Wnt/β-catenin signaling acts upstream of N-myc, BMP4, and FGF signaling to regulate proximal-distal patterning in the lung

Weiguo Shu; Susan Guttentag; Zhishan Wang; Thomas Andl; Philip Ballard; Min Min Lu; Stefano Piccolo; Walter Birchmeier; Jeffrey A. Whitsett; Sarah E. Millar; Edward E. Morrisey

doi:10.1016/j.ydbio.2005.04.014

Wnt/β-catenin signaling acts upstream of N-myc, BMP4, and FGF signaling to regulate proximal-distal patterning in the lung

Weiguo Shu
, Susan Guttentag
, Zhishan Wang
, Thomas Andl
, Philip Ballard
, Min Min Lu
, Stefano Piccolo
, Walter Birchmeier
, Jeffrey A. Whitsett
, Sarah E. Millar
, Edward E. Morrisey

Markey Cancer Center / Cancer Research Priority Initiative

Producción científica: Article › revisión exhaustiva

269 Citas (Scopus)

Resumen

Branching morphogenesis in the lung serves as a model for the complex patterning that is reiterated in multiple organs throughout development. β-catenin and Wnt signaling mediate critical functions in cell fate specification and differentiation, but specific functions during branching morphogenesis have remained unclear. Here, we show that Wnt/β-catenin signaling regulates proximal-distal differentiation of airway epithelium. Inhibition of Wnt/β-catenin signaling, either by expression of Dkk1 or by tissue-specific deletion of β-catenin, results in disruption of distal airway development and expansion of proximal airways. Wnt/β-catenin functions upstream of BMP4, FGF signaling, and N-myc. Moreover, we show that β-catenin and LEF/TCF activate the promoters of BMP4 and N-myc. Thus, Wnt/β-catenin signaling is a critical upstream regulator of proximal-distal patterning in the lung, in part, through regulation of N-myc, BMP4, and FGF signaling.

Idioma original	English
Páginas (desde-hasta)	226-239
Número de páginas	14
Publicación	Developmental Biology
Volumen	283
N.º	1
DOI	https://doi.org/10.1016/j.ydbio.2005.04.014
Estado	Published - jul 1 2005

Nota bibliográfica

Funding Information:
The authors would like to thank Peter Klein for the TCF3 expression plasmids, Arnold Levine for the β-catenin/4145 expression plasmid, and Constance Scharff for SU5402. The authors thank Jonathan Epstein for helpful suggestions during these studies. These studies were supported by funding from the NIH to E.E.M. (P01 HL075215) and S.E.M. (R01 AR47709). E.E.M. is an Established Investigator of the American Heart Association.

Financiación

The authors would like to thank Peter Klein for the TCF3 expression plasmids, Arnold Levine for the β-catenin/4145 expression plasmid, and Constance Scharff for SU5402. The authors thank Jonathan Epstein for helpful suggestions during these studies. These studies were supported by funding from the NIH to E.E.M. (P01 HL075215) and S.E.M. (R01 AR47709). E.E.M. is an Established Investigator of the American Heart Association.

Financiadores	Número del financiador
National Institutes of Health (NIH)	R01 AR47709
National Heart, Lung, and Blood Institute (NHLBI)	P01HL075215

ASJC Scopus subject areas

Molecular Biology
Developmental Biology
Cell Biology

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10.1016/j.ydbio.2005.04.014

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title = "Wnt/β-catenin signaling acts upstream of N-myc, BMP4, and FGF signaling to regulate proximal-distal patterning in the lung",

abstract = "Branching morphogenesis in the lung serves as a model for the complex patterning that is reiterated in multiple organs throughout development. β-catenin and Wnt signaling mediate critical functions in cell fate specification and differentiation, but specific functions during branching morphogenesis have remained unclear. Here, we show that Wnt/β-catenin signaling regulates proximal-distal differentiation of airway epithelium. Inhibition of Wnt/β-catenin signaling, either by expression of Dkk1 or by tissue-specific deletion of β-catenin, results in disruption of distal airway development and expansion of proximal airways. Wnt/β-catenin functions upstream of BMP4, FGF signaling, and N-myc. Moreover, we show that β-catenin and LEF/TCF activate the promoters of BMP4 and N-myc. Thus, Wnt/β-catenin signaling is a critical upstream regulator of proximal-distal patterning in the lung, in part, through regulation of N-myc, BMP4, and FGF signaling.",

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author = "Weiguo Shu and Susan Guttentag and Zhishan Wang and Thomas Andl and Philip Ballard and Lu, \{Min Min\} and Stefano Piccolo and Walter Birchmeier and Whitsett, \{Jeffrey A.\} and Millar, \{Sarah E.\} and Morrisey, \{Edward E.\}",

note = "Funding Information: The authors would like to thank Peter Klein for the TCF3 expression plasmids, Arnold Levine for the β-catenin/4145 expression plasmid, and Constance Scharff for SU5402. The authors thank Jonathan Epstein for helpful suggestions during these studies. These studies were supported by funding from the NIH to E.E.M. (P01 HL075215) and S.E.M. (R01 AR47709). E.E.M. is an Established Investigator of the American Heart Association.",

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AU - Shu, Weiguo

AU - Guttentag, Susan

AU - Wang, Zhishan

AU - Andl, Thomas

AU - Ballard, Philip

AU - Lu, Min Min

AU - Piccolo, Stefano

AU - Birchmeier, Walter

AU - Whitsett, Jeffrey A.

AU - Millar, Sarah E.

AU - Morrisey, Edward E.

N1 - Funding Information: The authors would like to thank Peter Klein for the TCF3 expression plasmids, Arnold Levine for the β-catenin/4145 expression plasmid, and Constance Scharff for SU5402. The authors thank Jonathan Epstein for helpful suggestions during these studies. These studies were supported by funding from the NIH to E.E.M. (P01 HL075215) and S.E.M. (R01 AR47709). E.E.M. is an Established Investigator of the American Heart Association.

PY - 2005/7/1

Y1 - 2005/7/1

N2 - Branching morphogenesis in the lung serves as a model for the complex patterning that is reiterated in multiple organs throughout development. β-catenin and Wnt signaling mediate critical functions in cell fate specification and differentiation, but specific functions during branching morphogenesis have remained unclear. Here, we show that Wnt/β-catenin signaling regulates proximal-distal differentiation of airway epithelium. Inhibition of Wnt/β-catenin signaling, either by expression of Dkk1 or by tissue-specific deletion of β-catenin, results in disruption of distal airway development and expansion of proximal airways. Wnt/β-catenin functions upstream of BMP4, FGF signaling, and N-myc. Moreover, we show that β-catenin and LEF/TCF activate the promoters of BMP4 and N-myc. Thus, Wnt/β-catenin signaling is a critical upstream regulator of proximal-distal patterning in the lung, in part, through regulation of N-myc, BMP4, and FGF signaling.

AB - Branching morphogenesis in the lung serves as a model for the complex patterning that is reiterated in multiple organs throughout development. β-catenin and Wnt signaling mediate critical functions in cell fate specification and differentiation, but specific functions during branching morphogenesis have remained unclear. Here, we show that Wnt/β-catenin signaling regulates proximal-distal differentiation of airway epithelium. Inhibition of Wnt/β-catenin signaling, either by expression of Dkk1 or by tissue-specific deletion of β-catenin, results in disruption of distal airway development and expansion of proximal airways. Wnt/β-catenin functions upstream of BMP4, FGF signaling, and N-myc. Moreover, we show that β-catenin and LEF/TCF activate the promoters of BMP4 and N-myc. Thus, Wnt/β-catenin signaling is a critical upstream regulator of proximal-distal patterning in the lung, in part, through regulation of N-myc, BMP4, and FGF signaling.

KW - BMP

KW - Dickkopf-1

KW - FGF

KW - Lung development

KW - Wnt

KW - β-catenin

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Wnt/β-catenin signaling acts upstream of N-myc, BMP4, and FGF signaling to regulate proximal-distal patterning in the lung

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

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