RNA Binding Motif Protein 39 (or Caperα) is a conserved RBP that is known to act as an alternative splicing activator. Caper (RBM39 homolog in Drosophila) has been studied in the development and maintenance of the nervous system, and in cancers. Deficiency in Caper/RBM-39 compromises dendrite morphology, sensory neuron development, neuromuscular junction morphogenesis, and lifespan, mainly in Drosophila model. However, very few studies have been conducted in other organisms. For example, in C. elegans, its full phenotypic effect remains obscured due to the absence of a knockout mutant. Using C. elegans as a model, we have successfully generated an rbm-39 knockout mutant (cnj4) via CRISPR. We found that the homozygous deletion of rbm-39 leads to severe developmental defects, including sterility, early death, and larval arrest. We used a genetic balancer tmC25 to maintain the recessive sterile allele in heterozygotes. Indeed, a previous study has found that Caper knockdown in Drosophila reduces animal life span. However, further investigation is required to understand the mechanism at the molecular level for larval mortality. Since the sterile phenotype was prominent, we decided to conduct a phenotypic analysis of germline development defects in rbm-39 mutants to learn potential causes of mutant sterility. Our results show that rbm-39(cnj4) animals have either delayed or failed in oogenesis. We found that the mitotic zone length of the germ line was shorter in the homozygous rbm-39(cnj4) than N2 (wild type) and heterozygotes, suggesting disruptions in proliferation and/or maintenance of the germline stem cells. Gonad visualization also revealed abnormal oocytes that were seemingly endomitotic in rbm-39(cnj4) animals. Taken together, RBM-39 is essential for proper germline development and oogenesis. Since RBM-39 is predominantly an alternative splicing factor, genes that control aspects of germline development may be mis-spliced in the mutant. In general, our study highlights the importance of this conserved splicing factor, RBM-39, in reproductive and early development. We have established a novel mutant strain for future investigations while also expanding the knowledge of this protein's functions in C. elegans. Given that germline development in C. elegans is well studied and the processes are highly coordinated with defined signaling pathways, the mechanism of RBM-39 in germline development can be studied using the rbm-39(cnj4) strain. Future directions should identify the specific signaling pathways and pre-mRNA targets. Additionally, rbm-39(cnj4) mutants exhibited mild uncoordinated locomotion, strongly associated with neuronal or muscular defects. Future studies should examine the RBM-39 knockout phenotype in neurons and dendritic branches.