cerevisiae ~200 million years ago, and in which glucose repression evolved independently. Lactic acid also induced -like epigenetic states in fungi that diverged from S. This trait had the defining genetic properties of, and did not require utilization of lactic acid as a carbon source. Transient exposure to lactic acid caused yeast cells to heritably circumvent glucose repression. Here we identify the common bacterial metabolite lactic acid as a strong inducer. Diverse bacteria can elicit yeast cells to acquire, although the molecular details of this interaction remain unknown. This program can be circumvented by a protein-based genetic element, the prion, permitting simultaneous metabolism of glucose and other carbon sources. Robust preference for fermentative glucose metabolism has motivated domestication of the budding yeast Saccharomyces cerevisiae. Garcia, David M Dietrich, David Clardy, Jon Jarosz, Daniel F This suggests that repressive changes of the glucose transport mechanism occur in brain endothelial cells in response to increased plasma glucose.Ī common bacterial metabolite elicits prion-based bypass of glucose repression
When plasma glucose was lowered to normal values, the glucose transport rate into brain was 20 percent below normal. In rats with chronic hyperglycemia the maximum glucose transport capacity of the blood-brain barrier decreased from 400 to 290 micromoles per 100 grams per minute. The symptoms may indicate insufficient transport of glucose from blood to brain.
PMID:8755906īlood-Brain Glucose Transfer: Repression in Chronic Hyperglycemiaĭiabetic patients with increased plasma glucose concentrations may develop cerebral symptoms of hypoglycemia when their plasma glucose is rapidly lowered to normal concentrations. A late response is only achieved when Hxk2p is present. An early repression response requires any one of the three glucose kinases present in S. This process may be resolved into several steps. Glucose repression may involve processes with different sugar kinase requirements.Īdding glucose to Saccharomyces cerevisiae cells growing among nonfermentable carbon sources leads to glucose repression. This review describes effects of glucose repression on yeast carbon metabolism with a focus on roles of the Snf3/Rgt2 glucose-sensing pathway and Snf1 signal transduction in establishment and relief of glucose repression. This dominant effect of glucose on yeast carbon metabolism is coordinated by several signaling and metabolic interactions that mainly regulate transcriptional activity but are also effective at post-transcriptional and post-translational levels.
Although yeast cells can utilize a wide range of carbon sources, presence of glucose suppresses molecular activities involved in the use of alternate carbon sources as well as it represses respiration and gluconeogenesis. Glucose is the primary source of energy for the budding yeast Saccharomyces cerevisiae. Glucose repression in Saccharomyces cerevisiae.
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