Bakkers Group

Cardiac development and genetics

Wide ranges of congenital and acquired human diseases are associated with pathological conditions in heart formation. To understand the complex genetics of congenital heart defects we study cardiac development in the zebrafish model. We use forward and reverse genetics to identify novel genes that are required for normal heart development and use molecular and cellular techniques to characterize gene function in vivo. Subsequently, we use this information to screen for genetic variations in patients with congenital heart defects to better understand the genetics of the disease.
Our research group is incorporated in the Interuniversity Cardiology Institute of the Netherlands (ICIN).

About the research

Key publications
Smith, K.A., Joziasse, I.C., Chocron, S., van Dinther,M., Guryev, V., Verhoeven, M.C., Rehmann, H., van der Smagt, J.J., Doevendans, P.A., Cuppen, E., Mulder, B.J., ten Dijke, P., Bakkers, J. (2009) Dominant-negative ALK2 allele associates with congenital heart defects. Circulation 119: 3062-3069.

Bakkers, J., Verhoeven, M.C., Abdelilah-Seyfried, S. (2009) Shaping the zebrafish heart: from left-right axis specification to epithelial tissue morphogenesis. Dev. Biol. 330: 213-220.

de Pater, E., Clijsters, L., Marques, S., Lin, Y., Garavito-Aguilar, Z.V., Yelon, D., Bakkers, J. (2009) Distinct phases of cardiomyocyte differentiation regulate growth of the zebrafish heart. Development 136: 1633-1641.

Smith, K.A., Chocron, S., von der Hardt, S., de Pater, E., Soufan, A., Bussmann, J., Schulte-Merker, S., Hammerschmidt, M.,  Bakkers, J. (2008) Rotation and asymmetric development of the zebrafish heart requires directed migration of cardiac progenitor cells.  Dev. Cell, 14: 287–297.

Knoell, R., Postel, R., Wang, J., Kraetzner, R., Hennecke, G., Murthy, K., Rana, B., Kube, D., Knoell, G., Schaefer, K., Hayashi, T., Kimura, A., Schork, N., Toliat, M., Nuernberg, P., Schultheiss, P., Schaper, W., Schaper, J., Bos, E., van Eeden, F., Peters, P., Hasenfuss, G., Chien, K., Bakkers, J. (2007). Laminin alpha 4 and integrin-linked kinase mutations cause human cardiomyopathy via simultaneous defects in cardiomyocytes and in endothelial cells. Circulation 116: 515-525.

Publication list