Cell division and protein homeostasis are fundamental processes required for organismal development. Disruption of either can lead to severe cellular and organismal abnormalities. In Caenorhabditis elegans, our laboratory identified PQN-59 as a component of stress granules and a key protein in early cell division and embryonic development. However, its precise function remains unclear. Here, we performed a structure–function analysis of PQN-59 to investigate a potential separation-of-function mutant between the aberrant first cell division and the stress granule localization phenotypes, with a focus on the loss of function allele pqn-59(ΔUBA). We also identify a novel PQN-59 interacting partner, SAO-1, whose human homologue GIGYF2 suggests a novel role for PQN-59 in protein homeostasis. Consistently, proteomic analyses revealed 70% of the differentially expressed proteins were downregulated in pqn-59(RNAi) and pqn-59(ΔUBA) conditions. Together, our findings establish PQN-59 as a critical regulator of early embryonic cell division and protein homeostasis in C. elegans.