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Vogel Group

Prof. Dr. Tanja Vogel

Department of Molecular Embryology

Institute of Anatomy and Cell Biology

Albertstr. 17

79104 Freiburg

Tel: 0761 / 203 5086



Prof. Dr. Vogel

Open Positions


Developemental Neurogenetics Lab

Group Members




1. Functional dissection of epigenetic modifications of histones during development of the cerebral cortex

Precursor cells residing in ventricular and subventricular zones give rise to the adult cerebral cortex that consists of six layers formed in an “inside-out manner” during development.
Functionally specialized areas of the neocortex are formed through a gradient of gene expression in the neuroepithelium. This relies on a time-dependent cell fate decision of precursor cells.
We have highlighted the contribution of histone methylation in the neuronal specification of upper layer neurons in an Af9-mutant mouse (Buttner et al. 2010). AF9-interaction partner DOT1L regulates the expression of the transcription factor TBR1 through methylation of Histone H3 at position K79. We highlighted that DOT1L activity prevents the activation of the ER-stress related transcriptional program in vitro (Roidl et al. 2016). Our interests are to further elucidate the transcriptional network of AF9, and DOT1L and their implication in cortical, hippocampal, cerebellar and spinal cord development in vivo and in vitro. Recently we described DOT1L function in cerebellum (Bovio et al. 2018) and cortex (Franz et al. 2018).  We are currently using ChIP-protocols to characterise in detail the distribution of H3K79 methylation in these various neuroanatomical locations to establish this histone mark as essential in balancing proliferation and differentiation of neural stem cells (Bovio et al. 2018). A part of the DFG-funded research training group 2344 "MeInBio" we aim to explore histone modifications and transcriptional regulation in small cell samples and on single cell level.

2. FOXG1 and the aetiology of FOXG1-syndrome

We are currently interested to understand the diverse molecular functions of the forkheadbox transcription FOXG1, which is an essential player in the developing forebrain. Using in vitro and in vivo approaches we are currently studying the effects of reduced expression of the mouse FOXG1, mainly focussing on the hippocampus within the DFG-funded SPP1738.

3. Functional relevance of Tgfβ-signalling for the development of the cerebral cortex

Transforming growth factor β (Tgfβ) mediated neurogenesis has been reported to be increased in older (E16.5) embryonic cortical progenitor cells as compared to that in E13.5 and adult spheres (Vogel et al. 2010). In this project we aimed to reveal key genes that highlight the functions of Tgfβ-signalling during cortical and hippocampal development and function, and how Tgfβ affects neurogenesis in an age-dependent manner.
We investigated the cross-talk and mutually exclusive signals of the PI3K-, mTorc- and Tgfβ-pathways which are implicated to balance proliferation and differentiation in the developing cerebral cortex (Wahane et al. 2014). We further showed that in early cortical development, IGF1/PI3K signalilng and the transcription factor FOXG1 inhibit FOXO- and Tgfβ-mediated Cdkn1a transcription. FOXG1 prevents cell cycle exit by binding to the SMAD/FOXO-protein complex and interferes with Foxo1 and Tgfβ transcription (Vezzali et al. 2016).
Neurogenesis and angiogenesis are both processes influenced by the Tgfβ-signalling pathway. To investigate functions of Tgfβ in forebrain development in vivo, we used a Foxg1-cre-expressing mouse line to conditionally knock-out Tgfbr2. Mutant mice displayed severe haemorrhages mostly in the telencephalon and diencephalon beginning around E13.5. The embryos died between E16 to E17, when the entire forebrain is infiltrated with blood cells. Our work revealed that defective Tgfβ-signalling alters the neuronal secretome that impairs proper migration of endothelial cells (Hellbach et al. 2014). Our work further highlighted that Tgfβ-signalling is also implicated in controling expression of enzymes affecting DNA methylation and that it links to altered neuronal activity in response to stress (Grassi et al. 2017).