Role of the RNA silencing machinery in the regulation of FLC.

迪恩实验室对了解是什么控制了各种植物的开花时间很感兴趣。我们正在使用一种模式植物拟南芥来识别所有与控制开花有关的基因，因为在这种植物中，仅基于该基因的突变（病变）而不需要其他信息就可以很容易地克隆该基因。多年来，我们已经证明，在开花的调节中起关键作用的是一种叫做FLC的蛋白质。FLC通过阻止一组需要开花的基因的激活来阻止开花。FLC水平在冬天会降低，这就是为什么许多植物在春天开花。在所谓的自主促进途径中，一组基因组合在一起也会减少这种基因。我们最近还发现FLC水平受一种涉及非常小的RNA分子的新的基因调控途径的调节。对植物病毒抗性和蠕虫发育的研究表明，长度在21到24个核苷酸之间的RNA分子作为信使，可以攻击含有相同序列的更长的RNA分子。它们还嵌入到大型蛋白质复合体中，并引导它们到达细胞中的遗传物质（染色质=环绕在组蛋白周围的DNA），找到具有匹配序列的DNA。涉及小RNA的过程被称为RNA沉默途径，用于人类治疗中，以RNAi或RNA干扰的名义关闭基因。RNA沉默如何被激活以及它如何导致常规基因染色质结构的调节尚不清楚。我们想通过分析FLC调控来剖析这些过程。这个系统很可能产生与整个生物学中基因调控相关的概念。

The Dean laboratory is interested in understanding what controls the timing of flowering in a wide range of plants. We are using a model plant Arabidopsis thaliana to identify all the genes involved in controlling flowering as in this plant it is easy to clone the gene based on just having a mutation (a lesion) in that gene and no other information. Over the years we have shown that a key player in the regulation of flowering is a protein called FLC. FLC prevents flowering by stopping the activation of a set of genes needed to make flowers. FLC levels are reduced by a winter period which is why many plants flower in the spring. It is also reduced by a set of genes grouped together in the so-called autonomous promotion pathway. We have recently also found FLC levels are regulated by a new gene regulatory pathway involving very small RNA molecules. Studies on virus resistance in plants and development in worms has revealed that RNA molecules between 21 and 24 nucleotides long act as messengers to zap longer RNA molecules containing the same sequence. They also get embedded in large protein complexes and guide them to the genetic material in the cell (chromatin = DNA looped around proteins called histones) finding DNA with a matching sequence. The processes involving small RNAs have been called RNA silencing pathways and are used in human therapeutics to switch off genes under the name RNAi or RNA interference. How RNA silencing is activated and how it leads to regulation of the chromatin structure of regular genes is not known. We want to dissect these processes by analysing FLC regulation. This system is likely to produce concepts relevant to gene regulation throughout biology.