Disruption of Apc10/Doc1 in Three Alleles of Oligosyndactylism
| Autor: | Dimitrina D. Pravtcheva, Thomas L. Wise |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Chromosomes
Artificial Bacterial DNA Complementary Saccharomyces cerevisiae Proteins Transcription Genetic Molecular Sequence Data Gene Expression Cell Cycle Proteins Mice Transgenic Biology Abnormalities Radiation-Induced Mice Sequence Homology Nucleic Acid Gene expression Genetics Animals Humans Amino Acid Sequence Transgenes Cloning Molecular Allele Gene Mitosis Metaphase Alleles Sequence Deletion Anaphase Apc10 Subunit Anaphase-Promoting Complex-Cyclosome Gene Rearrangement Base Sequence Nucleic acid sequence Phenotype Molecular biology Mutation |
| Zdroj: | Genomics. 72:78-87 |
| ISSN: | 0888-7543 |
| DOI: | 10.1006/geno.2001.6474 |
| Popis: | Oligosyndactylism (Os) is a radiation-induced mouse mutation associated with recessive lethality and a dominant effect on limb and kidney development. The lethal effect of the mutation is due to a cell-autonomous block in the transition from metaphase to anaphase. We have previously characterized two transgene-induced mutations, 94-A and 94-K, which are allelic with Os. These mutations facilitated the identification of genomic segments and transcribed sequences in the affected region. One of the transcripts in this region corresponds to the mouse homolog of the anaphase-promoting complex component APC10/DOC1. The disruption of this gene can explain the mitotic arrest phenotype of all three alleles of Os. |
| Databáze: | OpenAIRE |
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