Maternal inputs to offspring early in development are initially high but the process of development suggests that ontogenetic shifts in the importance of maternal genetic variation relative to other sources should occur. We investigated additive genetic variance and covariance for direct (animal), sire, and maternal effects on embryonic length (EL), yolk sac volume (YSV), and alevin (after yolk sac resorption) length (AL) for 460 embryonic and 460 alevin brook charr (Salvelinus fontinalis) in 23 half-sib families (12 sires, 23 dams). There were no additive genetic effects of sires or individual animals on their own phenotype using sire-dam and maternal-animal models for YSV or EL (h2a < 0.05). However, at the alevin stage we detected low but significant heritability for AL (h2a = 0.14 ± 0.11). Conversely, maternal genetic effects were high for both embryonic traits (h2EL = 0.61 ± 0.05; h2YSV = 0.57 ± 0.06) but faded rapidly for postresorption length (h2AL = 0.18 ± 0.04). Maternal effects in the sire-dam model corresponded highly with those in the animal-dam model. We did not detect significant genetic covariance between progeny and dams for preresorption traits or between sires and dams for any trait. However, following resorption of the yolk sac, the genetic value of dams for AL was negatively correlated with that of individual progeny (rm,a = −0.38 ± 0.13), suggesting trade-offs and/or stabilizing selection between maternal and animal genetic trait value. This finding was supported by models of dam fecundity on offspring length and dam weight in phenotypic space. Heritability estimates using simple regression of embryo phenotype on adult parental phenotype produced upwardly biased estimates of genetic variance (h2 > 1.0). We propose that development through the embryo-alevin boundary may be a major point in salmonids for ontogenetic changes in the genetic architecture of embryo size from maternal genetic effects to those of the individual organism, and that maternal-offspring conflicts in resource allocation related to size may be partially indicated by negative genetic covariance.
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Vol. 58 • No. 9