaining glucose homeostasis. Data show that the BAR domain protein Rvs161 is required for proper transporter localization and function. 1 Recent reviews describes BAR domain containing proteins as curvature inducing/stabilizing proteins essential for affecting a wide variety of membrane remodeling processes, including endocytosis. 2 Endocytosis and degradation of transporters is critically important in maintaining glucose homeostasis in yeast as well as mammals. Saccharomyces cerevisiae is a well‐established model organism for the study of endocytosis. 3 Additionally, yeast share similar components of glucose signaling and glucose transporter pathways with mammalian counterparts making yeast a useful model system for studies of glucose transporter biology. 4, 5 Yeast strains lacking the RVS161 gene fail to grow under conditions of glucose limitation and harbor endocytosis defects. Our data indicate that overexpression of specific glucose transporters can suppress this defect. Additionally, our data suggests that glucose transporter interactions are required for proper transporter function and that Rvs161p is required for proper transporter localization and function. Support or Funding Information NA