The rbm-39 family of genes encode RNA-binding proteins that are predicted to regulate alternative RNA splicing. However, the exact biological and molecular roles of rbm-39 remain largely unexplored. To learn more, we investigated the role of rbm-39 in C. elegans (a worm used for genetic studies). Loss of rbm-39 leads to sterility, but the cause has not yet been explored. Using staining and microscopy techniques we found that rbm-39 knockout worms have reduced germline development and a smaller pool of germline stem cells. This suggests that rbm-39 is required for normal germline stem cell regulation and the regulation germline development. However, the somatic gonad cells that regulate germ cell development appears morphologically normal. In addition, we also tested the hypothesis that RBM-39 regulates alternative RNA splicing. By isolating and sequencing mRNA from controls and rbm-39 mutants, we found that rbm-39 is implicated in the alternative splicing of a large group of genes. Alternative splicing analysis revealed that rbm-39 mutants have a significant difference in the usage of alternative 3’ splice sites for the RNAs for many genes. Gene ontology (GO) enrichment revealed that some of these RNAs are highly associated with the Notch signaling pathway, a key part of C. elegans transcriptional regulation for germline development, some misspliced RNAs are implicated in the cellular response to amino acid stimuli, aminoacylase activity, and the NuRD and CHD-type complexes. rbm-39 mutants also had differences in 3’ alternative splice site usage for many other RNAs implicated as regulators of gene expression in germ cells, such as nos-3, pal-1, cye-1, and mex-3. Overall, misregulation of these genes may explain why rbm-39 mutants are sterile.