Frizzled 1 and frizzled 2 genes function in palate, ventricular septum and neural tube closure: General implications for tissue fusion processes

Huimin Yu, Philip M. Smallwood, Yanshu Wang, Roman Vidaltamayo, Randall Reed, Jeremy Nathans

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

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 frizzled 1 (Fz1) and frizzled 2 (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 gene Vangl2 (Vangl2Lp), Fz1 and/or Fz2 mutations also cause defects in neural tube closure and misorientation 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. © 2010. Published by The Company of Biologists Ltd.
Original languageEnglish
Pages (from-to)3707-3717
Number of pages11
JournalDevelopment
DOIs
Publication statusPublished - 1 Nov 2010

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Ventricular Septum
Neural Tube
Palate
Cell Polarity
Mutation
Embryology
Neural Tube Defects
Inner Ear
Urethra
Diaphragm
Genes
Alleles
Membranes
Growth

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology

Cite this

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abstract = "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 frizzled 1 (Fz1) and frizzled 2 (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 gene Vangl2 (Vangl2Lp), Fz1 and/or Fz2 mutations also cause defects in neural tube closure and misorientation 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. {\circledC} 2010. Published by The Company of Biologists Ltd.",
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Frizzled 1 and frizzled 2 genes function in palate, ventricular septum and neural tube closure: General implications for tissue fusion processes. / Yu, Huimin; Smallwood, Philip M.; Wang, Yanshu; Vidaltamayo, Roman; Reed, Randall; Nathans, Jeremy.

In: Development, 01.11.2010, p. 3707-3717.

Research output: Contribution to journalArticle

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AU - Nathans, Jeremy

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AB - 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 frizzled 1 (Fz1) and frizzled 2 (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 gene Vangl2 (Vangl2Lp), Fz1 and/or Fz2 mutations also cause defects in neural tube closure and misorientation 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. © 2010. Published by The Company of Biologists Ltd.

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