【生态与环境讲坛183讲】To transcribe or to splice: SKIP-mediated development and environmental fitness in Arabidopsis

2017年09月28日 于 金泉楼A239


马力耕 教授 首都师范大学生命科学学院院长 63

主讲人简介

       马力耕,教授,国家杰出青年基金获得者,北京市特聘教授,北京市高层次人才引进计划入选者。现为首都师范大学生命科学学院教授、博士研究生导师、生命科学学院院长。马力耕教授主要研究方向为植物发育和环境适应的分子机制,研究内容为基因表达调控在植物细胞分化和适应环境的作用和机制。他在植物分子遗传领域做出了具有世界影响力的科研成果,发表的论文被SCI收录超过50篇,被SCI引用总次数超过4000次,其中单篇论文最高引用超过370次。

      马力耕教授曾获得国家自然科学杰出青年基金、国家自然科学二等奖、教育部科技进步二等奖、河北省自然科学一等奖、河北省有突出贡献的中青年专家等荣誉称号;主持国家自然科学杰出青年基金项目、国家自然科学基金青年项目、国家自然科学基金项目、863重大专项课题等。

内容简介

SKIP is an evolutionarily conserved protein from yeast to humans. In plants, We verified that SKIP is a bifunctional regulator that works as a splicing factor as part of the spliceosome, and as a transcriptional activator by forming transcriptional regulator complex. SKIP interacts with ELF7, a core component of the Paf1 complex (Paf1c), to form the SKIP-Paf1c to represses the floral transition in Arabidopsis. SKIP interacts with MAC3A and MAC3B in the spliceosome, and that they are required for the proper functioning of the circadian clock and abiotic stress response in Arabidopsis. However, neither MAC3A nor MAC3B interacts physically and genetically with ELF7. The SKIP-MAC3A/B complex mediates circadian clock function and abiotic stress responses by controlling the alternative splicing of pre-mRNAs encoded by clock- and stress tolerance-related genes. The SKIP-Paf1c regulates the floral transition by activating FLC transcription. Therefore, SKIP regulates development and environmental fitness by forming two distinct complexes that regulate gene expression transcriptionally and post-transcriptionally, respectively, in Arabidopsis.