SUT2是酵母中cAMP/蛋白激酶a通路低活性的一种新型多拷贝抑制因子。

Michael Rützler, André Reissaus, Magdalena Budzowska, Wolfhard Bandlow
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引用次数: 12

摘要

SUT2是在Deltaras2Deltagpa2双缺失突变体合成慢生长表型的多拷贝抑制子筛选中发现的。然而,它未能治愈Deltaras1Deltaras2突变体的致死表型,这表明它在Ras的上游或平行途径中起作用。通过测试camp依赖性反应,包括储存碳水化合物的积累、假菌丝分化、减数分裂的进入以及FLO11报告活性的测量,我们发现Sut2p调节蛋白激酶A (PKA)的活性。此外,我们还发现细胞中的Ras2p水平受到Sut2p的影响,并且Sut2-GFPp在细胞核中显著积累。根据观察到的高剂量SUT2基因对PKA活性的影响,以及Sut2p与推定的转录因子Sut1p的同源性,我们认为Sut2p在转录水平上参与了PKA活性的调控。
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SUT2 is a novel multicopy suppressor of low activity of the cAMP/protein kinase A pathway in yeast.

SUT2 was found in a screen for multicopy suppressors of the synthetic slow growth phenotype of a Deltaras2Deltagpa2 double deletion mutant. It failed, however, to cure the lethal phenotype of a Deltaras1Deltaras2 mutant suggesting that it acts upstream of Ras or in a parallel pathway. By testing cAMP-dependent reactions including the accumulation of storage carbohydrates, pseudohyphal differentiation, entry of meiosis as well as the measurement of FLO11 reporter activity we show that Sut2p modulates the activity of protein kinase A (PKA). Additionally, we demonstrate that cellular levels of Ras2p are affected by Sut2p and that Sut2-GFPp accumulates significantly in the nucleus. Based on the observed influence of high SUT2 gene dosage on PKA activity as well as Sut2p's homology to the presumptive transcription factor Sut1p, we suggest that Sut2p contributes to regulation of PKA activity at the level of transcription.

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