During my doctoral work I focused my attention on the study of the role of the uncharacterized protein PQN-59 in two independent processes in C. elegans: cell division and stress granule formation. I found that the depletion of PQN-59 results in high embryonic lethality and in the appearance of several mitotic defects during the early C. elegans embryonic divisions. Although the molecular mechanism underlying this phenotype remain to be elucidated, these data indicate that PQN-59 plays a role in cell division and development. In parallel, the observation that the human ortholog of PQN-59 (UBAP2L) is involved in the regulation of stress granule formation in mammalian cells, prompted me to explore the role of PQN-59 in this process and to study the mechanisms governing stress granule assembly in C. elegans. I found that PQN-59 is a component of stress granules in C. elegans and that it is required for the formation of numerous and well-structured cytoplasmic stress granules, demonstrating the importance of PQN-59 in this process.