During <i>C. elegans</i> development, 1090 somatic cells are generated of which 131 reproducibly die, many through apoptosis. The <i>C. elegans</i> BH3-only gene <i>
egl-1</i> is the key activator of apoptosis in somatic tissues, and it is predominantly expressed in 'cell death' lineages i.e. lineages in which apoptotic cell death occurs. <i>
egl-1</i> expression is regulated at the transcriptional and post-transcriptional level. For example, we previously showed that the miR-35 and miR-58 families of miRNAs repress <i>
egl-1</i> expression in mothers of 'unwanted' cells by binding to the 3' UTR of <i>
egl-1</i> mRNA, thereby increasing <i>
egl-1</i> mRNA turnover. In a screen for RNA-binding proteins with a role in the post-transcriptional control of <i>
egl-1</i> expression, we identified EIF-3.H (ortholog of human eIF3H) and HRPR-1 (ortholog human hnRNP R/Q) as potential activators of <i>
egl-1</i> expression. In addition, we demonstrate that the knockdown of the <i>
eif-3.H</i> or <i>
hrpr-1</i> gene by RNA-mediated interference (RNAi) results in the inappropriate survival of unwanted cells during <i>C. elegans</i> development. Our study provides novel insight into how <i>
egl-1</i> expression is controlled to cause the reproducible pattern of cell death observed during <i>C. elegans</i> development.