Cytokeratins 8 and 19 in the Mouse Placental Development

To investigate the expression and biological roles of cytokeratin 19 (K19) in development and in adult tissues, we inactivated the mouse K19 gene (Krt1-19) by inserting a bacterial β-galactosidase gene (lacZ) by homologous recombination in embryonic stem cells, and established germ line mutant mice....

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Main Authors:	Tamai, Yoshitaka, Ishikawa, Tomo-o, Bösl, Michael R., Mori, Masahiko, Nozaki, Masami, Baribault, Heléne, Oshima, Robert G., Taketo, Makoto M.
Format:	Online
Language:	English
Published:	The Rockefeller University Press 2000
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185583/

id	pubmed-2185583
recordtype	oai_dc
spelling	pubmed-21855832008-05-01 Cytokeratins 8 and 19 in the Mouse Placental Development Tamai, Yoshitaka Ishikawa, Tomo-o Bösl, Michael R. Mori, Masahiko Nozaki, Masami Baribault, Heléne Oshima, Robert G. Taketo, Makoto M. Original Article To investigate the expression and biological roles of cytokeratin 19 (K19) in development and in adult tissues, we inactivated the mouse K19 gene (Krt1-19) by inserting a bacterial β-galactosidase gene (lacZ) by homologous recombination in embryonic stem cells, and established germ line mutant mice. Both heterozygous and homozygous mutant mice were viable, fertile, and appeared normal. By 7.5–8.0 days post coitum (dpc), heterozygous mutant embryos expressed lacZ in the notochordal plate and hindgut diverticulum, reflecting the fact that the notochord and the gut endoderm are derived from the axial mesoderm-originated cells. In the adult mutant, lacZ was expressed mainly in epithelial tissues. To investigate the possible functional cooperation and synergy between K19 and K8, we then constructed compound homozygous mutants, whose embryos died ∼10 dpc. The lethality resulted from defects in the placenta where both K19 and K8 are normally expressed. As early as 9.5 dpc, the compound mutant placenta had an excessive number of giant trophoblasts, but lacked proper labyrinthine trophoblast or spongiotrophoblast development, which apparently caused flooding of the maternal blood into the embryonic placenta. These results indicate that K19 and K8 cooperate in ensuring the normal development of placental tissues. The Rockefeller University Press 2000-10-30 /pmc/articles/PMC2185583/ /pubmed/11062258 Text en © 2000 The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Tamai, Yoshitaka Ishikawa, Tomo-o Bösl, Michael R. Mori, Masahiko Nozaki, Masami Baribault, Heléne Oshima, Robert G. Taketo, Makoto M.
spellingShingle	Tamai, Yoshitaka Ishikawa, Tomo-o Bösl, Michael R. Mori, Masahiko Nozaki, Masami Baribault, Heléne Oshima, Robert G. Taketo, Makoto M. Cytokeratins 8 and 19 in the Mouse Placental Development
author_facet	Tamai, Yoshitaka Ishikawa, Tomo-o Bösl, Michael R. Mori, Masahiko Nozaki, Masami Baribault, Heléne Oshima, Robert G. Taketo, Makoto M.
author_sort	Tamai, Yoshitaka
title	Cytokeratins 8 and 19 in the Mouse Placental Development
title_short	Cytokeratins 8 and 19 in the Mouse Placental Development
title_full	Cytokeratins 8 and 19 in the Mouse Placental Development
title_fullStr	Cytokeratins 8 and 19 in the Mouse Placental Development
title_full_unstemmed	Cytokeratins 8 and 19 in the Mouse Placental Development
title_sort	cytokeratins 8 and 19 in the mouse placental development
description	To investigate the expression and biological roles of cytokeratin 19 (K19) in development and in adult tissues, we inactivated the mouse K19 gene (Krt1-19) by inserting a bacterial β-galactosidase gene (lacZ) by homologous recombination in embryonic stem cells, and established germ line mutant mice. Both heterozygous and homozygous mutant mice were viable, fertile, and appeared normal. By 7.5–8.0 days post coitum (dpc), heterozygous mutant embryos expressed lacZ in the notochordal plate and hindgut diverticulum, reflecting the fact that the notochord and the gut endoderm are derived from the axial mesoderm-originated cells. In the adult mutant, lacZ was expressed mainly in epithelial tissues. To investigate the possible functional cooperation and synergy between K19 and K8, we then constructed compound homozygous mutants, whose embryos died ∼10 dpc. The lethality resulted from defects in the placenta where both K19 and K8 are normally expressed. As early as 9.5 dpc, the compound mutant placenta had an excessive number of giant trophoblasts, but lacked proper labyrinthine trophoblast or spongiotrophoblast development, which apparently caused flooding of the maternal blood into the embryonic placenta. These results indicate that K19 and K8 cooperate in ensuring the normal development of placental tissues.
publisher	The Rockefeller University Press
publishDate	2000
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2185583/
_version_	1611426725139316736

Cytokeratins 8 and 19 in the Mouse Placental Development

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