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Genetics, Vol. 175, 527-544, February 2007, Copyright © 2007
doi:10.1534/genetics.106.065714

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Recurrent Locus-Specific Mutation Resulting From a Cryptic Ectopic Insertion in Neurospora

David D. Perkins*, Michael Freitag{dagger},1, Virginia C. Pollard*, Lori A. Bailey-Shrode{ddagger}, Eric U. Selker{dagger} and Daniel J. Ebbole{ddagger}

* Department of Biological Sciences, Stanford University, Stanford, California 94305-5020, {dagger} Institute of Molecular Biology and Department of Biology, University of Oregon, Eugene, Oregon 97403-1229 and {ddagger} Program for the Biology of Filamentous Fungi, Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 77843-2132

1 Corresponding author: Department of Biochemistry and Biophysics, Oregon State University, Corvallis, OR 97331-7305.
E-mail: freitagm{at}onid.orst.edu

New mutations are found among ~20% of progeny when one or both parents carry eas allele UCLA191 (easUCLA, easily wettable, hydrophobin-deficient, linkage group II). The mutations inactivate the wild-type allele of cya-8 (cytochrome aa3 deficient, linkage group VII), resulting in thin, "transparent" mycelial growth. Other eas alleles fail to produce cya-8 mutant progeny. The recurrent cya-8 mutations are attributed to repeat-induced point mutation (RIP) resulting from a duplicated copy of cya-8+ that was inserted ectopically at eas when the UCLA191 mutation occurred. As expected for RIP, easUCLA-induced cya-8 mutations occur during nuclear proliferation prior to karyogamy. When only one parent is easUCLA, the new mutations arise exclusively in easUCLA nuclei. Mutation of cya-8 is suppressed when a long unlinked duplication is present. Stable cya-8 mutations are effectively eliminated in crosses homozygous for rid, a recessive suppressor of RIP. The easUCLA allele is associated with a long paracentric inversion. A discontinuity is present in easUCLA DNA. The eas promoter is methylated in cya-8 progeny of easUCLA, presumably by the spreading of methylation beyond the adjoining RIP-inactivated duplication. These findings support a model in which an ectopic insertion that created a mutation at the target site acts as a locus-specific mutator via RIP.




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R. H. Davis
Tending Neurospora: David Perkins, 1919-2007, and Dorothy Newmeyer Perkins, 1922-2007
Genetics, April 1, 2007; 175(4): 1543 - 1548.
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