Edc3, or enhancer of mRNA decapping 3, is a crucial protein for P-body assembly. It functions in promoting mRNA decapping and P-body formation, playing a vital role in regulating mRNA stability and translation, which are key processes in determining protein abundance within cells [1,2,3,4,5,6,7,8]. It is involved in various biological pathways related to post-transcriptional control, and its study in genetic models can provide insights into these regulatory mechanisms.

In prostate cancer cells, EDC3 phosphorylation at serine 161 (S161) by Pim1 and 3 protein kinases modifies P-body assembly. A mutation at S161 (EDC3 S161A) leads to decreased cell growth, migration, and invasion, along with reduced expression of integrin β1 and α6 [1]. In PRRSV-infected cells, overexpression of EDC3 inhibits PRRSV proliferation by upregulating MyD88, while knockdown promotes virus transcription and protein expression [3]. In yeast, Edc3 and Scd6 act redundantly with Dhh1 in post-transcriptional repression of starvation-induced pathways, and Edc3 is involved in the decay of specific mRNAs like RPS28B [4,5]. In Candida albicans, the edc3/edc3 deletion strain shows increased stress resistance, lower ROS levels, and decreased CaMCA1 expression [9].

In conclusion, Edc3 is essential for regulating mRNA-related processes such as decapping, P-body formation, and translation. Its dysregulation is associated with cancer-related functions like cell growth and invasion in prostate cancer, and it also impacts viral proliferation in PRRSV-infected cells, stress response in Candida albicans, and starvation-induced pathways in yeast. Studies using loss-of-function models, although not always in KO/CKO mouse models, have significantly enhanced our understanding of these functions and their implications in different biological contexts and disease conditions.