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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation [ChIP-Seq]

ABSTRACT: We provide a set of genes that are directly bound by Dhx9 in CD8 T cells from LCMV infected mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE161694 | GEO | 2020/11/19

REPOSITORIES: GEO

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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation

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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation

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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation [ChIP-Seq]

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Innate sensor Dhx9 orchestrates TCR signaling and controls CD8 T cell immunity against viral infection [ATAC-Seq]

Project description:Nuclear sensor molecules of innate cells recognize pathogenic DNA or RNA to activate innate immunity and defense against bacteria and virus infection. Although some sensors exhibit their preliminary functions in T cells, it is still unclear about the underlying mechanism. Here we found a nuclear sensor-Dhx9, was enhanced its expression in effector CD8 T cells. T cell specific deletion of Dhx9 caused an impaired CD8 T cell expansion, memory formation and virus clearance. Mechanically, Dhx9 could directly regulate id2 transcription and in turn control effector CD8 T cell differentiation. Importantly, Dhx9 could bind to Lck protein, mediate Zap70 phosphorylation, and promoting TCR downstream signaling - ERK pathway to protect effector CD8 T cells from apoptosis. The DSRM and DEXDc-Helicase domain is required for Lck binding and Id2 transcription, respectively. Therefore, we revealed a novel regulatory mechanism that innate nuclear sensor regulates T cell fate and function through modulating adaptive pathways.

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Project description:The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach. Comparison of gene expression in large intestine of mice with or without reduced expression of DHX9.

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DHX9 and NPM1 silencing RNA-seq

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RNA damage compartmentalization by DHX9 granules

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