Lsm14b, a member of the LSM family, is an oocyte-specific RNA-binding protein. It is essential for maternal mRNA metabolism and oocyte development. Lsm14b is associated with networks crucial for oogenesis, and its function is pivotal in ensuring the success of oogenesis and the quality of eggs. Genetic models, such as knockout mouse models, have been instrumental in studying its function [1].

Deletion of Lsm14b in mice leads to female-specific infertility. The knockout oocytes are incompetent to complete meiosis and early embryogenesis. Lsm14b knockout disrupts the proper storage and timely clearance of mRNAs like Cyclin B1 and Btg4, by interfering with the assembly of the mitochondria-associated ribonucleoprotein domain (MARDO) during oocyte growth and meiotic maturation. It also affects the assembly of P-body-like granules in non-growing oocytes, impairs maternal mRNA accumulation and translation in fully grown oocytes, and causes abnormal oocyte MII arrest, along with aberrant transcriptional activation and chromosome assembly and segregation [1,2,3,4].

In conclusion, Lsm14b is indispensable for female fertility as it controls oocyte mRNA storage and stability, and coordinates protein component expression in the P-body to regulate oocyte maturation. The study of Lsm14b knockout mouse models has significantly enhanced our understanding of its role in female reproductive processes and the mechanisms underlying female infertility [1,2,3,4].