The opposing homeobox genes Goosecoid and Vent1/2 self-regulate Xenopus patterning.

Publisher: Wiley Blackwell Country of Publication: England NLM ID: 8208664 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0261-4189 (Print) Linking ISSN: 02614189 NLM ISO Abbreviation: EMBO J Subsets: MEDLINE

Publication: 2014- : London : Wiley Blackwell
Original Publication: Eynsham, Oxford, England : Published for the European Molecular Biology Organization by IRL Press, [c1982-

Body Patterning* ; Genes, Homeobox*; Goosecoid Protein/*genetics ; Homeodomain Proteins/*genetics ; Transcription Factors/*genetics ; Xenopus/*embryology ; Xenopus Proteins/*genetics; Animals ; Base Sequence ; DNA Primers ; Glycoproteins/physiology ; Intercellular Signaling Peptides and Proteins/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Homology, Nucleic Acid ; Xenopus/genetics

We present a loss-of-function study using antisense morpholino (MO) reagents for the organizer-specific gene Goosecoid (Gsc) and the ventral genes Vent1 and Vent2. Unlike in the mouse Gsc is required in Xenopus for mesodermal patterning during gastrulation, causing phenotypes ranging from reduction of head structures-including cyclopia and holoprosencephaly-to expansion of ventral tissues in MO-injected embryos. The overexpression effects of Gsc mRNA require the expression of the BMP antagonist Chordin, a downstream target of Gsc. Combined Vent1 and Vent2 MOs strongly dorsalized the embryo. Unexpectedly, simultaneous depletion of all three genes led to a rescue of almost normal development in a variety of embryological assays. Thus, the phenotypic effects of depleting Gsc or Vent1/2 are caused by the transcriptional upregulation of their opposing counterparts. A principal function of Gsc and Vent1/2 homeobox genes might be to mediate a self-adjusting mechanism that restores the basic body plan when deviations from the norm occur, rather than generating individual cell types. The results may shed light on the molecular mechanisms of genetic redundancy.

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R01 HD021502 United States HD NICHD NIH HHS; R01 HD021502-21A1 United States HD NICHD NIH HHS; R37 HD021502 United States HD NICHD NIH HHS; R37 HD 21502-21 United States HD NICHD NIH HHS

0 (DNA Primers)
0 (Glycoproteins)
0 (Goosecoid Protein)
0 (Homeodomain Proteins)
0 (Intercellular Signaling Peptides and Proteins)
0 (Transcription Factors)
0 (Xenopus Proteins)
0 (ventx2.1 protein, Xenopus)
93586-27-7 (chordin)

Date Created: 20070526 Date Completed: 20070920 Latest Revision: 20220409

20231215

PMC1894760

10.1038/sj.emboj.7601705

17525737