scholarly journals A selfish genetic element linked to increased lifespan impacts metabolism in female house mice

2019 ◽  
Vol 223 (1) ◽  
pp. jeb212704
Author(s):  
Patricia C. Lopes ◽  
Anna K. Lindholm
2018 ◽  
Vol 285 (1888) ◽  
pp. 20181333 ◽  
Author(s):  
Jan-Niklas Runge ◽  
Anna K. Lindholm

Life is built on cooperation between genes, which makes it vulnerable to parasitism. Selfish genetic elements that exploit this cooperation can achieve large fitness gains by increasing their transmission relative to the rest of the genome. This leads to counter-adaptations that generate unique selection pressures on the selfish genetic element. This arms race is similar to host–parasite coevolution, as some multi-host parasites alter the host’s behaviour to increase the chance of transmission to the next host. Here, we ask if, similarly to these parasites, a selfish genetic element in house mice, the t haplotype, also manipulates host behaviour, specifically the host’s migration propensity. Variants of the t that manipulate migration propensity could increase in fitness in a meta-population. We show that juvenile mice carrying the t haplotype were more likely to emigrate from and were more often found as migrants within a long-term free-living house mouse population. This result may have applied relevance as the t has been proposed as a basis for artificial gene drive systems for use in population control.


2018 ◽  
Author(s):  
Jan-Niklas Runge ◽  
Anna K. Lindholm

AbstractLife is built on cooperation between genes, which makes it vulnerable to parasitism. However, selfish genetic elements that exploit this cooperation can achieve large fitness gains by increasing their transmission unfairly relative to the rest of the genome. This leads to counter-adaptations that generate unique selection pressures on the selfish genetic element. This arms race is similar to host-parasite co-evolution. Some multi-host parasites alter the host’s behaviour to increase the chance of transmission to the next host. Here we ask if, similarly to these parasites, a selfish genetic element in house mice, the t haplotype, also manipulates host behaviour, specifically the host’s migration propensity. Variants of the t that manipulate migration propensity could increase in fitness in a meta-population. We show that juvenile mice carrying the t haplotype were more likely to emigrate from and were more often found as migrants within a long-term free-living house mouse population. This result may have applied relevance as the t has been proposed as a basis for artificial gene drive systems for use in population control.


2008 ◽  
Vol 105 (29) ◽  
pp. 10085-10089 ◽  
Author(s):  
M. D. Lorenzen ◽  
A. Gnirke ◽  
J. Margolis ◽  
J. Garnes ◽  
M. Campbell ◽  
...  

Science ◽  
2007 ◽  
Vol 316 (5824) ◽  
pp. 597-600 ◽  
Author(s):  
Chun-Hong Chen ◽  
Haixia Huang ◽  
Catherine M. Ward ◽  
Jessica T. Su ◽  
Lorian V. Schaeffer ◽  
...  

2019 ◽  
Vol 286 (1910) ◽  
pp. 20191414 ◽  
Author(s):  
Sam Ronan Finnegan ◽  
Nathan Joseph White ◽  
Dixon Koh ◽  
M. Florencia Camus ◽  
Kevin Fowler ◽  
...  

A number of species are affected by Sex-Ratio (SR) meiotic drive, a selfish genetic element located on the X-chromosome that causes dysfunction of Y-bearing sperm. SR is transmitted to up to 100% of offspring, causing extreme sex ratio bias. SR in several species is found in a stable polymorphism at a moderate frequency, suggesting there must be strong frequency-dependent selection resisting its spread. We investigate the effect of SR on female and male egg-to-adult viability in the Malaysian stalk-eyed fly, Teleopsis dalmanni . SR meiotic drive in this species is old, and appears to be broadly stable at a moderate (approx. 20%) frequency. We use large-scale controlled crosses to estimate the strength of selection acting against SR in female and male carriers. We find that SR reduces the egg-to-adult viability of both sexes. In females, homozygous females experience greater reduction in viability ( s f = 0.242) and the deleterious effects of SR are additive ( h = 0.511). The male deficit in viability ( s m = 0.214) is not different from that in homozygous females. The evidence does not support the expectation that deleterious side effects of SR are recessive or sex-limited. We discuss how these reductions in egg-to-adult survival, as well as other forms of selection acting on SR, may maintain the SR polymorphism in this species.


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