The Digital Divide

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Science  20 Nov 2009:
Vol. 326, Issue 5956, pp. 1043
DOI: 10.1126/science.326.5956.1043-a
CREDIT: SUZUKI ET AL., DEV. BIOL. 335, 396 (2009)

Programmed cell death is an important process in development, with mammalian digits being just one such example. The bone morphogenetic proteins (BMPs) and their downstream targets, the Msx genes, are known to participate in digit separation. If these components are absent, fingers and toes do not separate, resulting in soft tissue syndactyly. Suzuki et al. find that the small GTP-binding protein Rac1, which previously has been shown to function in cell adhesion, migration, and proliferation, also figures in digit development. When Rac1 was inactivated in the mesenchyme of the mouse limb bud, skeletal defects were apparent (such as the malformed sternum shown), yet a striking feature was soft tissue syndactyly due to webbing of the interdigital skin. Epistasis analysis revealed that BMP and Msx genes were not expressed in the limbs of Rac1-deficient mice; the elimination of Rac1 prevented programmed cell death from removing interdigital limb mesenchymal cells, primarily between the 2nd and 3rd, and the 3rd and 4th digits.

Dev. Biol. 335, 396 (2009).

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