Dataset: Fz1Fz2 double knock out mouse palate microarray (E13.5)

The closure of an open anatomical structure by the directed growth and fusion of two tissue masses is a recurrent theme in mammalian embryology, and this process plays an integral role in the development of the palate, ventricular septum, neural tube, urethra, diaphragm, and eye. In mice, targeted mutations of the genes encoding frizzled1 (Fz1) and frizzled2 (Fz2) show that these highly homologous integral membrane receptors play an essential and partially redundant role in closure of the palate and ventricular septum, and in the correct positioning of the cardiac outflow tract. When combined with a mutant allele of the planar cell polarity (PCP) gene Vangl2 (Vangl2Lp), Fz1 and/or Fz2 mutations also cause defects in neural tube closure and mis-orientation of inner ear sensory hair cells. These observations indicate that frizzled signaling is involved in diverse tissue closure processes, defects in which account for some of the most common congenital anomalies in humans. Microdissect E13.5 palates from Fz1-/-;Fz2+/+ and Fz1-/-;Fz2-/- embryos and compare transcript abundances by hybridization to Affymetrix 430 2.0 gene chips Supplementary file below reports fold change data.

Species:

mouse

Samples:

6

Source:

E-GEOD-24276

PubMed:

20940229

Updated:

Dec.12, 2014

Registered:

Nov.11, 2014