TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation

Ferri, F.; Parcelier, Aude; Petit, Vanessa; Gallouët, Anne-Sophie; Lewandowski, Daniel; Dalloz, Marion; Heuvel, Anita van den; Kolovos, Petros; Soler, Éric; Squadrito, Mario Leonardo; Palma, Michele De; Davidson, Irwin; Rousselet, Germain; Roméo, Paul-Henri

doi:10.1038/ncomms9900

Cited by 56 publications

(64 citation statements)

References 43 publications

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“…Macrophages then neutrophils (in this order) are the most PU.1-dependent leukocyte cell types. In mammals, TRIM33 was found able to interact physically with PU.1, co-bind with it to hematopoietic gene regulatory elements (Kusy et al, 2011), and more recently, to regulate the transcriptional response of the interferon-β gene specifically in macrophages in a PU.1-dependent manner (Ferri et al, 2015). We therefore surmise that the profound navigation defect shown by macrophages and neutrophils in Trim33-deficient developing zebrafish likely reflects the mis-regulation in these cells of genes co-regulated by Pu.1 and Trim33.…”

Section: Discussionmentioning

confidence: 99%

“…To assess whether such a role of Trim33 would be conserved in mammals, we took advantage of the recent availability of mice harbouring Trim33 gene disruption specifically in myeloid leukocytes (Ferri et al, 2015). We derived macrophages from the bone marrow of these or control mice, and quantified their M-CSFdependent mobility in vitro in a 3D-fibrous collagen gel, which triggers macrophage amoeboid ( protease-independent) mobility, or in Matrigel, which triggers a 'mesenchymal' ( protease-dependent) mode of macrophage migration (Van Goethem et al, 2010).…”

Section: Trim33-deficient Mouse Macrophages Are Impaired In Their Amomentioning

confidence: 99%

“…One of them turned out to be trim33. Trim33, previously known as transcriptional intermediary factor 1γ (Tif1-γ), is a nuclear protein endowed with ubiquitin ligase activity, that does not directly bind to DNA but regulates gene transcription by associating with various DNA-binding transcription factors, such as SMADs, PU.1 (also known as Spi1) and Scl (also known as Tal1) (Xi et al, 2011;Hesling et al, 2011;Bai et al, 2010;Kusy et al, 2011;Ferri et al, 2015). Trim33 has notably been implicated in TGF-β-mediated regulation of gene expression (Xi et al, 2011;Hesling et al, 2011), erythropoiesis (Ransom et al, 2004;He et al, 2006;Bai et al, 2010), the long-term fate of hematopoietic stem cells (Kusy et al, 2011;Quere et al, 2014) and epithelial mesenchymal transitions (Hesling et al, 2011(Hesling et al, , 2013, and is considered a tumour suppressor (Aucagne et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Trim33 is essential for macrophage and neutrophil mobilization to developmental or inflammatory cues

Demy

Tauzin

Lancino

et al. 2017

Journal of Cell Science

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Macrophages infiltrate and establish in developing organs from an early stage, often before these have become vascularized. Similarly, leukocytes, in general, can quickly migrate through tissues to any site of wounding. This unique capacity is rooted in their characteristic amoeboid motility, the genetic basis of which is poorly understood. Trim33 (also known as Tif1-γ), a nuclear protein that associates with specific DNA-binding transcription factors to modulate gene expression, has been found to be mainly involved in hematopoiesis and gene regulation mediated by TGF-β. Here, we have discovered that in Trim33-deficient zebrafish embryos, primitive macrophages are unable to colonize the central nervous system to become microglia. Moreover, both macrophages and neutrophils of Trim33-deficient embryos display a reduced basal mobility within interstitial tissues, and a profound lack of a response to inflammatory recruitment signals, including local bacterial infections. Correlatively, Trim33-deficient mouse bone marrow-derived macrophages display a strongly reduced three-dimensional amoeboid mobility in fibrous collagen gels. The transcriptional regulator Trim33 is thus revealed as being essential for the navigation of macrophages and neutrophils towards developmental or inflammatory cues within vertebrate tissues

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Section: Discussionmentioning

confidence: 99%

Section: Trim33-deficient Mouse Macrophages Are Impaired In Their Amomentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Trim33 is essential for macrophage and neutrophil mobilization to developmental or inflammatory cues

Demy

Tauzin

Lancino

et al. 2017

Journal of Cell Science

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“…TR body is known to appear after treatment with type I interferon . There are several possible links between interferons and TRIM proteins . Thus, TR body and TIF1 expression may be connected through the type I interferon pathway.…”

Section: Discussionmentioning

confidence: 99%

Anti‐TIF1γ antibody and the expression of TIF1γ in idiopathic inflammatory myopathies

et al. 2018

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Objective: Anti-transcriptional intermediary factor 1 (TIF1) antibody is associated with idiopathic inflammatory myopathies (IIMs). The aim of this study was to investigate the expression of TIF1s in IIMs.Method: TIF1α, β or γ expression in the skin and muscle of patients and controls was studied by immunohistochemistry. Serum myositis-specific autoantibodies were detected by immunoblot.Results: TIF1α was expressed in the skin of most dermatomyositis (DM) patients but not in the controls (80% vs 0%, P < 0.001). TIF1β was expressed in all tissues of patients and controls. TIF1γ was expressed in the muscle of DM patients compared to controls (42.1% vs 0%, P = 0.039) and associated with tubuloreticular bodies (P = 0.003). Anti-TIF1γ was related with TIF1γ expression in the muscle (P = 0.042). Conclusion: TIF1α expression in the skin and TIF1γ in the muscle of DM was increased compared to controls. TIF1γ expression in the muscle of IIMs was related to anti-TIF1γ antibody. K E Y W O R D S autoantibody, dermatomyositis, idiopathic inflammatory myopathy, polymyositis, transcriptional intermediary factor 1

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“…Macrophages are a major cell type involved in innate immune responses and have been especially difficult to modify using available CRISPR methods. In particular, genome editing of macrophage cell lines using all-in-one CRISPR-Cas9 techniques has been inefficient (16) and although newer methods have yielded improved results (17–19), some of these approaches require antibiotic selection and clonal isolation that dramatically delays the phenotyping timeline and risks the loss of original cell properties. To enable high-throughput CRISPR-Cas9 genome-wide knockout (KO) library screens, the murine RAW264.7 macrophage (RAW) cell line has been modified to constitutively express Cas9 for efficient genome editing (20).…”

Section: Introductionmentioning

confidence: 99%

Efficient Immune Cell Genome Engineering with Improved CRISPR Editing Tools

Chan

Gottschalk

Yao

et al. 2020

Preprint

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23CRISPR (clustered regularly interspaced short palindromic repeats)-based methods have 24 revolutionized genome engineering and the study of gene-phenotype relationships. However, 25 modifying cells of the innate immune system, especially macrophages, has been challenging 26 because of cell pathology and low targeting efficiency resulting from nucleic acid activation of 27 sensitive intracellular sensors. Likewise, lymphocytes of the adaptive immune system are largely 28 refractory to CRISPR-enhanced homology-directed repair (HDR) due to inefficient or toxic 29 delivery of donor templates via transient transfection methods. To overcome these challenges and 30 limitations, we developed three improved methods for CRISPR-based genome editing using a hit-31 and-run transient expression strategy to minimize off-target effects and generate more precise 32 genome editing. Overall, our enhanced CRISPR tools and strategies designed to tackle both 33 murine and human immune cell genome engineering are expected to be widely applicable not only 34 in hematopoietic cells but also other mammalian cell types of interest. 35 minimizes off-target effects. Another straight-forward strategy to reduce CRISPR-Cas9 off-target 46 effects is to limit the expression duration of Cas9 or guide-RNA (gRNA), the same rationale behind 47 the use of Cas9 inhibitors. While this can be achieved using transient transfection methods, the 48 on-target editing efficiency can be compromised (15) as compared to the stable lentiviral 49 transduction methods. 50Despite many advances in CRISPR technology, to date there have been very few reports of 51 using the Cas9 nickase strategy for immune cell (myeloid cell or lymphocyte) genome engineering. 52Macrophages are a major cell type involved in innate immune responses and have been especially 53 difficult to modify using available CRISPR methods. In particular, genome editing of macrophage 54 cell lines using all-in-one CRISPR-Cas9 techniques has been inefficient (16) and although newer 55 methods have yielded improved results (17)(18)(19), some of these approaches require antibiotic 56 selection and clonal isolation that dramatically delays the phenotyping timeline and risks the loss 57 of original cell properties. To enable high-throughput CRISPR-Cas9 genome-wide knockout (KO) 58 library screens, the murine RAW264.7 macrophage (RAW) cell line has been modified to 59 constitutively express Cas9 for efficient genome editing (20). While constitutive Cas9 and gRNA 60 expression can lead to the accumulation of off-target mutations in the long run, the doxycycline-61 inducible system pCW-Cas9 (21) helps resolve both issues by controlling the genome editing time 62 window to minimize long-term off-target effects and allowing immediate phenotyping before the 63 onset of potential compensating mechanisms. However, the lack of a live cell marker makes it 64 difficult to identify and isolate the Cas9-expressing population for further analysis. Here we 65 describe a modified method to enable doxycycline-induced Cas...

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TRIM33 switches off Ifnb1 gene transcription during the late phase of macrophage activation

Cited by 56 publications

References 43 publications

Trim33 is essential for macrophage and neutrophil mobilization to developmental or inflammatory cues

Trim33 is essential for macrophage and neutrophil mobilization to developmental or inflammatory cues

Anti‐TIF1γ antibody and the expression of TIF1γ in idiopathic inflammatory myopathies

Efficient Immune Cell Genome Engineering with Improved CRISPR Editing Tools

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