Canalization and Developmental Instability of the FetalSkull in a Mouse Model of Maternal Nutritional Stress

Abstract

Nutritional imbalance is one of themain sources of stress in both extant and extinct humanpopulations. Restricted availability of nutrients isthought to disrupt the buffering mechanisms that con-tribute to developmental stability and canalization,resulting in increased levels of fluctuating asymmetry(FA) and phenotypic variance among individuals. How-ever, the literature is contradictory in this regard. Thisstudy assesses the effect of prenatal nutritional stresson FA and among-individual variance in cranial shapeand size using a mouse model of maternal proteinrestriction. Two sets of landmark coordinates were digi-tized in three dimensions from skulls of control and pro-tein restricted specimens at E17.5 and E18.5. We foundthat, by the end of gestation, maternal protein restric-tion resulted in a significant reduction of skull size.Fluctuating asymmetry in size and shape exceeded theamount of measurement error in all groups, but no sig-nificant differences in the magnitude of FA were foundbetween treatments. Conversely, the pattern of shapeasymmetry was affected by the environmental perturba-tion since the angles between the first eigenvectorsextracted from the covariance matrix of shape asymmet-ric component of protein restricted and control groupswere not significantly different from the expected forrandom vectors. In addition, among-individual variancein cranial shape was significantly higher in the proteinrestricted than the control group at E18.5. Overall, theresults obtained from a controlled experiment do notsupport the view of fluctuating asymmetry of cranialstructures as a reliable index for inferring nutritionalstress in human populations.