Wnt6 signaling regulates heart muscle development during organogenesis

Danielle L. Lavery, Jennifer Martin, Yvonne D. Turnbull, Stefan Hoppler

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Mesodermal tissue with heart forming potential (cardiogenic mesoderm) is induced during gastrulation. This cardiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart tissue. Inhibition of Wnt/beta-catenin signaling is known to be required early for induction of cardiogenic mesoderm: however, the identity of the inhibiting Writ signal itself is still elusive. We have identified Wnt6 in Xenopus as an endogenous Writ signal, which is expressed in tissues close to and later inside the developing heart. Our loss-of-function experiments show that Wnt6 function is required in the embryo to prevent development of an abnormally large heart muscle. We find, however, that Wnt6 is not required as expected during gastrulation stages, but later during organogenesis stages just before cells of the cardiogenic mesoderm begin to differentiate into heart muscle (myocardium). Our gain-of-function experiments show that Wnt6 and also activated canonical Wnt/beta-catenin signaling are capable of restricting heart muscle development at these relatively late stages of development. This repressive role of Wilt signaling is mediated initially via repression of cardiogenic transcription factors, since reinstatement of GATA function can rescue expression of other cardiogenic transcription factors and downstream cardiomyogenic differentiation genes. (C) 2008 Elsevier Inc. All rights reserved.

Original languageEnglish
Pages (from-to)177-188
Number of pages12
JournalDevelopmental Biology
Volume323
Issue number2
Early online date9 Sep 2008
DOIs
Publication statusPublished - 15 Nov 2008

Keywords

  • Wnt
  • xenopus
  • heart
  • organogenesis
  • embryonic stem-cells
  • cardiac troponin-I
  • xenopus embryos
  • gene-expression
  • beta-catenin
  • laevis
  • cardiomyogenesis
  • specification
  • morphogenesis
  • transcription

Cite this

Wnt6 signaling regulates heart muscle development during organogenesis. / Lavery, Danielle L.; Martin, Jennifer; Turnbull, Yvonne D.; Hoppler, Stefan.

In: Developmental Biology, Vol. 323, No. 2, 15.11.2008, p. 177-188.

Research output: Contribution to journalArticle

Lavery, Danielle L. ; Martin, Jennifer ; Turnbull, Yvonne D. ; Hoppler, Stefan. / Wnt6 signaling regulates heart muscle development during organogenesis. In: Developmental Biology. 2008 ; Vol. 323, No. 2. pp. 177-188.
@article{b9eaa0b6465d4d088217a252eb9c08a0,
title = "Wnt6 signaling regulates heart muscle development during organogenesis",
abstract = "Mesodermal tissue with heart forming potential (cardiogenic mesoderm) is induced during gastrulation. This cardiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart tissue. Inhibition of Wnt/beta-catenin signaling is known to be required early for induction of cardiogenic mesoderm: however, the identity of the inhibiting Writ signal itself is still elusive. We have identified Wnt6 in Xenopus as an endogenous Writ signal, which is expressed in tissues close to and later inside the developing heart. Our loss-of-function experiments show that Wnt6 function is required in the embryo to prevent development of an abnormally large heart muscle. We find, however, that Wnt6 is not required as expected during gastrulation stages, but later during organogenesis stages just before cells of the cardiogenic mesoderm begin to differentiate into heart muscle (myocardium). Our gain-of-function experiments show that Wnt6 and also activated canonical Wnt/beta-catenin signaling are capable of restricting heart muscle development at these relatively late stages of development. This repressive role of Wilt signaling is mediated initially via repression of cardiogenic transcription factors, since reinstatement of GATA function can rescue expression of other cardiogenic transcription factors and downstream cardiomyogenic differentiation genes. (C) 2008 Elsevier Inc. All rights reserved.",
keywords = "Wnt, xenopus, heart, organogenesis, embryonic stem-cells, cardiac troponin-I, xenopus embryos, gene-expression, beta-catenin, laevis, cardiomyogenesis, specification , morphogenesis, transcription",
author = "Lavery, {Danielle L.} and Jennifer Martin and Turnbull, {Yvonne D.} and Stefan Hoppler",
year = "2008",
month = "11",
day = "15",
doi = "10.1016/j.ydbio.2008.08.032",
language = "English",
volume = "323",
pages = "177--188",
journal = "Developmental Biology",
issn = "0012-1606",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Wnt6 signaling regulates heart muscle development during organogenesis

AU - Lavery, Danielle L.

AU - Martin, Jennifer

AU - Turnbull, Yvonne D.

AU - Hoppler, Stefan

PY - 2008/11/15

Y1 - 2008/11/15

N2 - Mesodermal tissue with heart forming potential (cardiogenic mesoderm) is induced during gastrulation. This cardiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart tissue. Inhibition of Wnt/beta-catenin signaling is known to be required early for induction of cardiogenic mesoderm: however, the identity of the inhibiting Writ signal itself is still elusive. We have identified Wnt6 in Xenopus as an endogenous Writ signal, which is expressed in tissues close to and later inside the developing heart. Our loss-of-function experiments show that Wnt6 function is required in the embryo to prevent development of an abnormally large heart muscle. We find, however, that Wnt6 is not required as expected during gastrulation stages, but later during organogenesis stages just before cells of the cardiogenic mesoderm begin to differentiate into heart muscle (myocardium). Our gain-of-function experiments show that Wnt6 and also activated canonical Wnt/beta-catenin signaling are capable of restricting heart muscle development at these relatively late stages of development. This repressive role of Wilt signaling is mediated initially via repression of cardiogenic transcription factors, since reinstatement of GATA function can rescue expression of other cardiogenic transcription factors and downstream cardiomyogenic differentiation genes. (C) 2008 Elsevier Inc. All rights reserved.

AB - Mesodermal tissue with heart forming potential (cardiogenic mesoderm) is induced during gastrulation. This cardiogenic mesoderm later differentiates into heart muscle tissue (myocardium) and non-muscular heart tissue. Inhibition of Wnt/beta-catenin signaling is known to be required early for induction of cardiogenic mesoderm: however, the identity of the inhibiting Writ signal itself is still elusive. We have identified Wnt6 in Xenopus as an endogenous Writ signal, which is expressed in tissues close to and later inside the developing heart. Our loss-of-function experiments show that Wnt6 function is required in the embryo to prevent development of an abnormally large heart muscle. We find, however, that Wnt6 is not required as expected during gastrulation stages, but later during organogenesis stages just before cells of the cardiogenic mesoderm begin to differentiate into heart muscle (myocardium). Our gain-of-function experiments show that Wnt6 and also activated canonical Wnt/beta-catenin signaling are capable of restricting heart muscle development at these relatively late stages of development. This repressive role of Wilt signaling is mediated initially via repression of cardiogenic transcription factors, since reinstatement of GATA function can rescue expression of other cardiogenic transcription factors and downstream cardiomyogenic differentiation genes. (C) 2008 Elsevier Inc. All rights reserved.

KW - Wnt

KW - xenopus

KW - heart

KW - organogenesis

KW - embryonic stem-cells

KW - cardiac troponin-I

KW - xenopus embryos

KW - gene-expression

KW - beta-catenin

KW - laevis

KW - cardiomyogenesis

KW - specification

KW - morphogenesis

KW - transcription

U2 - 10.1016/j.ydbio.2008.08.032

DO - 10.1016/j.ydbio.2008.08.032

M3 - Article

VL - 323

SP - 177

EP - 188

JO - Developmental Biology

JF - Developmental Biology

SN - 0012-1606

IS - 2

ER -