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Journal of Heredity Advance Access published online on September 19, 2006
Journal of Heredity, doi:10.1093/jhered/esl029
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© The American Genetic Association. 2006. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.
Received January 16, 2006
Accepted July 16, 2006

Article

The Mutated S1-Haplotype in Sour Cherry Has an Altered S-Haplotype-Specific F-Box Protein Gene

Nathanael R. Hauck 1, Kazuo Ikeda 2, Ryutaro Tao 2, and Amy F. Iezzoni 1 *

1 From the Department of Horticulture, Michigan State University, East Lansing, MI 48824
2 From the Laboratory of Pomology, Graduate School of Agriculture, Kyoto University, Kyoto 606-8502, Japan

* To whom correspondence should be addressed.
Amy F. Iezzoni, E-mail: iezzoni{at}msu.edu


  Abstract

Gametophytic self-incompatibility (GSI) is an outcrossing mechanism in flowering plants that is genetically controlled by 2 separate genes located at the highly polymorphic S-locus, termed S-haplotype. This study characterizes a pollen part mutant of the S1-haplotype present in sour cherry (Rosaceae, Prunus cerasus L.) that contributes to the loss of GSI. Inheritance of S-haplotypes from reciprocal interspecific crosses between the self-compatible sour cherry cultivar Újfehértói Fürtös carrying the mutated S1-haplotype (S1'S4SdSnull) and the self-incompatible sweet cherry (Prunus avium L.) cultivars carrying the wild-type S1-haplotype revealed that the mutated S1-haplotype confers unilateral incompatibility with a functional pistil component and a nonfunctional pollen component. The altered sour cherry S1-haplotype pollen part mutant, termed S1', contains a 615-bp Ds-like element within the S1-haplotype-specific F-box protein gene (SFB1'). This insertion generates a premature in-frame stop codon that would result in a putative truncated SFB1 containing only 75 of the 375 amino acids present in the wild-type SFB1. S1' along with 2 other previously characterized Prunus S-haplotype mutants, Sf and S6m, illustrate that mobile element insertion is an evolutionary force contributing to the breakdown of GSI.


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