Cellular Immunology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi, India.
IUBMB Life. 2018 Sep;70(9):845-854. doi: 10.1002/iub.1887. Epub 2018 Aug 18.
Previously, we reported that infection of human macrophages with Mycobacterium tuberculosis (Mtb) results in massive alterations in the pattern of RNA splicing in the host. The finding gained significance since alternate spliced variants of a same gene may have substantially different structure, function, stability, interaction partners, localization, and so forth, owing to inclusion or exclusion of specific exons. To establish a proof-of-concept; on how infection-induced RNA splicing could impact protein functions, here we used RNA-seq data from THP-1 macrophages that were infected with clinical isolate of Mtb. In addition to re-establishing the fact that Mtb infection may cause strain specific alterations in RNA splicing, we also developed a new analysis pipeline resulting in characterization of domain maps of the transcriptome post-infection. For the sake of simplicity, we restricted our analysis to all the kinases in the human genome and considered only pfam classified protein domains and checked their frequency of inclusion or exclusion due to alternate splicing across the conditions and time points. We report massive alterations in the domain architecture of most regulated proteins across the entire kinases highlighting the physiological importance of such an understanding. This study paves way for more detailed analysis of different functional classes of proteins and perturbations to their domain architecture as a consequence of mycobacterial infections. Such analysis would yield unprecedented depth to our understanding of host-pathogen interaction and allow in a more systematic manner targeting of host pathways for controlling the infections. © 2018 The Authors. IUBMB Life published by Wiley Periodicals, Inc. on behalf of International Union of Biochemistry and Molecular Biology, 70(9):845-854, 2018.
此前,我们报道称结核分枝杆菌(Mtb)感染人类巨噬细胞会导致宿主中 RNA 剪接模式发生大规模改变。这一发现意义重大,因为同一基因的可变剪接变体可能由于外显子的包含或排除而具有截然不同的结构、功能、稳定性、相互作用伙伴、定位等。为了建立一个感染诱导的 RNA 剪接如何影响蛋白质功能的概念验证;在这里,我们使用了来自感染结核分枝杆菌临床分离株的 THP-1 巨噬细胞的 RNA-seq 数据。除了重新确立 Mtb 感染可能导致 RNA 剪接特异性改变的事实外,我们还开发了一种新的分析管道,对感染后转录组的结构域图谱进行了特征描述。为了简单起见,我们将分析仅限于人类基因组中的所有激酶,并仅考虑 pfam 分类的蛋白质结构域,并检查它们由于可变剪接在不同条件和时间点的包含或排除频率。我们报告了大多数调节蛋白的结构域架构在整个激酶中发生了大规模改变,突出了这种理解的生理重要性。这项研究为更详细地分析不同功能类别的蛋白质及其结构域架构的扰动铺平了道路,作为分枝杆菌感染的结果。这种分析将以前所未有的深度加深我们对宿主-病原体相互作用的理解,并允许更系统地针对宿主途径来控制感染。