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Lethal gene drive selects inbreeding.

James J Bull^1,2,3

¹Department of Integrative Biology, University of Texas, Austin, TX, USA bull@utexas.edu.

Evolution, Medicine, and Public Health

|December 26, 2016

Summary

This summary is machine-generated.

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Selfish gene drive systems can cause population suppression. However, evolution of selfing (inbreeding) can restore fitness, acting as a natural resistance mechanism against gene drive technology.

Area of Science:

Population genetics
Evolutionary biology
Molecular genetics

Background:

Gene drive systems, particularly homing endonuclease genes (HEGs), offer theoretical potential for population suppression.
CRISPR technology has enabled the creation of HEGs that cause homozygote lethality and 100% segregation distortion.
The evolution of resistance mechanisms could limit the effectiveness of gene drive strategies.

Purpose of the Study:

To investigate the evolution of inbreeding (selfing) as a response to a recessively lethal HEG with complete segregation distortion.
To determine if selfing can counteract the population suppression effects of gene drive.
To assess the role of inbreeding depression in the evolution of selfing and fitness restoration.

Main Methods:

Population genetic modeling was employed to simulate the evolutionary dynamics.

Keywords:

evolution fitness genome engineering population genetics selfish gene

Related Experiment Videos

Numerical analyses were conducted to explore various outcomes under different conditions.

The models specifically focused on hermaphroditic populations (plants).

Main Results:

Selfing frequently evolved as a response to the HEG, partially restoring mean population fitness.
The extent to which selfing evolved and restored fitness was contingent upon the magnitude of inbreeding depression.
These findings suggest an underappreciated evolutionary mechanism that can resist the effects of selfish genes.

Conclusions:

Selfing can act as an evolutionary buffer against gene drive-induced population suppression.
Population suppression by gene drive may be counteracted by inherent evolutionary responses independent of the gene drive's molecular basis.
Future research should extend these models to populations with separate sexes to broaden applicability.