Publication details

Asymmetric size and shape variation in the Central European transect across the house mouse hybrid zone

Authors

MIKULA Ondřej AUFFRAY Jean-Christophe MACHOLÁN Miloš

Year of publication 2010
Type Article in Periodical
Magazine / Source Biological Journal of the Linnean Society
MU Faculty or unit

Faculty of Science

Citation
Web https://doi.org/10.1111/j.1095-8312.2010.01490.x
Doi http://dx.doi.org/10.1111/j.1095-8312.2010.01490.x
Keywords asymmetric variation; developmental instability; fluctuating asymmetry; mandible; Mus musculus; skull
Description We studied asymmetric variation of the mandible in the Central European portion of the hybrid zone between two house mouse subspecies, Mus musculus musculus and Mus musculus domesticus. Within introgression classes, defined by the share of diagnostic allozymes, we quantified the directional and fluctuating component of asymmetric variation, as well as skewness and kurtosis of individual asymmetry distributions. Furthermore, in the same manner we re-analysed asymmetric variation of the ventral side of the skull. According to the quadratic polynomial model, the mandible shape-fluctuating asymmetry, but not size-fluctuating asymmetry, was significantly decreased in the centre of the hybrid zone (with a minimum predicted for a hybrid index of 0.41). On the contrary, the skull shape-fluctuating asymmetry non-monotonically increased towards the musculus side of the hybrid zone (with a peak predicted for a hybrid index of 0.86). Thus, the impact of hybridization on fluctuating asymmetry is trait-specific in this portion of the house mouse hybrid zone. The only general feature of asymmetric variation we observed was the shift towards the platykurtosis of asymmetry distributions in the centre of the hybrid zone. Taken together, we suggest genetic variability for right-left asymmetries to be generally increased, but the developmental instability of mandible shape to be decreased, by hybridization. We hypothesize the decrease of developmental instability to be caused by overdominant effects on developmental dynamics rather than by increased heterozygosity.

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