Rnpc3, encoding the U11/U12-65K protein, is a specific component of the minor spliceosome. The minor spliceosome is involved in splicing minor (U12-type) introns present in about 700-800 human genes, accounting for approximately 0.35% of all introns [2]. It is crucial for normal development and gene expression regulation [3].

Germline Rnpc3-/-mouse embryos died before blastocyst implantation, indicating its importance in early development [3]. Conditional knockout in adult mice led to rapid weight loss, leukopenia, and degeneration of the gastrointestinal tract epithelial lining due to increased cell death and reduced cell proliferation [3]. In female Rnpc3 mutant mice, there was a reduction in pituitary GH content, while male mice had no obvious phenotype [1]. Also, conditional ablation of RNPC3 in activated B cells in mice showed defective antibody generation due to impaired germinal center B cell response [4].

In conclusion, Rnpc3 is essential for early development, gastrointestinal homeostasis, and B-cell-mediated immune responses. Mouse models, including gene knockout and conditional knockout, have revealed its role in pituitary and ovarian development, as well as in diseases such as hypopituitarism and primary ovarian insufficiency [1]. These models are valuable for understanding the gene's function and its implications in disease.