Cell-cell communication is required for proper development and survival of an organism. One form of cell-cell communication uses signal transduction pathways such as the TGF-β pathway. TGF-β pathways are critical for developmental processes such as cell growth, cell division and organ development. TGF-β ligands signal through a type I and type II receptor and intracellular signal transducers called Smads. Binding of the ligand to its receptors allows for phosphorylation of Smads which then complex together and are shuttled to the nucleus and regulate target genes of the TGF-β pathway. The TGF-β ligands are conserved across animal phyla and a homolog of TGF-β in the nematode C. elegans is DBL-1. We previously established DBL-1 signaling in the epidermis of the worm as necessary and sufficient for normal body size. However, it is not clear which genes are directly responsible for changes in body size and what is the mechanism leading to a small worm. We present evidence implicating cuticle collagen genes as the effector genes responsible for the small body size phenotype resulting from defects in DBL-1 signaling. First, we show through EMSA and analysis of ChIP-seq data that specific collagen genes are direct or indirect targets of Smad regulation. Next, we establish through RNAi inhibition and overexpression that DBL-1-regulated cuticle collagen genes are positive and negative regulators of body size. Future work aims to determine whether changes in the exoskeleton structure of the worm affects DBL-1 signaling.