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磷酸化蛋白质组学分析揭示了裂谷热病毒感染后Smad蛋白家族的激活。

Phosphoproteomic analysis reveals Smad protein family activation following Rift Valley fever virus infection.

作者信息

de la Fuente Cynthia, Pinkham Chelsea, Dabbagh Deemah, Beitzel Brett, Garrison Aura, Palacios Gustavo, Hodge Kimberley Alex, Petricoin Emanuel F, Schmaljohn Connie, Campbell Catherine E, Narayanan Aarthi, Kehn-Hall Kylene

机构信息

National Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason University, Manassas, Virginia, United States of America.

United States Army Medical Research Institute of Infectious Diseases, Frederick, Maryland, United States of America.

出版信息

PLoS One. 2018 Feb 6;13(2):e0191983. doi: 10.1371/journal.pone.0191983. eCollection 2018.

DOI:10.1371/journal.pone.0191983
PMID:29408900
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5800665/
Abstract

Rift Valley fever virus (RVFV) infects both ruminants and humans leading to a wide variance of pathologies dependent on host background and age. Utilizing a targeted reverse phase protein array (RPPA) to define changes in signaling cascades after in vitro infection of human cells with virulent and attenuated RVFV strains, we observed high phosphorylation of Smad transcription factors. This evolutionarily conserved family is phosphorylated by and transduces the activation of TGF-β superfamily receptors. Moreover, we observed that phosphorylation of Smad proteins required active RVFV replication and loss of NSs impaired this activation, further corroborating the RPPA results. Gene promoter analysis of transcripts altered after RVFV infection identified 913 genes that contained a Smad-response element. Functional annotation of these potential Smad-regulated genes clustered in axonal guidance, hepatic fibrosis and cell signaling pathways involved in cellular adhesion/migration, calcium influx, and cytoskeletal reorganization. Furthermore, chromatin immunoprecipitation confirmed the presence of a Smad complex on the interleukin 1 receptor type 2 (IL1R2) promoter, which acts as a decoy receptor for IL-1 activation.

摘要

裂谷热病毒（RVFV）可感染反刍动物和人类，导致一系列因宿主背景和年龄而异的病理变化。利用靶向反相蛋白质阵列（RPPA）来确定用强毒和减毒RVFV毒株体外感染人类细胞后信号级联反应的变化，我们观察到Smad转录因子的高度磷酸化。这个进化上保守的家族被TGF-β超家族受体磷酸化并转导其激活。此外，我们观察到Smad蛋白的磷酸化需要活跃的RVFV复制，而NSs的缺失会损害这种激活，进一步证实了RPPA的结果。对RVFV感染后改变的转录本进行基因启动子分析，鉴定出913个含有Smad反应元件的基因。这些潜在的Smad调节基因的功能注释集中在轴突导向、肝纤维化以及参与细胞粘附/迁移、钙内流和细胞骨架重组的细胞信号通路中。此外，染色质免疫沉淀证实白细胞介素1受体2型（IL1R2）启动子上存在Smad复合物，该启动子作为IL-1激活的诱饵受体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/e58171095b8c/pone.0191983.g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/a46631b9c41d/pone.0191983.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/3e0cd6c91394/pone.0191983.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/80053e22434f/pone.0191983.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/e58171095b8c/pone.0191983.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/17a6afd3bd32/pone.0191983.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/312a30183103/pone.0191983.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/97e189b73cff/pone.0191983.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/a46631b9c41d/pone.0191983.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/3e0cd6c91394/pone.0191983.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/80053e22434f/pone.0191983.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9a6/5800665/e58171095b8c/pone.0191983.g007.jpg

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