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First published online 8 December 2005
doi: 10.1242/dev.02183
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Department of Molecular and Cell Biology, Division of Genetics, Genomics, and Development, and the Center for Integrative Genomics, University of California, Berkeley, CA 94720-3204, USA.
* Author for correspondence (e-mail: harland{at}socrates.berkeley.edu)
Accepted 25 October 2005
We have examined lbx1 expression in early X. laevis tadpoles. In contrast to amniotes, lbx1 is expressed in all of the myoblasts that contribute to the body wall musculature, as well as in a group of cells that migrate into the head. Despite this different expression, the function of lbx1 appears to be conserved. Morpholino (MO) knockdown of lbx1 causes a specific reduction of body wall muscles and hypoglossal muscles originating from the somites. Although myoblast migratory defects are observed in antisense MO injected tadpoles targeting lbx1, this results at least in part from a lack of myoblast proliferation in the hypaxial muscle domain. Conversely, overexpression of lbx1 mRNA results in enlarged somites, an increase in cell proliferation, but a lack of differentiated muscle. The control of cell proliferation is linked to a strong downregulation of myoD expression in gain-of-function experiments. Co-injection of myoD mRNA with lbx1 mRNA eliminates the overproliferation phenotype observed when lbx1 is injected alone. The results indicate that a primary function of lbx1 in hypaxial muscle development is to repress myoD, allowing myoblasts to proliferate before the eventual onset of terminal differentiation.
Key words: Hypaxial, Rectus abdominus, Rectus cervicus, Geniohyoideus, lbx1, myoD, myf5, Xenopus laevis, Cell proliferation, Myogenesis
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