School of Life Sciences
 

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Fred Sablitzky

Emeritus Professor of Genetics,

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Biography

1999-2018 Professor of Genetics, Genetics, Biology, Life Sciences, Molecular Cell & Developmental Biology, University of Nottingham

1998-1999 Reader in Molecular Genetics, Dept. of Medicine, UCL, London

1995-1999 Wellcome Trust Europ. Senior Res. Fellow, Dept. of Medicine, UCL, London

1989-1995 Head of Dev. Haematology Unit, Max-Delbrück-Laboratory, Max-Planck-Society, Cologne

1987-1989 Post-doctoral position, Prof Bob Phillips, University of Toronto

1985-1987 Post-doctoral position, Prof Klaus Rajewsky, University of Cologne

1996 Habilitation (venia legendi) in Genetics, University of Cologne

1985 PhD Genetics/Immunology, Prof Klaus Rajewsky, University of Cologne

1981 Diploma in Biology/Immunology, Prof Klaus Rajewsky, University of Cologne

1976-1980 Biology UG study, University of Cologne

Research Summary

Molecular regulators of cell fate

Utilising molecular, cell biology and biochemical techniques including gain- and loss-of-function analysis in vertebrate model systems such as mice and zebrafish, we are analysing several genes to determine their functional role in cell fate and function during development and the adult.

We identified Id4 (Riechmann et al, 1994), the fourth member of the Id protein family (Norton et al, 1998) and through analysis of knockout and transgenic mouse models established that Id4 plays a crucial role in neural and glial progenitor cell proliferation and timing of differentiation (Bedford et al, 2005). Several subsequent fruitful collaborations revealed that Id4 promotes osteoblast differentiation (Tokuzawa et al, 2010) and acts as tumour suppressor gene in chronic lymphocytic leukemia (CLL) (Chen et al, 2011). In addition, Id4 regulates mammary gland development by suppressing p38MAPK activity and recently it was shown that Id4 levels dictate the stem cell state in mouse spermatogonia (Helsel et al, 2017).

Lyl-1 and scl /tal-1, two related bHLH transcription factors, display highly overlapping expression patterns during cardiovascular and hematopoietic ontogeny (Giroux et al, 2007). Analysis of lyl-1/lacZ knockin mice revealed that lyl-1-deficient bone marrow cells have a reduced capacity to repopulate lymphoid and myeloid lineages (Capron et al, 2006). Importantly, either lyl1 or scl/tal1, a related bHLH transcription factor, is required for survival of adult haematopoietic stem and progenitor cells (Souroullas et al, 2009). In addition, lyl-1 activity is required for the maturation of newly formed blood vessels in adult mice (Pirot et al, 2010) and lyl-1-dificiency induces a stress erythropoiesis (Capron et al, 2011).

We discovered DEF6 (Hotfilder et al, 1999), an atypical Rho-family guanine nucleotide exchange factor (Mavrakis et al, 2004) that is predominantly expressed in T cells. DEF6 (also known as IBP or SLAT) is recruited to the immunological synapse upon T cell activation and localisation of DEF6 to the centre of the immune synapse is dependent upon ITK, a Tec-family kinase that phosphorylates DEF6 (Hey et al, 2012) and regulates the spatiotemporal organisation of components of T cell signalling pathways and Cdc42-dependent actin polymerisation. In zebrafish, def6a is required for convergent extension cell movements during zebrafish gastrulation downstream of Wnt5b signalling (Goudevenou et al, 2011).

https://scholar.google.co.uk/citations?user=JT6mspYAAAAJ&hl=en

School of Life Sciences

University of Nottingham
Medical School
Queen's Medical Centre
Nottingham NG7 2UH

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