Summary The quaking (qk) locus on mouse chromosome 17 has been defined by a single viable quaking allele. Three new alleles of quaking were selected after ENU mutagenesis by their failure to complement the quaking phenotype. Theqkk2allele was induced on wild-type chromatin and theqkkt1andqkkt4alleles were induced ont-chromatin. Each is a recessive embryonic lethal mutation. They fail to complement each other and are not complemented by the deletion,TtOrl. Homozygotes and hemizygotes die at 8–9·5 days gestation, but not at a single precise time. Because the classical quaking mutation complements the lethality of these new alleles, but they fail to complement its quaking phenotype (myelination defect), we conclude that the quaking+function is required for embryonic survival as well as for myelination.
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Justice et al. (1988) studied this question.
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