105學年度「學术特别演讲」系列讲座-106/03/16-黄馥博士【Roles of the KAT6/Enok acetyltransferase in transcription and cell proliferation.】(10:00-12:00)
开始日期
2017-03-16 10:00:00
结束日期
2017-03-16 12:00:00
活动说明
105學年度「學术特别演讲」系列讲座
日期：106年03月16日（星期四）10:00-12:00
地点：台北医學大學医學综合大楼後栋16楼演讲厅
主讲人：黄馥 博士
讲题：Roles of the KAT6/Enok acetyltransferase in transcription and cell proliferation.
The KAT6 acetyltransferases are highly conserved in a wide range of organisms, and are generally involved in transcriptional regulation and cell proliferation. However, how KAT6 regulates transcription and cell cycle progression remained elusive. We have discovered that the Drosophila KAT6 acetyltransferase, Enok, is the major enzyme for establishing the histone H3K23 acetylation (H3K23ac) mark. Interestingly, loss of functional Enok in the germline causes defective localization of Oskar in oocytes, resulting in loss of germline cells and abdominal segments in embryos. Further investigation using RNA-seq analysis, ChIP assay and genetic rescue suggests that Enok-mediated H3K23ac promotes expression of the spir gene, which is critical for the proper localization of Oskar in oocytes. Therefore, this study provides a specific mechanism linking KAT6 to transcription and oogenesis. We have also identified the PCNA-unloader Elg1 complex as a novel interacting partner of the Enok complex. Depletion of Enok in cultured cells results in a progression block at the G1/S transition, and this G1/S block is partially dependent on Elg1. Furthermore, knocking down enok decreases the levels of chromatin-bound PCNA, suggesting that Enok interacts with Elg1 and inhibits its PCNA-unloading function to promote the G1/S transition. In agreement with this hypothesis, knocking down enok in the germline partially rescued the endoreplication defects in Elg1-depleted nurse cells. Taken together, our studies provide novel insights into the roles of KAT6 HATs in regulation of transcription and cell cycle progression.
