Role of casein kinase 1 in the glucose sensor-mediated signaling pathway in yeastReport as inadecuate

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BMC Cell Biology

, 11:17

First Online: 07 March 2010Received: 02 December 2008Accepted: 07 March 2010


BackgroundIn yeast, glucose-dependent degradation of the Mth1 protein, a corepressor of the glucose transporter gene HXT repressor Rgt1, is a crucial event enabling expression of several HXT. This event occurs through a signaling pathway that involves the Rgt2 and Snf3 glucose sensors and yeast casein kinase 1 and 2 Yck1-2. In this study, we examined whether the glucose sensors directly couple with Yck1-2 to convert glucose binding into an intracellular signal that leads to the degradation of Mth1.

ResultsHigh levels of glucose induce degradation of Mth1 through the Rgt2-Snf3 glucose signaling pathway. Fluorescence microscopy analysis indicates that, under glucose-limited conditions, GFP-Mth1 is localized in the nucleus and does not shuttle between the nucleus and cytoplasm. If glucose-induced degradation is prevented due to disruption of the Rgt2-Snf3 pathway, GFP-Mth1 accumulates in the nucleus. When engineered to be localized to the cytoplasm, GFP-Mth1 is degraded regardless of the presence of glucose or the glucose sensors. In addition, removal of Grr1 from the nucleus prevents degradation of GFP-Mth1. These results suggest that glucose-induced, glucose sensor-dependent Mth1 degradation occurs in the nucleus. We also show that, like Yck2, Yck1 is localized to the plasma membrane via C-terminal palmitoylation mediated by the palmitoyl transferase Akr1. However, glucose-dependent degradation of Mth1 is not impaired in the absence of Akr1, suggesting that a direct interaction between the glucose sensors and Yck1-2 is not required for Mth1 degradation.

ConclusionGlucose-induced, glucose sensor-regulated degradation of Mth1 occurs in the nucleus and does not require direct interaction of the glucose sensors with Yck1-2.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2121-11-17 contains supplementary material, which is available to authorized users.

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Author: Satish Pasula - Samujjwal Chakraborty - Jae H Choi - Jeong-Ho Kim


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