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Am. J. Trop. Med. Hyg., 75(1), 2006, pp. 70-77
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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POPULATION DYNAMICS OF AN ENDOGENOUS MEIOTIC DRIVE SYSTEM IN AEDES AEGYPTI IN TRINIDAD

SUNG-JAE CHA, DAVE D. CHADEE, AND DAVID W. SEVERSON*
Center for Tropical Disease Research and Training, Department of Biological Sciences University of Notre Dame, Notre Dame, Indiana; Department of Life Sciences, University of the West Indies, St. Augustine, Trinidad, West Indies

An endogenous meiotic drive system was previously reported to be segregating in the yellow fever mosquito Aedes aegypti L. (Diptera: Culicidae) population in Trinidad. The meiotic driver (MD) is tightly linked to the male determining locus and selectively targets sensitive responders linked to the female determining allele, causing fragmentation of female gametes. This results in highly male-biased progeny. The MD system was initially studied as a genetic tool for population control with limited success, but recently interest has focused on its potential for population replacement. This study examines the distribution and dynamics of the MD system in Trinidad natural populations. We obtained ovitrap samples from seven geographically distinct regions and determined the allele frequencies of the driver (MD) and sensitive (ms) versus insensitive (mi) responders, respectively. Frequencies of the MD allele ranged from 0.1 to 0.5 and were low at the two major port cities, Port of Spain and San Fernando, suggesting the effects of frequent immigration by non-driving genotypes. Frequencies of the mi allele ranged from 0.4 to 0.7, suggesting the effects of strong selection by the driver. In addition, our results show that the driver and sensitivity of responders in the Trinidad populations are highly polymorphic. Continued studies of the dynamics of the MD system in natural populations are critical to considerations of its use in population replacement.


Received October 27, 2005. Accepted for publication March 13, 2006.

Financial support: This work was supported by NIH NIAID Grant PO1-AI45123.

* Address correspondence to David W. Severson, Center for Tropical Disease Research and Training, Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556. E-mail: severson.1{at}nd.edu

Authors’ addresses: Sung-Jae Cha, Johns Hopkins School of Public Health, Malaria Research Institute, Department of Molecular Microbiology and Immunology, 615 North Wolfe Street, Baltimore, MD 21205, E-mail: scha{at}jhsph.edu. Dave D. Chadee, Department of Life Sciences, University of the West Indies, St. Augustine, Trinidad, West Indies, E-mail: chadee{at}tstt.net.tt. David W. Severson, Center for Tropical Disease Research and Training, Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556.

Reprint requests: David W. Severson, Center for Tropical Disease Research and Training, Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, E-mail: severson.1{at}nd.edu.




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Copyright © 2006 by the American Society of Tropical Medicine and Hygiene.