Abstract
BackgroundIn recent years it has become increasingly apparent that physical inactivity can predispose individuals to a host of health problems. While many studies have analyzed the effect of various environmental factors on activity, we know much less about the genetic control of physical activity. Some studies in mice have discovered quantitative trait loci (QTL) influencing various physical activity traits, but mostly have analyzed inter-individual variation rather than variation in activity within individuals over time. We conducted a genome scan to identify QTLs controlling the distance, duration, and time run by mice over seven consecutive three-day intervals in an F2 population created by crossing two inbred strains (C57L/J and C3H/HeJ) that differed widely (average of nearly 300%) in their activity levels. Our objectives were (a) to see if we would find QTLs not originally discovered in a previous investigation that assessed these traits over the entire 21-day period and (b) to see if some of these QTLs discovered might affect the activity traits only in the early or in the late time intervals.ResultsThis analysis uncovered 39 different QTLs, over half of which were new. Some QTLs affected the activity traits only in the early time intervals and typically exhibited significant dominance effects whereas others affected activity only in the later age intervals and exhibited less dominance. We also analyzed the regression slopes of the activity traits over the intervals, and found several QTLs affecting these traits that generally mapped to unique genomic locations.ConclusionsIt was concluded that the genetic architecture of physical activity in mice is much more complicated than has previously been recognized, and may change considerably depending on the age at which various activity measures are assessed.
Highlights
In recent years it has become increasingly apparent that physical inactivity can predispose individuals to a host of health problems
There is a wealth of knowledge about the environmental factors that predispose individuals to physical inactivity, it is somewhat surprising that we still know comparatively little about the genetic control of voluntary exercise
Our results are applicable only to the specific F2 population we generated from crossing the C57L/J and C3H/HeJ strains, and as quantitative trait loci (QTL) studies are performed with other progenitor strains, we should expect additional QTLs to be found, including on the four chromosomes where we found none
Summary
In recent years it has become increasingly apparent that physical inactivity can predispose individuals to a host of health problems. Activity levels vary considerably among populations, sexes, and/or age cohorts [1,2], in most populations, typically only a fraction of all individuals engage in vigorous or sustained exercise [3,4] This is unfortunate since it has become increasingly apparent that physical inactivity can predispose individuals to a host of diseases such as heart failure and cancer [5,6,7,8]. Several recent studies in mice [11,12,13,14,15,16,17,18,19] have been successful in uncovering a number of QTLs for various wheel-running traits These studies have given us information about the numbers and modes of action of the QTLs governing these traits, and have been useful in providing a preliminary view of the genetic control of physical activity in mice
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