Cloning and characterization of a novel MyoD enhancer-binding factor

Masakazu Yamamoto, Christopher D. Watt, Ryan J. Schmidt, Unsal Kuscuoglu, Roger Miesfeld, David J. Goldhamer

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Glucocorticoid-induced gene-1 (Gig1) was identified in a yeast one-hybrid screen for factors that interact with the MyoD core enhancer. The Gig1 gene encodes a novel C2H2 zinc finger protein that shares a high degree of sequence similarity with two known DNA binding proteins in humans, Glut4 enhancer factor and papillomavirus binding factor (PBF). The mouse ortholog of PBF was also isolated in the screen. The DNA binding domain of Gig1, which contains TCF-E-tail CR1 and CR2 motifs shown to mediate promoter specificity of TCF-E-tail isoforms, was mapped to a C-terminal domain that is highly conserved in Glut4 enhancer factor and PBF. In mouse embryos, in situ hybridization revealed a restricted pattern of expression of Gig1 that overlaps with MyoD expression. A nuclear-localized lacZ knockin null allele of Gig1 was produced to study Gig1 expression with greater resolution and to assess Gig1 functions. X-gal staining of Gig1nlacZ heterozygous embryos revealed Gig1 expression in myotomal myocytes, skeletal muscle precursors in the limb, and in nascent muscle fibers of the body wall, head and neck, and limbs through E14.5 (latest stage examined). Gig1 was also expressed in a subset of Scleraxis-positive tendon precursors/rudiments of the limbs, but not in the earliest tendon precursors of the somite (syndetome) defined by Scleraxis expression. Additional regions of Gig1 expression included the apical ectodermal ridge, neural tube roof plate and floor plate, apparent motor neurons in the ventral neural tube, otic vesicles, notochord, and several other tissues representing all three germ layers. Gig1 expression was particularly well represented in epithelial tissues and in a number of cells/tissues of neural crest origin. Expression of both the endogenous MyoD gene and a reporter gene driven by MyoD regulatory elements was similar in wild-type and homozygous null Gig1nlacZ embryos, and mutant mice were viable and fertile, indicating that the functions of Gig1 are redundant with other factors.

Original languageEnglish (US)
Pages (from-to)715-728
Number of pages14
JournalMechanisms of Development
Volume124
Issue number9-10
DOIs
StatePublished - Sep 2007

Fingerprint

Glucocorticoids
Organism Cloning
Genes
Gene Expression
Neural Tube
Embryonic Structures
Extremities
Tendons
Tail
Notochord
Germ Layers
Somites
Neural Crest
DNA-Binding Proteins
Motor Neurons
Reporter Genes
Muscle Cells
In Situ Hybridization
Ear
Protein Isoforms

Keywords

  • Core enhancer
  • Gene targeting
  • Gig1
  • lacZ knockin
  • Mouse
  • MyoD
  • Myogenesis
  • Papillomavirus binding factor
  • Pbf
  • Tendon precursor
  • Transcription

ASJC Scopus subject areas

  • Developmental Biology
  • Developmental Neuroscience

Cite this

Yamamoto, M., Watt, C. D., Schmidt, R. J., Kuscuoglu, U., Miesfeld, R., & Goldhamer, D. J. (2007). Cloning and characterization of a novel MyoD enhancer-binding factor. Mechanisms of Development, 124(9-10), 715-728. https://doi.org/10.1016/j.mod.2007.07.002

Cloning and characterization of a novel MyoD enhancer-binding factor. / Yamamoto, Masakazu; Watt, Christopher D.; Schmidt, Ryan J.; Kuscuoglu, Unsal; Miesfeld, Roger; Goldhamer, David J.

In: Mechanisms of Development, Vol. 124, No. 9-10, 09.2007, p. 715-728.

Research output: Contribution to journalArticle

Yamamoto, M, Watt, CD, Schmidt, RJ, Kuscuoglu, U, Miesfeld, R & Goldhamer, DJ 2007, 'Cloning and characterization of a novel MyoD enhancer-binding factor', Mechanisms of Development, vol. 124, no. 9-10, pp. 715-728. https://doi.org/10.1016/j.mod.2007.07.002
Yamamoto, Masakazu ; Watt, Christopher D. ; Schmidt, Ryan J. ; Kuscuoglu, Unsal ; Miesfeld, Roger ; Goldhamer, David J. / Cloning and characterization of a novel MyoD enhancer-binding factor. In: Mechanisms of Development. 2007 ; Vol. 124, No. 9-10. pp. 715-728.
@article{234fe9680c1348468db93c384ebfbc5b,
title = "Cloning and characterization of a novel MyoD enhancer-binding factor",
abstract = "Glucocorticoid-induced gene-1 (Gig1) was identified in a yeast one-hybrid screen for factors that interact with the MyoD core enhancer. The Gig1 gene encodes a novel C2H2 zinc finger protein that shares a high degree of sequence similarity with two known DNA binding proteins in humans, Glut4 enhancer factor and papillomavirus binding factor (PBF). The mouse ortholog of PBF was also isolated in the screen. The DNA binding domain of Gig1, which contains TCF-E-tail CR1 and CR2 motifs shown to mediate promoter specificity of TCF-E-tail isoforms, was mapped to a C-terminal domain that is highly conserved in Glut4 enhancer factor and PBF. In mouse embryos, in situ hybridization revealed a restricted pattern of expression of Gig1 that overlaps with MyoD expression. A nuclear-localized lacZ knockin null allele of Gig1 was produced to study Gig1 expression with greater resolution and to assess Gig1 functions. X-gal staining of Gig1nlacZ heterozygous embryos revealed Gig1 expression in myotomal myocytes, skeletal muscle precursors in the limb, and in nascent muscle fibers of the body wall, head and neck, and limbs through E14.5 (latest stage examined). Gig1 was also expressed in a subset of Scleraxis-positive tendon precursors/rudiments of the limbs, but not in the earliest tendon precursors of the somite (syndetome) defined by Scleraxis expression. Additional regions of Gig1 expression included the apical ectodermal ridge, neural tube roof plate and floor plate, apparent motor neurons in the ventral neural tube, otic vesicles, notochord, and several other tissues representing all three germ layers. Gig1 expression was particularly well represented in epithelial tissues and in a number of cells/tissues of neural crest origin. Expression of both the endogenous MyoD gene and a reporter gene driven by MyoD regulatory elements was similar in wild-type and homozygous null Gig1nlacZ embryos, and mutant mice were viable and fertile, indicating that the functions of Gig1 are redundant with other factors.",
keywords = "Core enhancer, Gene targeting, Gig1, lacZ knockin, Mouse, MyoD, Myogenesis, Papillomavirus binding factor, Pbf, Tendon precursor, Transcription",
author = "Masakazu Yamamoto and Watt, {Christopher D.} and Schmidt, {Ryan J.} and Unsal Kuscuoglu and Roger Miesfeld and Goldhamer, {David J.}",
year = "2007",
month = "9",
doi = "10.1016/j.mod.2007.07.002",
language = "English (US)",
volume = "124",
pages = "715--728",
journal = "Mechanisms of Development",
issn = "0925-4773",
publisher = "Elsevier Ireland Ltd",
number = "9-10",

}

TY - JOUR

T1 - Cloning and characterization of a novel MyoD enhancer-binding factor

AU - Yamamoto, Masakazu

AU - Watt, Christopher D.

AU - Schmidt, Ryan J.

AU - Kuscuoglu, Unsal

AU - Miesfeld, Roger

AU - Goldhamer, David J.

PY - 2007/9

Y1 - 2007/9

N2 - Glucocorticoid-induced gene-1 (Gig1) was identified in a yeast one-hybrid screen for factors that interact with the MyoD core enhancer. The Gig1 gene encodes a novel C2H2 zinc finger protein that shares a high degree of sequence similarity with two known DNA binding proteins in humans, Glut4 enhancer factor and papillomavirus binding factor (PBF). The mouse ortholog of PBF was also isolated in the screen. The DNA binding domain of Gig1, which contains TCF-E-tail CR1 and CR2 motifs shown to mediate promoter specificity of TCF-E-tail isoforms, was mapped to a C-terminal domain that is highly conserved in Glut4 enhancer factor and PBF. In mouse embryos, in situ hybridization revealed a restricted pattern of expression of Gig1 that overlaps with MyoD expression. A nuclear-localized lacZ knockin null allele of Gig1 was produced to study Gig1 expression with greater resolution and to assess Gig1 functions. X-gal staining of Gig1nlacZ heterozygous embryos revealed Gig1 expression in myotomal myocytes, skeletal muscle precursors in the limb, and in nascent muscle fibers of the body wall, head and neck, and limbs through E14.5 (latest stage examined). Gig1 was also expressed in a subset of Scleraxis-positive tendon precursors/rudiments of the limbs, but not in the earliest tendon precursors of the somite (syndetome) defined by Scleraxis expression. Additional regions of Gig1 expression included the apical ectodermal ridge, neural tube roof plate and floor plate, apparent motor neurons in the ventral neural tube, otic vesicles, notochord, and several other tissues representing all three germ layers. Gig1 expression was particularly well represented in epithelial tissues and in a number of cells/tissues of neural crest origin. Expression of both the endogenous MyoD gene and a reporter gene driven by MyoD regulatory elements was similar in wild-type and homozygous null Gig1nlacZ embryos, and mutant mice were viable and fertile, indicating that the functions of Gig1 are redundant with other factors.

AB - Glucocorticoid-induced gene-1 (Gig1) was identified in a yeast one-hybrid screen for factors that interact with the MyoD core enhancer. The Gig1 gene encodes a novel C2H2 zinc finger protein that shares a high degree of sequence similarity with two known DNA binding proteins in humans, Glut4 enhancer factor and papillomavirus binding factor (PBF). The mouse ortholog of PBF was also isolated in the screen. The DNA binding domain of Gig1, which contains TCF-E-tail CR1 and CR2 motifs shown to mediate promoter specificity of TCF-E-tail isoforms, was mapped to a C-terminal domain that is highly conserved in Glut4 enhancer factor and PBF. In mouse embryos, in situ hybridization revealed a restricted pattern of expression of Gig1 that overlaps with MyoD expression. A nuclear-localized lacZ knockin null allele of Gig1 was produced to study Gig1 expression with greater resolution and to assess Gig1 functions. X-gal staining of Gig1nlacZ heterozygous embryos revealed Gig1 expression in myotomal myocytes, skeletal muscle precursors in the limb, and in nascent muscle fibers of the body wall, head and neck, and limbs through E14.5 (latest stage examined). Gig1 was also expressed in a subset of Scleraxis-positive tendon precursors/rudiments of the limbs, but not in the earliest tendon precursors of the somite (syndetome) defined by Scleraxis expression. Additional regions of Gig1 expression included the apical ectodermal ridge, neural tube roof plate and floor plate, apparent motor neurons in the ventral neural tube, otic vesicles, notochord, and several other tissues representing all three germ layers. Gig1 expression was particularly well represented in epithelial tissues and in a number of cells/tissues of neural crest origin. Expression of both the endogenous MyoD gene and a reporter gene driven by MyoD regulatory elements was similar in wild-type and homozygous null Gig1nlacZ embryos, and mutant mice were viable and fertile, indicating that the functions of Gig1 are redundant with other factors.

KW - Core enhancer

KW - Gene targeting

KW - Gig1

KW - lacZ knockin

KW - Mouse

KW - MyoD

KW - Myogenesis

KW - Papillomavirus binding factor

KW - Pbf

KW - Tendon precursor

KW - Transcription

UR - http://www.scopus.com/inward/record.url?scp=34548522064&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548522064&partnerID=8YFLogxK

U2 - 10.1016/j.mod.2007.07.002

DO - 10.1016/j.mod.2007.07.002

M3 - Article

C2 - 17693064

AN - SCOPUS:34548522064

VL - 124

SP - 715

EP - 728

JO - Mechanisms of Development

JF - Mechanisms of Development

SN - 0925-4773

IS - 9-10

ER -