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Originally published as Genetics Published Articles Ahead of Print on January 19, 2009.
Genetics, Vol. 181, 1437-1450, April 2009, Copyright © 2009
doi:10.1534/genetics.108.100057
Reduced Fertility of Drosophila melanogaster Hybrid male rescue (Hmr) Mutant Females Is Partially Complemented by Hmr Orthologs From Sibling Species
S. Aruna1, Heather A. Flores and Daniel A. Barbash2
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853
2 Corresponding author: Department of Molecular Biology and Genetics, 401 Biotechnology Bldg., Cornell University, Ithaca, NY 14853-2703.
E-mail: dab87{at}cornell.edu
The gene Hybrid male rescue (Hmr) causes lethality in interspecific hybrids between Drosophila melanogaster and its sibling species. Hmr has functionally diverged for this interspecific phenotype because lethality is caused specifically by D. melanogaster Hmr but not by D. simulans or D. mauritiana Hmr. Hmr was identified by the D. melanogaster partial loss-of-function allele Hmr1, which suppresses hybrid lethality but has no apparent phenotype within pure-species D. melanogaster. Here we have investigated the possible function of Hmr in D. melanogaster females using stronger mutant alleles. Females homozygous for Hmr mutants have reduced viability posteclosion and significantly reduced fertility. We find that reduced fertility of Hmr mutants is caused by a reduction in the number of eggs laid as well as reduced zygotic viability. Cytological analysis reveals that ovarioles from Hmr mutant females express markers that distinguish various stages of wild-type oogenesis, but that developing egg chambers fail to migrate posteriorly. D. simulans and D. mauritiana Hmr+ partially complement the reduced fertility of a D. melanogaster Hmr mutation. This partial complementation contrasts with the complete functional divergence previously observed for the interspecific hybrid lethality phenotype. We also investigate here the molecular basis of hybrid rescue associated with a second D. melanogaster hybrid rescue allele, In(1)AB. We show that In(1)AB is mutant for Hmr function, likely due to a missense mutation in an evolutionarily conserved amino acid. Two independently discovered hybrid rescue mutations are therefore allelic.
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