Dis3l, also known as Dis3L1, is a catalytic exoribonuclease associated with the cytoplasmic exosome complex. It degrades cytoplasmic RNAs and is involved in RNA decay processes, playing a role in mRNA metabolism which is crucial for proper protein synthesis. It is associated with pathways like RNA degradation, and its malfunction has implications in various diseases including cancers [3,4]. Genetic models, such as KO and CKO mouse models, are valuable for studying its functions.

In a Dis3l cKO mouse model where DIS3L was ablated from the principal cells of the initial segment of the epididymis, spermatogenesis, IS differentiation, and the IS transcriptome were normal. Sperm count, morphology, motility, and acrosome reaction frequency were comparable to the control, indicating normal male fertility. Thus, DIS3L inactivation in the IS is nonessential for sperm maturation and male fertility [1].

In another KO mouse model study, disruption of DIS3L led to severe embryo degeneration and death soon after implantation. However, preimplantation Dis3l -/- embryos were normal in morphology and ability to produce functional embryonic stem cells. Although there were no major transcriptome changes in ES cells and blastocysts, Dis3l KO inhibited global protein synthesis, highlighting the essential role of DIS3L in embryo development [2].

In conclusion, model-based research reveals that Dis3l is essential for embryo development but not for cell viability in mice. The Dis3l KO/CKO mouse models contribute to understanding its non-essential role in sperm maturation in the epididymis. These findings provide insights into the biological functions of Dis3l and its potential implications in related disease areas, such as embryo-related disorders.