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Three ENU-induced alleles of the murine quaking locus are recessive embryonic lethal mutations

Published online by Cambridge University Press:  14 April 2009

Monica J. Justice  and
Vernon C. Bode
Monica J. Justice
Affiliation:
Kansas State University, Division of Biology, Ackert Hall, Manhattan, Kansas 66506, USA
Vernon C. Bode
Affiliation:
Kansas State University, Division of Biology, Ackert Hall, Manhattan, Kansas 66506, USA

Summary

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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. The qkk2 allele was induced on wild-type chromatin and the qkkt1 and qkkt4 alleles were induced on t-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.

Type
Research Article
Information
Genetics Research , Volume 51 , Issue 2 , April 1988 , pp. 95 - 102
Copyright
Copyright © Cambridge University Press 1988

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