Stephane Zaffran
  • E-mail :[email]
  • Phone : +33 4 91 32 43 86
  • Location : Marseille, France
Last update 2011-04-05 11:07:47.041

Stephane Zaffran PhD Developmental Biology

Course and current status

Academic Training and Degrees

March 2005: Habilitation (HDR), University of Paris VII, Paris, France.

Sept 2003: Qualification for experimental manipulation on animal (Level 1)(#13-394).

2001-2002: Postdoctoral training, Department of Developmental Biology, URA 2578,

Pasteur Institute, Paris, France. (Advisor: Pr. M. Buckingham).

Topic: Cardiac development in mouse embryo.

1997-2001: Postdoctoral training, Brookdale Department of Mol, Cell and Dev Biol,

Mount Sinai School of Medicine, New York, USA. (Advisor: Pr. M. Frasch)

Topic: Formation of cardiac and visceral musculatures in Drosophila embryo.

1993-1997: PhD, Developmental Biology Institute, University of Marseille, France.

(Advisor: Dr. M. Sémériva)

Title: Morphogenesis of the dorsal vessel in Drosophila melanogaster.

1987-1992: MSc, Cell Biology, Specialization in Genetics.

 

Appointments

2009-present: Group Leader, INSERM. Research Director (DR2)

UMR_S910 Inserm

Director: Pr. N. Lévy

2006-2008: C.N.R.S. research Fellow (CR1)

Developmental Biology Institute of Marseille-Luminy, France.

Director: Dr. Geneviève Rougon

2002-2005: C.N.R.S. research Fellow (CR1)

Staff member of the Department of Developmental Biology,

Director: Pr. Margaret Buckingham

Pasteur Institute, Paris, France.

Scientific summary

My main interest is to understand the etiology of congenital heart diseases. I have extensive experience in cardiac development, explant cultures and molecular genetics. Using these techniques, I have shown that the second heart field (SHF) contributes to the right ventricle and that atrial myocardium derives from the posterior region of the SHF (Zaffran et al., 2004; Galli et al., 2008). Since 2006, my team has been working on Raldh2 mutant mice. We have recently demonstrated that the heart phenotype of Raldh2 mutants is mainly the result of abnormal development of the SHF (Ryckebusch et al., 2008). In collaboration with other labs, we have shown that retinoic acid (RA) might be involved in variability observed in DiGeorge syndrome patients (Ryckebusch et al., 2010). Moreover, in this analysis on the function of RA in the embryonic heart, focusing on regional anterior-posterior patterning we have identified that Hoxa1, Hoxb1 and Hoxa3 genes are expressed in cardiac progenitor cells in the SHF that contribute to both the arterial and venous poles of the heart (Bertrand et al., 2011). We will continue our investigation on the function of Hox genes in cardiac development by using mouse and chick models.

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