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揭示了新型抗原表达调控的单寄生虫转录图谱。

A single-parasite transcriptional atlas of reveals novel control of antigen expression.

机构信息

Department of Bioengineering, Stanford University, Stanford, United States.

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, United States.

出版信息

Elife. 2020 Feb 17;9:e54129. doi: 10.7554/eLife.54129.

DOI:10.7554/eLife.54129
PMID:32065584
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7180058/
Abstract

a protozoan parasite, undergoes a complex and poorly understood developmental process that is critical for establishing a chronic infection in its intermediate hosts. Here, we applied single-cell RNA-sequencing (scRNA-seq) on >5,400 Toxoplasma in both tachyzoite and bradyzoite stages using three widely studied strains to construct a comprehensive atlas of cell-cycle and asexual development, revealing hidden states and transcriptional factors associated with each developmental stage. Analysis of SAG1-related sequence (SRS) antigenic repertoire reveals a highly heterogeneous, sporadic expression pattern unexplained by measurement noise, cell cycle, or asexual development. Furthermore, we identified AP2IX-1 as a transcription factor that controls the switching from the ubiquitous SAG1 to rare surface antigens not previously observed in tachyzoites. In addition, comparative analysis between and scRNA-seq results reveals concerted expression of gene sets, despite fundamental differences in cell division. Lastly, we built an interactive data-browser for visualization of our atlas resource.

摘要

一种原生动物寄生虫，经历了一个复杂且尚未被充分理解的发育过程，该过程对于在其中间宿主中建立慢性感染至关重要。在这里，我们对处于速殖子和缓殖子阶段的超过 5400 个弓形虫应用单细胞 RNA 测序 (scRNA-seq)，使用三种广泛研究的菌株构建了一个全面的细胞周期和无性发育图谱，揭示了与每个发育阶段相关的隐藏状态和转录因子。对 SAG1 相关序列 (SRS) 抗原库的分析揭示了一种高度异质的、散在的表达模式，无法用测量噪声、细胞周期或无性发育来解释。此外，我们确定了 AP2IX-1 作为一种转录因子，它控制着从无处不在的 SAG1 向以前在速殖子中未观察到的罕见表面抗原的转换。此外，尽管在细胞分裂方面存在根本差异，但 和 scRNA-seq 结果之间的比较分析显示基因集的协调表达。最后，我们构建了一个交互式数据浏览器，用于可视化我们的图谱资源。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb69/7180058/3c90f7e781cc/elife-54129-fig6-figsupp1.jpg
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