Journal Article

DZNE-2025-00300

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Impaired primitive erythropoiesis and defective vascular development in Trim71-KO embryos.

Beckröge, T. ; Jux, B. ; Seifert, H. ; Theobald, H. ; De Domenico, E.DZNE* ; Paulusch, S.DZNE* ; Beyer, M.DZNE* ; Schlitzer, A. ; Mass, E. ; Kolanus, W.

2025
EMBO Press Heidelberg

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Please use a persistent id in citations: doi:10.26508/lsa.202402956

Abstract: The transition of an embryo from gastrulation to organogenesis requires precisely coordinated changes in gene expression, but the underlying mechanisms remain unclear. The RNA-binding protein Trim71 is essential for development and serves as a potent regulator of post-transcriptional gene expression. Here, we show that global deficiency of Trim71 induces severe defects in mesoderm-derived cells at the onset of organogenesis. Murine Trim71-KO embryos displayed impaired primitive erythropoiesis, yolk sac vasculature, heart function, and circulation, explaining the embryonic lethality of these mice. Tie2 Cre Trim71 conditional knockout did not induce strong defects, showing that Trim71 expression in endothelial cells and their immediate progenitors is dispensable for embryonic survival. scRNA-seq of E7.5 global Trim71-KO embryos revealed that transcriptomic changes arise already at gastrulation, showing a strong up-regulation of the mesodermal pioneer transcription factor Eomes. We identify Eomes as a direct target of Trim71-mediated mRNA repression via the NHL domain, demonstrating a functional link between these important regulatory genes. Taken together, our data suggest that Trim71-dependent control of gene expression at gastrulation establishes a framework for proper development during organogenesis.

Keyword(s): Animals (MeSH) ; Erythropoiesis: genetics (MeSH) ; Mice (MeSH) ; Mice, Knockout (MeSH) ; Gene Expression Regulation, Developmental: genetics (MeSH) ; Embryo, Mammalian: metabolism (MeSH) ; Organogenesis: genetics (MeSH) ; Yolk Sac: metabolism (MeSH) ; Yolk Sac: blood supply (MeSH) ; Yolk Sac: embryology (MeSH) ; T-Box Domain Proteins: genetics (MeSH) ; T-Box Domain Proteins: metabolism (MeSH) ; Gastrulation: genetics (MeSH) ; Endothelial Cells: metabolism (MeSH) ; Female (MeSH) ; RNA-Binding Proteins: metabolism (MeSH) ; RNA-Binding Proteins: genetics (MeSH) ; Mesoderm: metabolism (MeSH) ; Mesoderm: embryology (MeSH) ; T-Box Domain Proteins ; RNA-Binding Proteins

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Contributing Institute(s):

1. Clinical Single Cell Omics (CSCO) / Systems Medicine (AG Schultze)
2. Platform for Single Cell Genomics and Epigenomics (PRECISE)
3. Immunogenomics and Neurodegeneration (AG Beyer)

Research Program(s):

1. 354 - Disease Prevention and Healthy Aging (POF4-354) (POF4-354)
2. 352 - Disease Mechanisms (POF4-352) (POF4-352)
3. 351 - Brain Function (POF4-351) (POF4-351)

Appears in the scientific report 2025

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