Dcp1a, the mRNA decapping factor, is a key player in post-transcriptional regulation of gene expression in eukaryotes. It is involved in mRNA cap removal before degradation and is associated with P-bodies. Its function impacts various biological processes, making it biologically significant. Genetic models, such as mouse models, have been valuable in studying its functions in vivo [1].

In mice, Dcp1a-deficient embryos generated using the CRISPR/Cas9 system showed embryonic lethality around E10.5, along with growth retardation and cardiac developmental defects, indicating its essential role in embryonic growth [1]. In mouse embryonic stem cells (ESCs), DCP1A, phosphorylated by MEK, regulates ESC self-renewal and differentiation through modulating P-body formation [2]. In the context of porcine deltacoronavirus (PDCoV) infection, PDCoV nsp5 cleaves DCP1A, reducing its antiviral activity, and this cleavage is a common immune evasion mechanism among different coronaviruses [3]. In gastric cancer, high DCP1a expression is associated with cancer development, poor prognosis, and chemotherapy resistance, and down-regulating its expression can reduce these effects [4].

In conclusion, Dcp1a is essential for embryonic growth, regulates the self-renewal and differentiation of embryonic stem cells, and is involved in viral immune evasion and cancer-related processes. Studies using gene-knockout mouse models have significantly contributed to understanding its role in these biological and disease-related contexts, providing insights into potential therapeutic targets for conditions like hepatocellular carcinoma and gastric cancer [1,2,3,4].