Congenital heart defects are some of the most common birth defects. To understand the nature of thesedefects it is important to study signaling pathways, like Retinoic Acid (RA) signaling, which is required fornormal heart development. RA signaling is important for cell differentiation in adult and embryonic tissues.Loss of RA signaling in adult tissues can lead to cancer and in embryos leads to developmental defects.Too much RA signaling can also be teratogenic. Thus, modulation of RA signaling levels is important forproper cell differentiation. The Yelon, using zebrafish, recently discovered a new role for RA signaling inproper cardiomyocyte progenitor selection. Without RA signaling, too many cardiomyocyte progenitorsdifferentiate within a discrete area. The molecular mechanisms that influence cardiomyocyte progenitorselection have not been investigated. Moreover, we are unaware of what is regulating RA signaling.Therefore, the specific aims of my post-doctoral research are: 1) to determine how RA signaling levels affectdifferentiation of cardiomyocyte progenitors in zebrafish; 2) to determine which RA receptors regulatecardiomyocyte progenitors differentiation; 3) and to identify novel regulators of RA signaling.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32HL083591-02
Application #
7207940
Study Section
Special Emphasis Panel (ZRG1-F05 (20))
Program Officer
Meadows, Tawanna
Project Start
2006-03-01
Project End
2008-02-29
Budget Start
2007-03-01
Budget End
2008-02-29
Support Year
2
Fiscal Year
2007
Total Cost
$48,796
Indirect Cost
Name
New York University
Department
Anatomy/Cell Biology
Type
Schools of Medicine
DUNS #
121911077
City
New York
State
NY
Country
United States
Zip Code
10016
Waxman, Joshua S; Yelon, Deborah (2011) Zebrafish retinoic acid receptors function as context-dependent transcriptional activators. Dev Biol 352:128-40
Feng, L; Hernandez, R E; Waxman, J S et al. (2010) Dhrs3a regulates retinoic acid biosynthesis through a feedback inhibition mechanism. Dev Biol 338:1-14
Waxman, Joshua S; Yelon, Deborah (2009) Increased Hox activity mimics the teratogenic effects of excess retinoic acid signaling. Dev Dyn 238:1207-13
Waxman, Joshua S; Keegan, Brian R; Roberts, Richard W et al. (2008) Hoxb5b acts downstream of retinoic acid signaling in the forelimb field to restrict heart field potential in zebrafish. Dev Cell 15:923-34
Waxman, Joshua S; Yelon, Deborah (2007) Comparison of the expression patterns of newly identified zebrafish retinoic acid and retinoid X receptors. Dev Dyn 236:587-95