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1.
Development ; 134(2): 251-60, 2007 Jan.
Article in English | MEDLINE | ID: mdl-17151016

ABSTRACT

During mouse gastrulation, endoderm cells of the dorsal foregut are recruited ahead of the ventral foregut and move to the anterior region of the embryo via different routes. Precursors of the anterior-most part of the foregut and those of the mid- and hind-gut are allocated to the endoderm of the mid-streak-stage embryo, whereas the precursors of the rest of the foregut are recruited at later stages of gastrulation. Loss of Mixl1 function results in reduced recruitment of the definitive endoderm, and causes cells in the endoderm to remain stationary during gastrulation. The observation that the endoderm cells are inherently unable to move despite the expansion of the mesoderm in the Mixl1-null mutant suggests that the movement of the endoderm and the mesoderm is driven independently of one another.


Subject(s)
Endoderm/cytology , Gastrula/cytology , Animals , Body Patterning/genetics , Cell Movement , Cell Transplantation , Digestive System/cytology , Digestive System/embryology , Female , Gene Expression Regulation, Developmental , Homeodomain Proteins/genetics , Mice , Mice, Knockout , Mice, Transgenic , Pregnancy
2.
Genesis ; 35(1): 57-62, 2003 Jan.
Article in English | MEDLINE | ID: mdl-12481299

ABSTRACT

We have optimized the technique of electroporation for introducing genetic markers into cells of the gastrulating mouse embryo to follow cell fates, tissue movement, and lineage differentiation. Using a plate-needle electrode combination and specific route of plasmid delivery, labeling could be targeted to discrete regions of the epiblast or the endoderm of the late gastrula. Among the various types of fluorescent and chromogenic reporter constructs tested, those driven by CMV promoter are efficient and strong expression can be detected as soon as 2-3 h after electroporation. The efficacy of marking cell lineages by CRE-mediated activation of reporters proved to be inefficient for tracking cell lineages due to an obligatory 8-9-h lag from the electroporation of constructs to the expression of reporter. This significant time lag also raises concern of the temporal precision at which tissue- or stage-specific knock-out or activation of genetic activity may be achieved by the Cre-loxP mechanism.


Subject(s)
Electroporation , Gastrula/physiology , Germ Layers/physiology , Alkaline Phosphatase/metabolism , Animals , Biomarkers , Cell Culture Techniques , Cell Lineage , Embryo, Mammalian/anatomy & histology , Genes, Reporter , Genetic Techniques , Green Fluorescent Proteins , Integrases/metabolism , Lac Operon/physiology , Luminescent Proteins/metabolism , Mice , Viral Proteins/metabolism
3.
Development ; 129(10): 2367-79, 2002 May.
Article in English | MEDLINE | ID: mdl-11973269

ABSTRACT

In the mouse, the definitive endoderm is derived from the epiblast during gastrulation, and, at the early organogenesis stage, forms the primitive gut tube, which gives rise to the digestive tract, liver, pancreas and associated visceral organs. The transcription factors, Sox17 (a Sry-related HMG box factor) and its upstream factors, Mixer (homeobox factor) and Casanova (a novel Sox factor), have been shown to function as endoderm determinants in Xenopus and zebrafish, respectively. However, whether the mammalian orthologues of these genes are also involved with endoderm formation is not known. We show that Sox17(-/-) mutant embryos are deficient of gut endoderm. The earliest recognisable defect is the reduced occupancy by the definitive endoderm in the posterior and lateral region of the prospective mid- and hindgut of the headfold-stage embryo. The prospective foregut develops properly until the late neural plate stage. Thereafter, elevated levels of apoptosis lead to a reduction in the population of the definitive endoderm in the foregut. In addition, the mid- and hindgut tissues fail to expand. These are accompanied by the replacement of the definitive endoderm in the lateral region of the entire length of the embryonic gut by cells that resemble the visceral endoderm. In the chimeras, although Sox17-null ES cells can contribute unrestrictedly to ectodermal and mesodermal tissues, few of them could colonise the foregut endoderm and they are completely excluded from the mid- and hindgut endoderm. Our findings indicate an important role of Sox17 in endoderm development in the mouse, highlighting the idea that the molecular mechanism for endoderm formation is likely to be conserved among vertebrates.


Subject(s)
DNA-Binding Proteins , Digestive System/embryology , Endoderm/pathology , High Mobility Group Proteins , Proteins/genetics , Transcription Factors , Xenopus Proteins , Zebrafish Proteins , Animals , Apoptosis/genetics , Digestive System Abnormalities , Female , Gene Expression Regulation, Developmental , Mice , Mice, Mutant Strains , Proteins/metabolism , SOXF Transcription Factors , Viscera/embryology , Viscera/pathology
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