Foxp2 regulates anatomical features that may be relevant for vocal behaviors and bipedal locomotion

Proc Natl Acad Sci U S A. 2018 Aug 28;115(35):8799-8804. doi: 10.1073/pnas.1721820115. Epub 2018 Aug 13.

Abstract

Fundamental human traits, such as language and bipedalism, are associated with a range of anatomical adaptations in craniofacial shaping and skeletal remodeling. However, it is unclear how such morphological features arose during hominin evolution. FOXP2 is a brain-expressed transcription factor implicated in a rare disorder involving speech apraxia and language impairments. Analysis of its evolutionary history suggests that this gene may have contributed to the emergence of proficient spoken language. In the present study, through analyses of skeleton-specific knockout mice, we identified roles of Foxp2 in skull shaping and bone remodeling. Selective ablation of Foxp2 in cartilage disrupted pup vocalizations in a similar way to that of global Foxp2 mutants, which may be due to pleiotropic effects on craniofacial morphogenesis. Our findings also indicate that Foxp2 helps to regulate strength and length of hind limbs and maintenance of joint cartilage and intervertebral discs, which are all anatomical features that are susceptible to adaptations for bipedal locomotion. In light of the known roles of Foxp2 in brain circuits that are important for motor skills and spoken language, we suggest that this gene may have been well placed to contribute to coevolution of neural and anatomical adaptations related to speech and bipedal locomotion.

Keywords: Foxp2; bipedalism; bone remodeling; cranial base; vocalization.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Bone Remodeling / genetics*
  • Forkhead Transcription Factors* / genetics
  • Forkhead Transcription Factors* / metabolism
  • Hindlimb / metabolism
  • Humans
  • Locomotion / genetics*
  • Mice
  • Mice, Knockout
  • Mutation*
  • Repressor Proteins* / genetics
  • Repressor Proteins* / metabolism
  • Skull / metabolism*
  • Vocalization, Animal*

Substances

  • Forkhead Transcription Factors
  • Foxp2 protein, mouse
  • Repressor Proteins