Martial Lab

(1) Molecular mechanisms controlling pancreas organogenesis and differentiation of pancreatic cells. Project leader: Bernard Peers

The goal of this project is to identify and study regulatory genes involved in the differentiation of pancreatic cells. Using zebrafish as animal model, we are studying the role of several transcription factors (i.e. Meis, Pbx, SOX4 factors) in pancreas development. The expression of these factors has been analysed during zebrafish embryogenesis by in situ hybridization. The role of these factors is studied by loss and gain of function strategies (injection of mRNA and antisens morphonino into zebrafish fertilized eggs). We have also generated zebrafish transgenic lines expressing GFP under the control of the HB9 and Pax6 promoters which are active in endocrine pancreatic cells. Observation of living transgenic embryos under fluorescent microscope allow to follow the formation of the endocrine islet. We are using these transgenic lines to perform a genetic screenning for zebrafish mutants having endocrine pancreatic defects.


(2) Molecular dissection of the role of the PLAG family members in oncogenesis and embryogenesis using the zebrafish as animal model. Project leader: Marianne Voz

PLAG gene family comprise three members, PLAG1, PLAGL1 and PLAGL2 which all seem to be involved in tumor formation. Moreover, PLAG1 and PLAGL2 are mainly expressed during fetal life suggesting important functions during development. To determine their physiological role, we analyse the expression pattern of the PLAG factors during zebrafish development by whole mount in situ and test their role by gain or loss function strategies(injection of mRNAs or of morpholinos/siRNAs). Transgenic approach to ectopically overexpress these factors will evaluate their oncogenic
potential in zebrafish.


(3) Study of the antiangiogenic factor 16K hPRL: understanding of its mechanism of action and evaluation of its therapeutic potential. Project leader: Ingrid Struman.

Our group is studying the 16 kDa N-terminal fragment of human prolactin, also named 16K hPRL that has been shown to be antiangiogenic in vitro and in vivo. Research conducted in our lab attempts to:
* Understand the molecular mechanisms by which 16K hPRL induces apoptosis and inhibits proliferation of endothelial cells.
* Identify the receptor involved in the antiangiogenic action of 16K hPRL.
* Search for minimal fragments of 16K hPRL that retain antiangiogenic activity.
* Determine the effect of 16K hPRL in early blood vessel development in zebrafish.
* Evaluate the potential use of 16K hPRL in an antiangiogenic therapy for cancer and other angiogenesis-related diseases.


(4) The organogenesis of the pituitary gland is characterized in the zebrafish and the regulatory factors governing this process in early embryonic development are investigated.