The Lyz1 gene encodes lysozyme C, a critical enzyme predominantly expressed in embryonic mesenchyme, intestine, liver, biliary system, and lungs. In mice, Paneth cells, specialized epithelial cells residing in the small intestine, serve as the principal source of lysozyme C. Studies have demonstrated that the targeted disruption of Lyz1 provides protection against experimental colitis. Loss of Lyz1 impairs the intestinal immune response to bacterial molecular patterns, thereby promoting the expansion of lysozyme-sensitive, mucus-dissolving bacterial populations ^[1].

The Lyz1-H2BmCherry-IRES-CreERT2 mice are constructed by knocking the H2BmCherry-IRES-CreERT2-rBG pA cassette into the mouse Lyz1 gene, a strategy that disrupts the expression of the endogenous Lyz1 gene. Without tamoxifen treatment, CreERT2 recombinase remains in the cytoplasm. After tamoxifen treatment, CreERT2 recombinase can enter the nucleus and exert its recombination function. Additionally, this model carries a red fluorescent protein (H2BmCherry) expression element, which can be used for lineage tracing of Lyz1-positive cells. When Lyz1-H2BmCherry-IRES-CreERT2 mice are crossed with mice containing loxP sites, tamoxifen-induced offspring will undergo Cre recombinase-mediated sequence recombination in Paneth cells of the small intestine. The red fluorescence expressed in this strain localizes to chromatin, facilitating detection.