Effectors of retrotransposon movement

项目摘要/摘要 反转录转座子运动效应因子 酵母菌的逆转录病毒样转座子Ty1是一个信息模型，可以用来了解 反转录转座子和逆转录病毒动员基因组，塑造基因组，并与宿主和编码的元件相互作用 各种因素。反转录元件复制周期的加性性质会导致拷贝的大量增加 如果未选中，则为数字。宿主细胞已经用几种防御系统进行了反击，包括驯化 反转录因子基因现在起到限制因素的作用，以最大限度地减少繁殖。我们发现了一个截断的 Ty1衣壳蛋白的一种形式，可抑制病毒样颗粒的组装和功能。这是自编码 限制因子扩大了针对衣壳的防御蛋白的谱系。我们的工作还突出了一个 耐人寻味的宿主-寄生虫策略。而不是通过驯化限制来抑制所有转座子的移动 基因作为一个不同的位点，酵母和Ty1可能已经共同进化出一种关系，允许高水平的 当拷贝数低时换位，随着拷贝数增加，换位逐渐减少。我们的目标 是为了了解Ty1拷贝数控制的机制和进化是由遗传、 基因组、细胞生物学、生化和结构方法。

PROJECT SUMMARY/ABSTRACT Effectors of retrotransposon movement The retrovirus-like transposon Ty1 of Saccharomyces is an informative model for understanding how retrotransposons and retroviruses mobilize, shape the genome, and interact with host and element encoded factors. The additive nature of the retroelement replication cycle can result in massive increases in copy number if left unchecked. Host cells have countered with several defense systems, including domestication of retroelement genes that now act as restriction factors to minimize propagation. We discovered a truncated form of the Ty1 capsid protein that inhibits virus-like particle assembly and function. This self-encoded restriction factor expands the repertoire of defense proteins targeting the capsid. Our work also highlights an intriguing host-parasite strategy. Instead of inhibiting all transposon movement by domesticating the restriction gene as a distinct locus, yeast and Ty1 may have coevolved a relationship that allows high levels of transposition when copy numbers are low and progressively less transposition as copy numbers rise. Our goal is to understand the mechanism and evolution of Ty1 copy number control by a combination of genetic, genomic, cell biological, biochemical and structural approaches.