Abstract
The mouse kreisler (kr) mutation causes segmentation abnormalities in the caudal hindbrain and defective inner ear development. Based on an inversion discovered in the original kr allele, we selected a candidate cDNA highly expressed in the developing caudal hindbrain. This cDNA encodes a basic domain-leucine zipper (bZIP) transcription factor and was confirmed to represent the kr gene by analysis of a second kr allele, generated by chemical mutagenesis, in which a serine is substituted for an asparagine residue conserved in the DNA-binding domain of all known bZIP family members. The identity, expression, and mutant phenotype of kr indicate an early role in axial patterning and provide insights into the molecular and embryologic mechanisms that govern hindbrain and otic development.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Avian Proteins*
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Base Sequence
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Chromosome Inversion
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Cloning, Molecular
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DNA-Binding Proteins / genetics*
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Ear / embryology
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Female
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In Situ Hybridization
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Leucine Zippers*
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MafB Transcription Factor
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Male
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Mice
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Mice, Mutant Strains / embryology*
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Models, Biological
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Molecular Sequence Data
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Mutation
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Oncogene Proteins*
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Point Mutation
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins c-maf
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RNA, Messenger / analysis
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Restriction Mapping
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Rhombencephalon / abnormalities
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Sequence Homology, Amino Acid
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Transcription Factors / genetics*
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Transcription, Genetic
Substances
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Avian Proteins
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DNA-Binding Proteins
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Maf protein, mouse
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MafB Transcription Factor
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Mafb protein, mouse
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Oncogene Proteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-maf
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RNA, Messenger
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Transcription Factors
Associated data
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GENBANK/L36434
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GENBANK/L36435