Nordberg Niklas, Olsson Ida, Carlsson Mattias, Hu Guo-Zhen, Orzechowski Westholm Jakub, Ronne Hans
Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden; Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden.
PLoS One. 2014 Jul 7;9(7):e95078. doi: 10.1371/journal.pone.0095078. eCollection 2014.
Rph1 and Gis1 are two related yeast zinc finger proteins that function as downstream effectors in the Ras/PKA, TOR and Sch9 nutrient signaling pathways. Both proteins also contain JmjC histone demethylase domains, but only Rph1 is known to be an active enzyme, demethylating lysine 36 of histone H3. We have studied to what extent the demethylase activity of Rph1 contributes to its role in nutrient signaling by performing gene expression microarray experiments on a yeast strain containing a catalytically inactive allele of RPH1. We find that the enzymatic activity of Rph1 is not essential for its role in growth phase dependent gene regulation. However, the ability of Rph1 to both activate and repress transcription is partially impaired in the active site mutant, indicating that the demethylase activity may enhance its function in vivo. Consistent with this, we find that the Rph1 mutation and a deletion of the histone H3 methylase Set2 affect the same target genes in opposite directions. Genes that are differentially expressed in the Rph1 mutant are also enriched for binding of Rpd3, a downstream effector in silencing, to their promoters. The expression of some subtelomeric genes and genes involved in sporulation and meiosis are also affected by the mutation, suggesting a role for Rph1-dependent demethylation in regulating these genes. A small set of genes are more strongly affected by the active site mutation, indicating a more pronounced role for the demethylase activity in their regulation by Rph1.
Rph1和Gis1是两个相关的酵母锌指蛋白,它们在Ras/PKA、TOR和Sch9营养信号通路中作为下游效应器发挥作用。这两种蛋白还都含有JmjC组蛋白去甲基化酶结构域,但只有Rph1被认为是一种活性酶,可使组蛋白H3的赖氨酸36去甲基化。我们通过对含有RPH1催化失活等位基因的酵母菌株进行基因表达微阵列实验,研究了Rph1的去甲基化酶活性在多大程度上对其在营养信号传导中的作用有贡献。我们发现,Rph1的酶活性对于其在生长阶段依赖性基因调控中的作用并非必不可少。然而,在活性位点突变体中,Rph1激活和抑制转录的能力部分受损,这表明去甲基化酶活性可能会增强其在体内的功能。与此一致的是,我们发现Rph1突变和组蛋白H3甲基转移酶Set2的缺失对相同的靶基因有相反方向的影响。在Rph1突变体中差异表达的基因,其启动子上也富集了沉默下游效应器Rpd3的结合。一些亚端粒基因以及参与孢子形成和减数分裂的基因的表达也受到该突变的影响,这表明Rph1依赖性去甲基化在调控这些基因中发挥作用。一小部分基因受活性位点突变的影响更大,这表明去甲基化酶活性在Rph1对它们的调控中发挥着更显著的作用。