david TUIL
  • E-mail :[email]
  • Phone : 01 44 41 24 23
  • Location : Paris, France
Last update 2011-04-04 18:11:32.768

david TUIL 1st class Researcher INSERM, PhD Biochemistry, Doctor ès sciences

Course and current status


1977: PhD Biochemistry, Paris 7 University, France

1980: Doctor ès Sciences, Paris 7 University, France

Scientific training:

1972-1977: PhD, Cochin University, Paris, France

1977-1983: Doctorate ès Sciences, Cochin University, Paris, France


1975-1980: Biochemistry Assistant of Biochemistry Department, Cochin University, Paris, France

1980-1983: 2nd class Researcher, INSERM (National Institute of Health and Medical Research)

1984-present: 1st class Researcher, INSERM

 Pioneer in SRF and CCArGG box sequence studies

Leader of SRF team (1993-2010) of Genetic and Development Department in Cochin Institute, INSERM 1016

Expert domains:

Gene Regulation and Function, Cardiomyogenesis, Cytoskeleton and Skeletal Myogenesis


31 papers in International Reviewed Journals

Scientific summary

 My major results concern:  The expression of the transferrin gene during development of non-hepatic tissues; the function of the CCArGG box sequence in the promoter of muscular genes and the crucial role of SRF (Serum Response Factor) a CCArGG binding-protein during proliferation and differentiation of C2 myogenic cells. Actually my research focuses on studies of SRF in the striated muscles with several SRF depletion mouse models. We adopted a Cre-loxP inactivation strategy in the mouse to search out in different tissues the function of the ubiquitous and conserved transcriptional factor SRF. Specific inducible or non inducible Cre transgenes allow to target the embryonic or adult Heart or skeletal muscles. SRF heart inactivation during mouse development is lethal. SRF induced for adult cardiac depletion displays decrease of expression of several cardiac genes, reduced cardiac contractility followed by progressive ventricular dilatation, heart failure (dilated cardiomyopathy) leading to death within 2 months. In this model cardiomyocytes showed highly stretched intercalated disks, myofibrillar disarray and low content of F-actin. Inactivation of SRF with a non inducible Cre transgene in the skeletal muscles resulted in severe myofibres maturation defects and deficient regenerative capacities associated with the decrease of skeletal alpha-actin expression as well as IL4 and IGF1. Inducible SRF depletion in adult skeletal muscles provokes their premature aging. My project aims to determine the function of SRF in skeletal muscles during hypertrophy, denervation and regeneration; to identify the whole set target genes regulated by SRF in cardiac and skeletal muscles; to analyse by transgenesis the attempted rescue of the phenotypes observed; to understand the respective contribution of some major targets such as cardiac alpha-actin and IGF1 genes, integrin signalling related genes and microRNAs in our models; to study in transgenic mice the consequence of inducible SRF overexpression in striated muscles; to characterize alterations or modifications of SRF protein isoforms, SRF specific targets, and SRF partners in experimental models of pathologies or human biopsies associated with a remodelling of muscular walls.

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