Genetic and Maternal Effects on Offspring Mortality in Mice

Abstract

Trade-offs occur when two traits have opposing fitness effects such that positive selection on one trait is constrained by the negative fitness consequences of the other trait. To understand why trade-off may arise we need to study the genetic and non-genetic factors that influence associated traits because these may respond differently to selective pressure. Research into trade-offs has largely focused on the genetic basis of associated traits, yet both maternal effects and epigenetic effects have recently been shown to affect life history traits that play a role in tradeoffs. In this study, we analyze genetic, epigenetic and lifehistory predictors of one of the most important trade-offs, that between offspring number and offspring mortality. Using a large-scale 3-generational intercross between two divergent mouse lines C57BL/6J and DBA/2J, we show that litter size differences between these lines, although significant, are surprisingly not the most important predictors of mortality. Offspring genotype, maternal effects and their interactions are the most influential factors determining mortality. We found significant paternal effects suggesting an important influence of paternal care or potentially the role of imprinted genes. Perhaps contrary to expectations our results further show that the trade-off between offspring number and mortality is not just a simple function of the two factors yielding, on average, an 'optimal' litter size at weaning. Indeed if one focused on litter size and mortality alone, the slope of relationship is the same for the two lines, yet they differ in the number of young at weaning. Our study reveals that a perceived tradeoff between two traits is governed by a more complex set of interactions between genetic and non-genetic effects.

Livebearing or egg-laying mammals: 27 decisive nucleotides of FAM168

“…Although the immune system is relatively undeveloped at birth and is developed during a lifetime of exposure to multiple foreign challenges (the so-called adaptive immune system), the development of the immune system, in particular innate immunity, starts early in fetal life for livebearing mammals (69)(70)(71). Considering this finding and our previous discoveries, the FAM168 gene family may contain crucial genes involved in the higher immune system and brain functions that are essential for mammals giving birth to live young (15,17,18,68).…”

“…Thus, this intermediate exon E4 seems to be a distinctive feature of livebearing mammals. Moreover, insertion of this new exon may have led to proteomic diversification by generating new gene functionality in FAM168A, the development of a higher immune system, which is essential for maturation in livebearing mammals (56,67,68) (Figure 4). Although the immune system is relatively undeveloped at birth and is developed during a lifetime of exposure to multiple foreign challenges (the so-called adaptive immune system), the development of the immune system, in particular innate immunity, starts early in fetal life for livebearing mammals (69)(70)(71).…”

Genotype-dependent responses to levels of sibling competition over maternal resources in mice

“…This seems particularly relevant to early development because levels of competition may be indicative of available resources during this crucial developmental period (Gyekis et al, 2011). Sibling competition over access to resources is common in species that provide significant parental care and have multiple offspring in a litter or brood (Mock and Parker, 1997).…”