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Genome-wide identification of BATF2 binding sites in HeLa-BATF2 cells

ABSTRACT: Basic leucine zipper transcription factors (BATFs) play profound roles in the regulatory networks of gene expression in tumor cells. BATF2, also known as SARI (suppressor of AP-1, regulated by interferon), was able to suppress both growth and migration of various cancers. In searching for BATF2/SARI-specific regulatory DNA elements, we first established a stable BATF2 over-expression HeLa cell line, then employed ChIP-Sequencing in order to identify the responsive DNA motifs for BATF2/SARI.

ORGANISM(S): Homo sapiens

PROVIDER: GSE67258 | GEO | 2015/03/26

SECONDARY ACCESSION(S): PRJNA279358

REPOSITORIES: GEO

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Microarray analyses using bone marrow-derived macrophages from Batf2−/− and wildtype mice that had been stimulated with R848

Project description:We assessed the role of basic leucine zipper transcription factor ATF-like 2 (Batf2), particularly its positive transcriptional activities via TLR signals. Because TLR7 agonists are clinically used against tumors and have proven effective as antitumor drugs, we assessed effect of Batf2 on the responses to the TLR7 ligand (R848).

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Batf2 is a regulator of interferon gamma signaling in astrocytes during neuroinflammation

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Effect of Batf2 deficiency on gene epxression in murine alveolar macrophages treated ex vivo with IFNg and K. pneumoniae supernatant

Project description:Basic leucine zipper transcription factor ATF-like 2 (BATF2) is a transcription factor that is emerging as an important regulator of the innate immune system. We previously identified BATF2 among the top upregulated genes in human alveolar macrophages treated with LPS, but the signaling pathways that induce BATF2 expression in response to Gram-negative stimuli are incompletely understood. In addition, the role of BATF2 in the host response to pulmonary infection with a Gram-negative pathogen like Klebsiella pneumoniae (Kp) is not known. We show that induction of Batf2 gene expression in macrophages in response to Kp in vitro requires TRIF and type I interferon (IFN) signaling, but not MyD88 signaling. Analysis of the impact of BATF2-deficiency on macrophage effector functions in vitro showed that BATF2 does not directly impact macrophage phagocytic uptake and intracellular killing of Kp. However, BATF2 markedly enhanced macrophage pro-inflammatory gene expression and Kp-induced cytokine responses. In vivo, we observed that Batf2 gene expression was elevated in the lung tissue of wild type (WT) mice 24 h after pulmonary Kp infection, and Kp-infected BATF2-deficient (Batf2-/-) mice displayed a modest but significant increase in bacterial burden in the lung, spleen and liver compared to WT mice. WT and Batf2-/- mice showed similar recruitment of leukocytes following infection, but in line with our in vitro observations, pro-inflammatory cytokine levels in the alveolar space were reduced in Batf2-/- mice. Altogether, these results suggest that BATF2 enhances pro-inflammatory cytokine responses in macrophages in response to Kp, and that as such, BATF2 contributes to the host defense against pulmonary Kp infection.

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Project description:Rattus norvegicus Batf2, basic leucine zipper ATF-like transcription factor 2 [Source:RGD Symbol;Acc:1311481], is expressed in 4 baseline experiment(s);

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