PUBLICATION

Trim33 / Tif1-γ is essential for macrophage and neutrophil mobilisation to developmental or inflammatory cues

Authors

Demy, D.L., Tauzin, M., Lancino, M., le Cabec, V., Redd, M., Murayama, E., Maridonneau-Parini, I., Trede, N., Herbomel, P.

ID

ZDB-PUB-170721-7

Date

2017

Source

Journal of Cell Science 130(17): 2797-2807 (Journal)

Registered Authors

Demy, Doris-Lou, Herbomel, Philippe, Lancino, Mylène, Murayama, Emi, Redd, Michael, Tauzin, Muriel, Trede, Nick

Keywords

Amoeboid motility, In vivo, Leukocyte recruitment, Macrophages, Neutrophils, Tif1-gamma, Trim33, Zebrafish

MeSH Terms

Transcription Factors/deficiency
Transcription Factors/genetics
Transcription Factors/metabolism*
Microglia/metabolism
Mice
Cell Movement
Bone Marrow Cells/metabolism
Neutrophils/metabolism*
Bacterial Infections/pathology
Macrophages/metabolism*
Retina/pathology
Inflammation/metabolism
Inflammation/pathology*
Zebrafish Proteins/genetics
Zebrafish Proteins/metabolism
Myeloid Cells/metabolism
Mutation/genetics
Animals
Central Nervous System/metabolism
Central Nervous System/pathology

(all 20)

PubMed

28724755 Full text @ J. Cell Sci.

Abstract

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.

Genes / Markers

Figures