Syndecan-3 and syndecan-4 specifically mark skeletal muscle satellite cells and are implicated in satellite cell maintenance and muscle regeneration.

Myogenesis in the embryo and the adult mammal consists of a highly organized and regulated sequence of cellular processes to form or repair muscle tissue that include cell proliferation, migration, and differentiation. Data from cell culture and in vivo experiments implicate both FGFs and HGF as critical regulators of these processes. Both factors require heparan sulfate glycosaminoglycans for signaling from their respective receptors. Since syndecans, a family of cell-surface transmembrane heparan sulfate proteoglycans (HSPGs) are implicated in FGF signaling and skeletal muscle differentiation, we examined the expression of syndecans 1-4 in embryonic, fetal, postnatal, and adult muscle tissue, as well as on primary adult muscle fiber cultures. We show that syndecan-1, -3, and -4 are expressed in developing skeletal muscle tissue and that syndecan-3 and -4 expression is highly restricted in adult skeletal muscle to cells retaining myogenic capacity. These two HSPGs appear to be expressed exclusively and universally on quiescent adult satellite cells in adult skeletal muscle tissue, suggesting a role for HSPGs in satellite cell maintenance or activation. Once activated, all satellite cells maintain expression of syndecan-3 and syndecan-4 for at least 96 h, also implicating these HSPGs in muscle regeneration. Inhibition of HSPG sulfation by treatment of intact myofibers with chlorate results in delayed proliferation and altered MyoD expression, demonstrating that heparan sulfate is required for proper progression of the early satellite cell myogenic program. These data suggest that, in addition to providing potentially useful new markers for satellite cells, syndecan-3 and syndecan-4 may play important regulatory roles in satellite cell maintenance, activation, proliferation, and differentiation during skeletal muscle regeneration.

A Caenorhabditis elegans homologue of hunchback is required for late stages of development but not early embryonic patterning.

We have cloned a Caenorhabditis elegans homologue of the Drosophila gap gene hunchback (hb) and have designated it hbl-1 (hunchback-like). hbl-1 encodes a predicted 982-amino-acid protein, containing two putative zinc-finger domains similar to those of Drosophila Hunchback. The gene is transcribed embryonically, but unlike the maternally expressed Drosophila hb, its mRNA is not detected in C. elegans oocytes. A hbl-1::gfp reporter is expressed primarily in ectodermal cells during embryonic and larval development. Double-stranded RNA-interference (RNAi) was used to indicate hbl-1 loss-of-function phenotypes. Progeny of hbl-1(RNAi) hermaphrodites exhibit a range of defects; the most severely affected progeny arrest as partially elongated embryos or as hatching, misshapen L1 larvae. Animals that survive to adulthood exhibit variably dumpy (Dpy), uncoordinated (Unc), and egg-laying defective (Egl) phenotypes, as well as defects in vulval morphology (Pvl). Abnormal organization of hypodermal cells and expression of a hypodermal marker in hbl-1(RNAi) animals suggests that most of the phenotypes observed could be due to improper specification of hypodermal cells. The pattern of hbl-1 expression is similar to that reported for the leech hunchback homologue Lzf-2, suggesting that these proteins may have similar biological functions in diverse species with cellular embryos.