701. Changes in embryonic cell fate produced by expression of an endodermal transcription factor, Xsox17.
- Author
-
Clements D and Woodland HR
- Subjects
- Animals, Cell Differentiation, Embryo, Nonmammalian metabolism, In Situ Hybridization, Models, Biological, RNA, Messenger metabolism, SOXF Transcription Factors, Transcription, Genetic, Xenopus laevis embryology, beta-Galactosidase metabolism, Cell Lineage, DNA-Binding Proteins, Ectoderm metabolism, Endoderm metabolism, High Mobility Group Proteins, Mesoderm metabolism, Proteins metabolism, Transcription Factors, Xenopus Proteins
- Abstract
Many molecules induce the ectopic expression of tissue-specific genes in Xenopus embryos. Conversely, interfering with their activity disrupts patterns of gene expression, implicating them in normal development. Does this mean that they control cell fate (i.e. position, as well as differentiation)? Xsox17alpha and beta can induce ectopic expression of endodermal markers; inhibiting their function suppresses expression of endodermal marker genes in the developing gut (Cell 91 (1997) 397). Here we show the effect of these manipulations on cell lineage. Expressing Xsox17 in a cells normally fated to become ectoderm causes their descendants either to relocate into the embryonic gut or to die at a late developmental stage. Conversely, disrupting Xsox17 activity in cells normally fated to be endodermal causes them to enter mesodermal and ectodermal lineages.
- Published
- 2000
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