Male reproductive strategies and maintenance of genetic variation in the bank vole, Myodes glareolus
Post-Doctoral researcher with Tapio Mappes and Esa Koskela,
University of Jyvaskyla, Finland
We found that male reproductive success correlates with testosterone (T) levels and there is strong selection for T (Mills et al., 2007a). Furthermore, male dominance, driven by T, is an honest signal of male viability to females because T is heritable, high T males have higher mating success and importantly for a trait to be an honest signal, T has costs in terms of reduced immune response and reduced survival (Mills et al., 2009). Olfactory signalling, also used in sexual advertisement, on the other hand does not have immune costs, only energetic costs (Radwan et al., 2006).
However, there is considerable genetic variation in male T levels and thus this trait has not been driven to fixation. Three possible reasons include 1) the trade off between T and immune response; 2) genotype by environment interaction (GxE); and 3) sexual antagonism driven by T.
We have found a negative association between immune response and both T and the male signal, dominance (Mills et al., 2010). Moreover, immune function regulates the trade off between the sexual signal and survival (Mills et al., 2009). This trade off may thus provide a proximate mechanism that maintains variation in life history traits.
Further we found that although male dominance is an honest signal of viability to females, dominance is not heritable when environments fluctuate and thus dominance is not a reliable signal to females when environments fluctuate (Mills et al., 2007b). We demonstrate that GxE is an additional mechanism whereby genetic variation for male fitness traits can be maintained.
Finally, we demonstrated the presence of sexual conflict for reproductive success governed by T (Mills et al., 2012; Mokkonen et al., 2011) and for multiple mating behaviour (Mokkonen et al., 2012) and such antagonism coupled with population cycles suggests that sexual conflict may be another mechanism that maintains both reliability in the dominance signal and its genetic variation (Mills et al., 2015).