Loss of Orphan Receptor Germ Cell Nuclear Factor Function Results in Ectopic Development of the Tail Bud and a Novel Posterior Truncation

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Published inMolecular and Cellular Biology Vol. 21; no. 2; pp. 663 - 677
Main Authors Chung, Arthur C.-K., Katz, Deborah, Pereira, Fred A., Jackson, Kathy J., DeMayo, Francesco J., Cooney, Austin J., O'Malley, Bert W.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.01.2001
Taylor & Francis
Subjects
Animals
Cell Differentiation
Choristoma - embryology
Choristoma - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Embryonic and Fetal Development
Fetal Death
GCNF gene
Gene Deletion
Gene Expression Regulation, Developmental
Gene Targeting
Genetic Markers
germ cell nuclear factor
Histocytochemistry
In Situ Hybridization
Limb Buds - abnormalities
Limb Buds - cytology
Limb Buds - embryology
Limb Buds - metabolism
Mammalian Genetic Models with Minimal or Complex Phenotypes
Mice
Mice, Knockout
Nuclear Receptor Subfamily 6, Group A, Member 1
Receptors, Cytoplasmic and Nuclear - genetics
Receptors, Cytoplasmic and Nuclear - metabolism
Recombination, Genetic - genetics
RNA, Messenger - analysis
RNA, Messenger - genetics
Somites - cytology
Somites - metabolism
Tail - abnormalities
Tail - cytology
Tail - embryology
Tail - metabolism
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The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of the GCNF gene in mice. Germ line mutation of the GCNF gene proves that the orphan nuclear receptor is essential for embryonic survival and normal development. GCNF −/− embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF −/− embryos suffer significant defects in posterior development. Unlike GCNF +/+ embryos, GCNF −/− embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. GCNF −/− embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF −/− embryos is 13 instead of 25 as in the GCNF +/+ embryos. Interestingly, the tailbud of GCNF −/− embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF −/− embryos, including the primitive streak, the node, and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.
The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of the GCNF gene in mice. Germ line mutation of the GCNF gene proves that the orphan nuclear receptor is essential for embryonic survival and normal development. GCNF(-/-) embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF(-/-) embryos suffer significant defects in posterior development. Unlike GCNF(+/+) embryos, GCNF(-/-) embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. GCNF(-/-) embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF(-/-) embryos is 13 instead of 25 as in the GCNF(+/+) embryos. Interestingly, the tailbud of GCNF(-/-) embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF(-/-) embryos, including the primitive streak, the node, and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.
The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of the GCNF gene in mice. Germ line mutation of the GCNF gene proves that the orphan nuclear receptor is essential for embryonic survival and normal development. GCNF super(-/-) embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF super(-/-) embryos suffer significant defects in posterior development. Unlike GCNF super(+/+) embryos GCNF super(-/-) embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. GCNF super(-/-) embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF super(-/-) embryos is 13 instead of 25 as in the GCNF super(+/+) embryos. Interestingly, the tailbud of GCNF super(-/-) embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF super(-/-) embryos, including the primitive streak, the node, and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.
The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of the GCNF gene in mice. Germ line mutation of the GCNF gene proves that the orphan nuclear receptor is essential for embryonic survival and normal development. GCNF −/− embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF −/− embryos suffer significant defects in posterior development. Unlike GCNF +/+ embryos, GCNF −/− embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. GCNF −/− embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF −/− embryos is 13 instead of 25 as in the GCNF +/+ embryos. Interestingly, the tailbud of GCNF −/− embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF −/− embryos, including the primitive streak, the node, and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.
Author Francesco J. DeMayo
Kathy J. Jackson
Bert W. O'Malley
Deborah Katz
Fred A. Pereira
Arthur C.-K. Chung
Austin J. Cooney
AuthorAffiliation Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030
AuthorAffiliation_xml – name: Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030
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  givenname: Arthur C.-K.
  surname: Chung
  fullname: Chung, Arthur C.-K.
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  surname: Katz
  fullname: Katz, Deborah
  organization: Department of Molecular and Cellular Biology, Baylor College of Medicine
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  organization: Department of Molecular and Cellular Biology, Baylor College of Medicine
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  surname: Jackson
  fullname: Jackson, Kathy J.
  organization: Department of Molecular and Cellular Biology, Baylor College of Medicine
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/11134352$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-6250. Fax: (713) 790-1275. E-mail: acooney@bcm.tmc.edu.
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early...
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StartPage 663
SubjectTerms Animals
Cell Differentiation
Choristoma - embryology
Choristoma - metabolism
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Embryonic and Fetal Development
Fetal Death
GCNF gene
Gene Deletion
Gene Expression Regulation, Developmental
Gene Targeting
Genetic Markers
germ cell nuclear factor
Histocytochemistry
In Situ Hybridization
Limb Buds - abnormalities
Limb Buds - cytology
Limb Buds - embryology
Limb Buds - metabolism
Mammalian Genetic Models with Minimal or Complex Phenotypes
Mice
Mice, Knockout
Nuclear Receptor Subfamily 6, Group A, Member 1
Receptors, Cytoplasmic and Nuclear - genetics
Receptors, Cytoplasmic and Nuclear - metabolism
Recombination, Genetic - genetics
RNA, Messenger - analysis
RNA, Messenger - genetics
Somites - cytology
Somites - metabolism
Tail - abnormalities
Tail - cytology
Tail - embryology
Tail - metabolism
Title Loss of Orphan Receptor Germ Cell Nuclear Factor Function Results in Ectopic Development of the Tail Bud and a Novel Posterior Truncation
URI http://mcb.asm.org/content/21/2/663.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.21.2.663-677.2001
https://www.ncbi.nlm.nih.gov/pubmed/11134352
https://search.proquest.com/docview/17761757
https://search.proquest.com/docview/70554166
https://pubmed.ncbi.nlm.nih.gov/PMC86646
Volume 21
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