Uprety Bhawana, Kaja Amala, Ferdoush Jannatul, Sen Rwik, Bhaumik Sukesh R
Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois, USA.
Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, Illinois, USA
Mol Cell Biol. 2016 Jan 11;36(6):992-1006. doi: 10.1128/MCB.00808-15.
NuA4 histone lysine (K) acetyltransferase (KAT) promotes transcriptional initiation of TATA-binding protein (TBP)-associated factor (TAF)-dependent ribosomal protein genes. TAFs have also been recently found to enhance antisense transcription from the 3' end of the GAL10 coding sequence. However, it remains unknown whether, like sense transcription of the ribosomal protein genes, TAF-dependent antisense transcription of GAL10 also requires NuA4 KAT. Here, we show that NuA4 KAT associates with the GAL10 antisense transcription initiation site at the 3' end of the coding sequence. Such association of NuA4 KAT depends on the Reb1p-binding site that recruits Reb1p activator to the GAL10 antisense transcription initiation site. Targeted recruitment of NuA4 KAT to the GAL10 antisense transcription initiation site promotes GAL10 antisense transcription. Like NuA4 KAT, histone H3 K4/36 methyltransferases and histone H2B ubiquitin conjugase facilitate GAL10 antisense transcription, while the Swi/Snf and SAGA chromatin remodeling/modification factors are dispensable for antisense, but not sense, transcription of GAL10. Taken together, our results demonstrate for the first time the roles of NuA4 KAT and other chromatin regulatory factors in controlling antisense transcription, thus illuminating chromatin regulation of antisense transcription.
NuA4组蛋白赖氨酸(K)乙酰转移酶(KAT)促进TATA结合蛋白(TBP)相关因子(TAF)依赖性核糖体蛋白基因的转录起始。最近还发现TAF可增强GAL10编码序列3'端的反义转录。然而,GAL10的TAF依赖性反义转录是否像核糖体蛋白基因的正义转录一样也需要NuA4 KAT,目前尚不清楚。在这里,我们表明NuA4 KAT与编码序列3'端的GAL10反义转录起始位点相关联。NuA4 KAT的这种关联取决于Reb1p结合位点,该位点将Reb1p激活剂招募到GAL10反义转录起始位点。将NuA4 KAT靶向招募到GAL10反义转录起始位点可促进GAL10反义转录。与NuA4 KAT一样,组蛋白H3 K4/36甲基转移酶和组蛋白H2B泛素缀合酶促进GAL10反义转录,而Swi/Snf和SAGA染色质重塑/修饰因子对于GAL10的反义转录是可有可无的,但对正义转录不是。综上所述,我们的结果首次证明了NuA4 KAT和其他染色质调节因子在控制反义转录中的作用,从而阐明了反义转录的染色质调控。