Ell3, an RNA polymerase II elongation factor, is involved in diverse biological processes. It is associated with pathways like the p53-Bcl2 axis, ERK1/2 signaling, and Wnt signaling. Ell3 plays a crucial role in embryonic development, stem cell regulation, and cancer-related processes, highlighting its overall biological importance. Genetic models, especially KO mouse models, are valuable for studying its functions [3-5, 7].

Maternal ELL3 knockout in mice leads to oocyte aneuploidy, subfertility, and embryonic defects. Mechanistically, ELL3 localizes to the spindle during meiosis, and its depletion increases meiotic spindle abnormality. It coordinates with TPX2 to ensure proper function of the microtubule motor KIF11, promoting spindle assembly and chromosome movement [2]. In mouse embryonic stem cells, ELL3 depletion dislodges TET1 and SIN3A from a subset of young LINE-1s (L1Md_Ts), but increases BRD4 enrichment, affecting gene regulation and naïve-primed transition [1].

In conclusion, Ell3 is essential for proper embryonic development, especially in preventing oocyte aneuploidy. Its role in regulating LINE-1-based enhancers in embryonic stem cells also showcases its significance in early development. The gene knockout mouse models have been instrumental in revealing these functions, which are relevant to understanding early miscarriage and embryonic development-related diseases [1,2].