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. 2017 Sep 29;12(9):e0185516. doi: 10.1371/journal.pone.0185516

Fig 10. Low RNAP III activity caused by Gly1007Ala point mutation in C128 RNAP III subunit, correlates with transcription of HXT2 gene by RNAP II, despite repressing conditions.

Fig 10

Activation of the Snf1-dependent glucose repression and Snf3/Rgt2-Rgt1 (SRR) signaling pathways do not repress the HXT2 transcription by RNAP II. We propose Ssn6-Tup1 complex as a HXT2 transcription coactivator in rpc128-1007. Under high-glucose conditions, Mth1 degradation occurs. Rgt1, which is phosphorylated by PKA, dissociates from the HXT2 promoter. Mig1, which is bound to the regulatory region, recruits Ssn6-Tup1. The complex transforms into a coactivator complex due to an unidentified intracellular signal and the expression of HXT2 is induced. Under non-fermentable growth conditions in the strain with low RNAP III activity, the Snf3/Rgt2-Rgt1 (SRR) pathway transduces the signal for unfavorable external conditions to Mth1, preventing its degradation. The Rgt1 and Tup1 corepressor complex transforms into an activator complex and strongly induces HXT2 expression.