Limits to Behavioral Evolution: The Quantitative Genetics of a Complex Trait Under Directional Selection

Abstract

Replicated selection experiments provide a powerful way to study how "multiple adaptive solutions" may lead to differences in the quantitative-genetic architecture of selected traits and whether this may translate into differences in the timing at which

Evolution of the additive genetic variance–covariance matrix under continuous directional selection on a complex behavioural phenotype

“…For all six behavioural traits, HR mice show an approximately fourfold lower predicted R than do C mice (figure 3; electronic supplementary material, table S4). Because the predicted responses for days 5 and 6 were still positive and statistically significant in generations 21-31, however, we can confidently rule out the possibility that changes in the form of G and/or b caused the selection plateaus that occurred in each of the four HR lines during generations 21-31, which is consistent with the conclusions of Careau et al [16].…”

“…We used the same data and pedigree for wheel running on days 5 and 6 as compiled and checked in a previous study [16]. Here, we added data on days 1 -4 and excluded an additional 572 individuals for which wheel running on a given day was obviously abnormal compared with wheel running on the other days (this often resulted from wheel problems that were detected and corrected during the first 4 days).…”

“…We chose to pool the data for replicate lines within C and HR, and divide the 32 generations into roughly three equal time periods: generations 0-10, 11-20 and 21-31. This offered the best tradeoff between having large sample size within each time period (electronic supplementary material, table S1) to allow estimation of G with adequate precision while at the same time examining temporal change in G over periods before (generations 0-10), during (generations [11][12][13][14][15][16][17][18][19][20] and mostly after (generations 21-31) the selection plateaus had been reached [16]. For each time period, we ran two separate models (one for C and one for HR mice) restricted to the pedigree and phenotypic data from that time period, yielding a total of six G matrices.…”

A Novel Intronic Single Nucleotide Polymorphism in the Myosin heavy polypeptide 4 Gene Is Responsible for the Mini-Muscle Phenotype Characterized by Major Reduction in Hind-Limb Muscle Mass in Mice

“…After 10 generations of selection, mice from the four replicate High Runner (HR) lines were running .70% more revolutions per day (on days 5 and 6) as compared with four nonselected control (C) lines (Swallow et al 1998). Wheel running continued to increase in the HR lines until generation 16-28 (depending on line and sex) and remained approximately at those levels through a subsequent 50 generations of selective breeding Swallow et al 2009;Kolb et al 2010;Careau et al 2012Careau et al , 2013.…”

“…Alternatively, the underlying allele might have pleiotropic effects that act on nonmuscle tissues and organs but still facilitate endurance running (e.g., reduced total body mass and fat mass; increased relative heart, liver, and kidney mass; longer hind-limb bones) (Garland et al 2002;Kelly et al 2006;Hannon et al 2008;Kolb et al 2010). However, at generation 22, wheel running of affected individuals did not differ statistically from those with normal-sized muscles (Garland et al 2002), and the magnitude of response to selection was not systematically higher in the two lines that had the mini-muscle phenotype as compared with the two that did not, indicating that multiple genetic "solutions" are possible in response to selection for high levels of voluntary exercise (Garland et al 2011a;Careau et al 2013). To date, obvious deleterious effects of the mini-muscle phenotype have not been identified (e.g., see Girard et al 2002), which is unusual for a gene of major effect (e.g., Carriére et al 1994;Rivero et al 2011).…”