Salim Abdelilah-Seyfried
Max Delbrück Center for
Molecular Medicine
Berlin-Buch
Robert-Rössle Str. 10
13125 Berlin
e-mail:
Salim Abdelilah-Seyfried studied Biology and Biochemistry at the Hein-
rich-Heine University Düsseldorf, the Manchester Institute of Science and
Technology, and the Eberhard Karls University Tübingen from 1988-2003.
For his Diploma and Ph.D. thesis work, he joined the lab of Wolfgang Drie-
ver at Harvard University (USA) where he participated in large-scale zeb-
rafsh developmental screens. After obtaining his Ph.D. in 1996, he started
his postdoctoral work in the lab of Yuh-Nung Jan at the University of
California in San Francisco where he worked on Drosophila and zebrafsh
cellular polarity. Since 2002 he has been heading his own research group
“Zebrafsh Cardiovascular Developmental Genetics” at the Max Delbrück
Center for Molecular Medicine in Berlin-Buch. In 2010, he was awarded a
Heisenberg Fellowship of the DFG.
nier, D.Y., and Abdelilah-Seyfried, S. (2001). Positional cloning of heart and soul reveals multiple
roles for PKC lambda in zebrafsh organogenesis. Curr Biol. 11, 1492-502.
Lecuit, T., Lenne, P.F., and Munro, E. (2011). Force generation, transmission, and integration du-
ring cell and tissue morphogenesis. Annu. Rev. Cell Dev. Biol. 27, 157-184.
Lenhart, K.F., Lin, S.Y., Titus, T.A., Postlethwait, J.H., and Burdine, R.D. (2011). Two additional
midline barriers function with midline lefty1 expression to maintain asymmetric Nodal signaling
during left-right axis specifcation in zebrafsh. Development. 138, 4405-10.
Lenhart, K.F., Holtzman, N.G., Williams, J.R., and Burdine, R.D. (2013). Integration of nodal and
BMP signals in the heart requires FoxH1 to create left-right differences in cell migration rates
that direct cardiac asymmetry. PLoS Genet. 9, e1003109.
Long, S., Ahmad, N., and Rebagliati, M. (2003). The zebrafsh nodal-related gene southpaw is
required for visceral and diencephalic left-right asymmetry. Development 130, 2303-2316.
Peterson, R. T., Mably, J. D., Chen, J. N., and Fishman, M. C., (2001). Convergence of distinct
pathways to heart patterning revealed by the small molecule concentramide and the mutation
heart-and-soul. Curr Biol. 11, 1481-91.
Rohr, S., Bit-Avragim, N., Abdelilah-Seyfried, S., (2006). Heart and soul/PRKCi and nagie oko/
Mpp5 regulate myocardial coherence and remodeling during cardiac morphogenesis. Develop-
ment. 133, 107-115.
Rohr, S., Otten, C., and Abdelilah-Seyfried,S. (2008). Asymmetric involution of the myocardial
feld drives heart tube formation in zebrafsh. Circ. Res. 102, e12-e19.
Schier, A.F. (2009). Nodal morphogens. Cold Spring Harb. Perspect. Biol. 1, a003459.
Schilling, T.F., Concordet, J.P., and Ingham, P.W. (1999). Regulation of left-right asymmetries in
the zebrafsh by Shh and BMP4. Dev. Biol. 210, 277-287.
Smith,K.A., Chocron,S., von der,H.S., de,P.E., Soufan,A., Bussmann,J., Schulte-Merker,S.,
Hammerschmidt,M., and Bakkers,J. (2008). Rotation and asymmetric development of the zebra-
fsh heart requires directed migration of cardiac progenitor cells. Dev. Cell 14, 287-297.
Smith, K.A., Noël, E., Thurlings, I., Rehmann, H., Chocron, S., and Bakkers, J. (2011). Bmp and
nodal independently regulate lefty1 expression to maintain unilateral nodal activity during left-
right axis specifcation in zebrafsh. PLoS Genet.7, e1002289.
Staudt, D. and Stainier, D.Y. (2012). Uncovering the molecular and cellular mechanisms of heart
development using the zebrafsh. Annu Rev Genet. 46, 397-418.
Trinh, L. A. and Stainier, D. Y. (2004). Fibronectin Regulates Epithelial Organization during Myo-
cardial Migration in Zebrafsh. Dev. Cell. 6, 371-382.
Veerkamp, J., Rudolph, F., Cseresnyes, Z., Priller, F., Otten, C., Renz, M., Schaefer, L., and Abdelilah-
Seyfried, S. (2013). Unilateral dampening of Bmp activity by nodal generates cardiac left-right
asymmetry. Dev Cell. 24, 660-667.
Widmann, T.J. and Dahmann, C. (2009). Dpp signaling promotes the cuboidal-to-columnar sha-
pe transition of Drosophila wing disc epithelia by regulating Rho1. J Cell Sci. 122, 1362-1373.
Zhang, H. and Bradley, A. (1996). Mice defcient for BMP2 are nonviable and have defects in
amnion/chorion and cardiac development. Development 122, 2977-2986.
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