Recombinant human BMPs are used clinically to repair and replace bone. Perturbation of BMP signaling levels can contribute to pathogenic conditions including bone disorders and cancers. The invertebrate Caenorhabditis elegans is an established genetic model system for studying BMP signaling. BMP member DBL-1 regulates post-embryonic body size and other phenotypes. Animals with increased DBL-1 signaling are longer than wild-type animals, while loss of signaling results in smaller animals. The body length phenotype develops during postembryonic development, and is not based on cell number, as this eutelic species has a fixed somatic cell number among its members. Studies to address how DBL-1 signaling regulates body size has revealed a canonical BMP signaling pathway exists to transmit the secreted DBL-1 signal from the cell membrane through a set of conserved receptors to the nucleus by Smad transcriptional regulators. The cellular focus of the body size phenotype is the hypodermis, an epidermal tissue that surrounds the animal��s internal tissues and synthesizes the nematode cuticle, a sturdy, protective extracellular matrix. The DBL-1 receptors, Smads, other regulatory factors, and a multitude of pathway targets are expressed in this tissue. However, the cellular mechanisms underlying the body size phenotype of this molecular pathway remain unclear. Previous work to address the question of how DBL-1 regulates body size has provided evidence of a partial contribution by endoreduplication within these hypodermal cells. Multiple studies show that expression of a number of transcriptional targets, including cuticular components, is altered by changes in DBL-1 signaling. Loss of single cuticular proteins can also alter nematode body length. Loss of DBL-1 signaling increases sensitivity to different drug types in C. elegans. While mutation of drug target genes can affect drug response of the Carbimazole animal, a compromised nematode permeability barrier is also associated with increased anesthetic sensitivity. While it has been Butacaine proposed that DBL-1 also affects drug entry, rather than affecting the function of the drug targets themselves, the basis of this DBL-1 function is unresolved.