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Genetic mapping of molar size relations identifies inhibitory locus for third molars in mice

Authors :
Nicolas Navarro
A. Murat Maga
École pratique des hautes études (EPHE)
Université Paris sciences et lettres (PSL)
Biogéosciences [UMR 6282] [Dijon] (BGS)
Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS)
Division of Craniofacial Medicine
University of Washington [Seattle]
Center for Developmental Biology and Regenerative Medicine
Seattle Children's Research Institute
Study supported partially by NIH/NIDCR Independence to Pathway Award, as well as a Seattle Children’s Research Institute seed fund, and by the National Institute of General Medical Sciences of the National Institutes of Health under grant number P41 GM103545-17.
Source :
Heredity, Heredity, Nature Publishing Group, 2018, 121 (1), pp.1-11. ⟨10.1038/s41437-017-0033-2⟩
Publication Year :
2018
Publisher :
Springer Science and Business Media LLC, 2018.

Abstract

11 pages; International audience; Molar size in Mammals shows considerable disparity and exhibits variation similar to that predicted by the Inhibitory Cascade model. The importance of such developmental systems in favoring evolutionary trajectories is also underlined by the fact that this model can predict macroevolutionary patterns. Using backcross mice, we mapped QTL for molar sizes controlling for their sequential development. Genetic controls for upper and lower molars appear somewhat similar, and regions containing genes implied in dental defects drive this variation. We mapped three relationship QTLs (rQTL) modifying the control of the mesial molars on the focal third molar. These regions overlap Shh, Sostdc1, and Fst genes, which have pervasive roles in development and should be buffered against new variation. It has theoretically been shown that rQTL produces new variation channeled in the direction of adaptive changes. Our results provide evidence that evolutionary/disease patterns of tooth size variation could result from such a non-random generating process.

Details

ISSN :
13652540 and 0018067X
Volume :
121
Database :
OpenAIRE
Journal :
Heredity
Accession number :
edsair.doi.dedup.....d4df2e7283ad3d18a22d90d58e413454