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Originally published as Genetics Published Articles Ahead of Print on December 18, 2006.
Genetics, Vol. 175, 1321-1333, March 2007, Copyright © 2007
doi:10.1534/genetics.106.067082
Inheritance of Gynandromorphism in the Parasitic Wasp Nasonia vitripennis
Albert Kamping*,
Vaishali Katju
,
,
Leo W. Beukeboom*,1 and
John H. Werren
* Evolutionary Genetics, Centre for Ecological and Evolutionary Studies, University of Groningen, NL-9750 AA Haren, The Netherlands,
Department of Biology, University of Rochester, Rochester, New York 14627 and
Department of Biology, University of New Mexico, Albuquerque, New Mexico 87131
1 Corresponding author: Evolutionary Genetics, Centre for Ecological and Evolutionary Studies, Biological Centre, University of Groningen, P.O. Box 14, NL-9750 AA Haren, The Netherlands.
E-mail: l.w.beukeboom{at}rug.nl
The parasitic wasp Nasonia vitripennis has haplo-diploid sex determination. Males develop from unfertilized eggs and are haploid, whereas females develop from fertilized eggs and are diploid. Females and males can be easily distinguished by their morphology. A strain that produces individuals with both male and female features (gynandromorphs) is studied. We provide data on female/male patterning within and between individuals, on environmental effects influencing the occurrence of gynandromorphism, and on its pattern of inheritance. A clear anterior/posterior pattern of feminization is evident in gynandromorphic individuals that developed from unfertilized haploid eggs. The proportion of gynandromorphic individuals can be increased by exposing the mothers to high temperature and also by exposing embryos at early stages of development. Selection for increased gynandromorph frequency was successful. Backcross and introgression experiments showed that a combination of a nuclear and a heritable cytoplasmic component causes gynandromorphism. Analyses of reciprocal F2 and F3 progeny indicate a maternal effect locus (gyn1) that maps to chromosome IV. Coupled with previous studies, our results are consistent with a N. vitripennis sex determination involving a maternal/zygotic balance system and/or maternal imprinting. Genetics and temperature effects suggest a temperature-sensitive mutation of a maternally produced masculinizing product that acts during a critical period in early embryogenesis.