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Published April 2011 | Accepted Version + Supplemental Material
Journal Article Open

Medea Selfish Genetic Elements as Tools for Altering Traits of Wild Populations: A Theoretical Analysis

Abstract

One strategy for controlling transmission of insect-borne disease involves replacing the native insect population with transgenic animals unable to transmit disease. Population replacement requires a drive mechanism to ensure the rapid spread of linked transgenes, the presence of which may result in a fitness cost to carriers. Medea selfish genetic elements have the feature that when present in a female, only offspring that inherit the element survive, a behavior that can lead to spread. Here, we derive equations that describe the conditions under which Medea elements with a fitness cost will spread, and the equilibrium allele frequencies are achieved. Of particular importance, we show that whenever Medea spreads, the non-Medea genotype is driven out of the population, and we estimate the number of generations required to achieve this goal for Medea elements with different fitness costs and male-only introduction frequencies. Finally, we characterize two contexts in which Medea elements with fitness costs drive the non-Medea allele from the population: an autosomal element in which not all Medea-bearing progeny of a Medea-bearing mother survive, and an X-linked element in species in which X/Y individuals are male. Our results suggest that Medea elements can drive population replacement under a wide range of conditions.

Additional Information

© 2010 The Author(s). Evolution © 2010 The Society for the Study of Evolution. Received June 11, 2010. Accepted October 22, 2010. Article first published online: 22 Dec. 2010. Associate Editor: S. Gandon. YH, ALL, and FG were supported by NIH grant R01-AI54954-OIA2 and a grant to the Regents of the University of California from the Foundation for the National Institutes of Health through the Grand Challenges in Global Health initiative. BAH, CMW, and JTS were supported by grants to BAH from NIH (R01 GM072879; R01 GM0711956: DPI OD003878), and the Weston Havens Foundation. Support was also provided by a grant to the Regents of the University of California from the Foundation for the National Institutes of Health through the Grand Challenges in Global Health initiative. We thank M. Legros for making helpful suggestions on model analysis.

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Accepted Version - nihms253412.pdf

Supplemental Material - EVO_1186_sm_SuppMat.pdf

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