Abstract
The Ten-a gene of Drosophila melanogaster encodes several alternative variants of a full length member of the Odz/Tenm protein family. A number of Ten-a mutants created by inexact excisions of a resident P-element insertion are embryonic lethal, but show no pair-rule phenotype. In contrast, these mutants, and deficiencies removing Ten-a, do enhance the segmentation phenotype of a weak allele of the paralog gene odz (or Ten-m) to the odz amorphic phenotype. Germ line clone derived Ten-a(-) embryos display a pair-rule phenotype which phenocopies that of odz. Post segmentation eye patterning phenotypes of Ten-a mutants establish it as a pleiotropic patterning co-partner of odz.
MeSH terms
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Alleles
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Alternative Splicing / genetics
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Animals
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Body Patterning*
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Cleavage Stage, Ovum / cytology
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Clone Cells
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DNA Transposable Elements
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Drosophila Proteins / metabolism*
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Drosophila melanogaster / embryology*
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Drosophila melanogaster / genetics*
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Embryo, Nonmammalian / cytology
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Exons / genetics
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Eye / embryology
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Eye / ultrastructure
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Gene Expression Regulation, Developmental
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Genes, Insect*
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Germ Cells
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Introns / genetics
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Mutagenesis, Insertional
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Mutation / genetics
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Phenotype
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Receptors, Cell Surface / metabolism*
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Tenascin / metabolism
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Transcription, Genetic
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Zygote
Substances
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DNA Transposable Elements
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Drosophila Proteins
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RNA, Messenger
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Receptors, Cell Surface
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Ten-a protein, Drosophila
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Ten-m protein, Drosophila
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Tenascin