In the embryo and in the adult, skeletal muscle growth is dependent on the proliferation and the differentiation of muscle progenitors present within muscle masses. Despite the importance of these progenitors, their embryonic origin is unclear. Here we use electroporation of green fluorescent protein in chick somites, video confocal microscopy analysis of cell movements, and quail-chick grafting experiments to show that the dorsal compartment of the somite, the dermomyotome, is the origin of a population of muscle progenitors that contribute to the growth of trunk muscles during embryonic and fetal life. Furthermore, long-term lineage analyses indicate that satellite cells, which are known progenitors of adult skeletal muscles, derive from the same dermomyotome cell population. We conclude that embryonic muscle progenitors and satellite cells share a common origin that can be traced back to the dermomyotome.

Myostatin, a TGF-␤ family member, is an important regulator of adult muscle size. While extensively studied in vitro, the mechanisms by which this molecule mediates its effect in vivo are poorly understood. We addressed this question using chick and mouse embryos. We show that while myostatin overexpression in chick leads to an exhaustion of the muscle progenitor population that ultimately results in muscle hypotrophy, myostatin loss of function in chick and mouse provokes an expansion of this population. Our data demonstrate that myostatin acts in vivo to regulate the balance between proliferation and differentiation of embryonic muscle progenitors by promoting their terminal differentiation through the activation of p21 and MyoD. Previous studies have suggested that myostatin imposes quiescence on muscle progenitors. Our data suggest that myostatin's effect on muscle progenitors is more complex than previously realized and is likely to be context-dependent. We propose a novel model for myostatin mode of action in vivo, in which myostatin affects the balance between proliferation and differentiation of embryonic muscle progenitors by enhancing their differentiation.[Keywords: Myostatin; skeletal muscle; embryo; p21] Supplemental material is available at http://www.genesdev.org.

The receptor protein tyrosine kinase 7 (PTK7) was recently shown to participate in noncanonical Wnt/planar cell polarity signalling during mouse and frog embryonic development. In this study, we report that PTK7 interacts with b-catenin in a yeast two-hybrid assay and mammalian cells. PTK7-deficient cells exhibit weakened b-catenin/T-cell factor transcriptional activity on Wnt3a stimulation. Furthermore, Xenopus PTK7 is required for the formation of Spemann's organizer and for Siamois promoter activation, events that require b-catenin transcriptional activity. Using epistatic assays, we demonstrate that PTK7 functions upstream from glycogen synthase kinase 3. Taken together, our data reveal a new and conserved role for PTK7 in the Wnt canonical signalling pathway.

Neural induction is the process that initiates nervous system development in vertebrates. Two distinct models have been put forward to describe this phenomenon in molecular terms. The default model states that ectoderm cells are fated to become neural in absence of instruction, and do so when bone morphogenetic protein (BMP) signals are abolished. A more recent view implicates a conserved role for FGF signaling that collaborates with BMP inhibition to allow neural fate specification. Using the Xenopus embryo, we obtained evidence that may unite the 2 views. We show that a dominant-negative R-Smad, Smad5-somitabun-unlike the other BMP inhibitors used previously-can trigger conversion of Xenopus epidermis into neural tissue in vivo. However, it does so only if FGF activity is uncompromised. We report that this activity may be encoded by FGF4, as its expression is activated upon BMP inhibition, and its knockdown suppresses endogenous, as well as ectopic, neural induction by Smad5-somitabun. Supporting the importance of FGF instructive activity, we report the isolation of 2 immediate early neural targets, zic3 and foxD5a. Conversely, we found that zic1 can be activated by BMP inhibition in the absence of translation. Finally, Zic1 and Zic3 are required together for definitive neural fate acquisition, both in ectopic and endogenous situations. We propose to merge the previous models into a unique one whereby neural induction is controlled by BMP inhibition, which activates directly, and, via FGF instructive activity, early neural regulators such as Zic genes. xenopus ͉ default model ͉ Smad5-sbn N eural induction is viewed as a decision made by gastrula ectodermal cells between neural and epidermal fates (1, 2). This process has been best studied in the Xenopus and chick embryos, which led to the emergence of distinct molecular models. The default model, based initially on Xenopus studies, has proposed that bone morphogenetic protein (BMP) inhibition is necessary and sufficient for neural induction (1). Studies in the chick have implicated additional instructive signals, among which FGF is an early and essential one (3, 4). However, one shared conclusion is that neural fate assignment requires the down-regulation of BMP signals (5, 6). What remains controversial is whether BMP inhibition could be sufficient for neural induction. Recently, we and others have introduced a paradigm to test the validity of the default model in frogs, which consists of micro-injection of cell-autonomously acting BMP inhibitors in ventral ectodermal cells of the 16-or 32-cell embryo (5, 6). Fate mapping combined to marker gene analysis indicate that these blastomeres normally give rise exclusively to epidermal cells (5). Those cells are competent for neuralization, but do not become neural if injected with Smad6 or a dominant-negative BMP receptor (5, 6). However, the epidermal-to-neural switch occurs when a low amount of FGF4 (called eFGF in the frog) is combined with those BMP inhibitors, supporting a combinatorial model (5, 6).It remaine...