表观遗传学的传统观点认为，组蛋白去乙酰化酶通常与转录抑制相关，但近年来的研究表明，去乙酰化酶也参与了转录的激活，因此对于该过程的研究是目前表观遗传领域的热点之一。SET3是一个在进化上很保守的组蛋白去乙酰化酶复合物，在酵母和哺乳动物中都有它的同源复合物。SET3复合物参与了基因的转录激活，但是该过程的分子机制仍不清楚。本课题将以裂殖酵母(Schizosaccharomyces pombe)作为模式生物，利用前期构建的缺失突变体文库及筛选平台,通过鉴定SET3复合物与其他表观遗传途径之间的联系，以及鉴定SET3复合物核心亚基的结合蛋白，来研究SET3复合物调控转录激活的分子机制。本课题还将进一步研究SET3复合物的作用机制在哺乳动物中的保守性。本研究将有助于阐明组蛋白去乙酰化酶调控转录激活的机制，同时为研究SET3同源复合物在人类疾病和发育中发挥的作用奠定基础。

According to the classic epigenetic theory, histone deacetylase is usually involved in the transcriptional repression. However, recent study revealed a role of histone deacetylase in transcriptional activation, which emerges as a hotspot in the epigenetic field. SET3 is a conserved histone deacetylase complex. Both yeast and mammalians contain its homologous complex. SET3 complex is implicated in the transcription activation, but detail mechanism is still unclear. In this study, we plan to use Schizosaccharomyces pombe as a model, to identify the binding partners of the core subunit of SET3 complex, and to identify the co-operations between SET3 complex and other epigenetic pathways during transcriptional activation. We will also check whether the mechanism of SET3 complex is conserved in mammals. This study seeks to provide a better understanding of general mechanism of transcriptional activation by histone deacetylase, and might also help to study the role of SET3 homologous complex in human disease and development.