School of Biological Sciences, Seoul National University, Seoul 08826, Korea; Research Center for Plant Plasticity, Seoul National University, Seoul 08826, Korea.
School of Biological Sciences, Seoul National University, Seoul 08826, Korea.
Mol Cells. 2024 Oct;47(10):100114. doi: 10.1016/j.mocell.2024.100114. Epub 2024 Sep 16.
Arabidopsis TATA-BINDING PROTEIN-ASSOCIATED FACTOR15b (TAF15b) is a plant-specific component of the transcription factor IID complex. TAF15b is involved in the autonomous pathway for flowering and represses the transcription of FLOWERING LOCUS C (FLC), a major floral repressor in Arabidopsis. While components of the autonomous flowering pathway have been extensively studied, scant attention has been directed toward elucidating the direct transcriptional regulators responsible for repressing FLC transcription. Here, we demonstrate that C-TERMINAL DOMAIN PHOSPHATASE-LIKE 1 (CPL1) is a physical and functional partner of TAF15b, playing a role in FLC repression. CPL1 is a protein phosphatase that dephosphorylates the C-terminal domain of RNA polymerase II (Pol II). Through the immunoprecipitation and mass spectrometry technique, we identified CPL1 as an interacting partner of TAF15b. Similar to taf15b, the cpl1 mutant showed a late-flowering phenotype caused by an increase in FLC levels. Additionally, the increase in cpl1 was correlated with the enrichment of phosphorylated Pol II in the FLC chromatin, as expected. We also discovered that CPL1 and TAF15b share additional common target genes through transcriptome analysis. These results suggest that TAF15b and CPL1 cooperatively repress transcription through the dephosphorylation of Pol II, especially at the FLC locus.
拟南芥 TATA 结合蛋白相关因子 15b(TAF15b)是转录因子IID 复合物中植物特异性的组成部分。TAF15b 参与开花的自主途径,并抑制拟南芥中主要的花抑制因子 FLOWERING LOCUS C(FLC)的转录。虽然自主开花途径的组成部分已经得到了广泛的研究,但很少有研究关注负责抑制 FLC 转录的直接转录调节因子。在这里,我们证明 C-末端结构域磷酸酶样 1(CPL1)是 TAF15b 的物理和功能伙伴,在 FLC 抑制中发挥作用。CPL1 是一种蛋白磷酸酶,可使 RNA 聚合酶 II(Pol II)的 C 末端结构域去磷酸化。通过免疫沉淀和质谱技术,我们鉴定出 CPL1 是 TAF15b 的相互作用伙伴。与 taf15b 相似,cpl1 突变体表现出晚花表型,这是由于 FLC 水平的增加引起的。此外,正如预期的那样,cpl1 的增加与 FLC 染色质中磷酸化 Pol II 的富集相关。我们还发现通过转录组分析,CPL1 和 TAF15b 共享其他共同的靶基因。这些结果表明,TAF15b 和 CPL1 通过 Pol II 的去磷酸化协同抑制转录,特别是在 FLC 基因座上。