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Choline kinase beta is required for normal endochondral bone formation.
Faculty Research 2014
  • Zhuo Li
  • Gengshu Wu
  • Roger B Sher
  • Zohreh Khavandgar
  • Martin Hermansson
  • Gregory A Cox, The Jackson Laboratory
  • Michael R Doschak
  • Monzur Murshed
  • Frank Beier
  • Dennis E Vance
Document Type
Publication Date
JAX Source
Biochim Biophys Acta 2014 Mar 14; 1840(7):2112-2122.

BACKGROUND: Choline kinase has three isoforms encoded by the genes Chka and Chkb. Inactivation of Chka in mice results in embryonic lethality, whereas Chkb(-/-) mice display neonatal forelimb bone deformations.

METHODS: To understand the mechanisms underlying the bone deformations, we compared the biology and biochemistry of bone formation from embryonic to young adult wild-type (WT) and Chkb(-/-) mice.

RESULTS: The deformations are specific to the radius and ulna during the late embryonic stage. The radius and ulna of Chkb(-/-) mice display expanded hypertrophic zones, unorganized proliferative columns in their growth plates, and delayed formation of primary ossification centers. The differentiation of chondrocytes of Chkb(-/-) mice was impaired, as was chondrocyte proliferation and expression of matrix metalloproteinases 9 and 13. In chondrocytes from Chkb(-/-) mice, phosphatidylcholine was slightly lower than in WT mice whereas the amount of phosphocholine was decreased by approximately 75%. In addition, the radius and ulna from Chkb(-/-) mice contained fewer osteoclasts along the cartilage/bone interface.

CONCLUSIONS: Chkb has a critical role in the normal embryogenic formation of the radius and ulna in mice.

GENERAL SIGNIFICANCE: Our data indicate that choline kinase beta plays an important role in endochondral bone formation by modulating growth plate physiology.

Biochim Biophys Acta 2014 Mar 14; 1840(7):2112-2122.

Citation Information
Zhuo Li, Gengshu Wu, Roger B Sher, Zohreh Khavandgar, et al.. "Choline kinase beta is required for normal endochondral bone formation." Vol. 1840 Iss. 7 (2014) p. 2112 - 2122 ISSN: 0006-3002
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