Goosecoid and cerberus-like do not interact during mouse embryogenesis

Mouse Cerberus-like (Cer-l) is a neural inducer molecule, capable of inhibiting Nodal and BMP-4 signals in the extracelular space. The cer-l expression domain in the Anterior Visceral Endoderm (AVE) and prechordal plate, tissues involved in head induction and patterning, respectively, suggested a ro...

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Bibliographic Details
Published inThe International journal of developmental biology Vol. 46; no. 2; pp. 259 - 262
Main Authors Borges, Ana C, Marques, Sara, Belo, José A
Format Journal Article
LanguageEnglish
Published Spain 01.03.2002
Subjects
Animals
BF-1 gene
Bone Morphogenetic Protein 4
Bone Morphogenetic Proteins - genetics
Bone Morphogenetic Proteins - metabolism
cer-1 gene
Crosses, Genetic
Gene Expression Regulation, Developmental
Genotype
Goosecoid Protein
gsc gene
HNF-3^b gene
Homeodomain Proteins - genetics
Homeodomain Proteins - physiology
In Situ Hybridization
Mice
Mice, Inbred C57BL
Mice, Transgenic
Mutation
Proteins - genetics
Proteins - physiology
Repressor Proteins
Six-3 gene
Transcription Factors
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Summary:Mouse Cerberus-like (Cer-l) is a neural inducer molecule, capable of inhibiting Nodal and BMP-4 signals in the extracelular space. The cer-l expression domain in the Anterior Visceral Endoderm (AVE) and prechordal plate, tissues involved in head induction and patterning, respectively, suggested a role for this gene in head formation. However, animals homozygous for the cer-l null allele failed to show any abnormality, leading us to propose the existence of other factor(s) that might compensate for cer-l loss-of-function. Since goosecoid (gsc) shares some domains of expression with cer-l and was shown to be essential for head morphogenesis, we tested its ability to interact genetically with cer-l. With this aim we generated cer-l;gsc double mutants. These animals were analyzed at birth for skeletal defects and revealed the same phenotype as gsc-/- single mutants. We also investigated the proper patterning of structures adjacent to the prechordal plate by performing in situ hybridization of HNF-3beta, Six-3 and BF-1, genes whose expression domains remained unchanged. In conclusion, the analysis carried out indicated that gsc does not compensate for cer-l loss-of-function and that these genes do not interact genetically.
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ISSN:0214-6282