Slc30a1, also known as the gene encoding zinc transporter ZnT1, is crucial for maintaining cellular and systemic zinc homeostasis. It is involved in diverse biological processes such as ion transport, cell proliferation, and survival. The protein is ubiquitously expressed and plays a role in various pathways related to zinc-mediated physiological functions [1,2,3,4,5]. Genetic models, like knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools for studying its functions.

Using tissue-specific KO mice, Slc30a1 in the intestine was found to be essential for survival, safeguarding intestinal barrier integrity and systemic zinc homeostasis [2]. In macrophages, Lyz2-Cre-driven Slc30a1 CKO mice showed increased susceptibility to Salmonella infection. Slc30a1-deficient macrophages had defective intracellular killing, reduced activation of nuclear factor kappa B, and decreased nitric oxide production, along with intracellular zinc accumulation [3]. In zebrafish, slc30a1a and slc30a1b double mutants had increased melanocytes, and in Slc30a1-deficient zebrafish, there was zinc accumulation in neural crest cells, affecting pharyngeal arch differentiation [4,5].

In conclusion, Slc30a1 is fundamental for maintaining zinc homeostasis across different tissues and cell types. Studies using KO and CKO mouse models and zebrafish mutants have revealed its significance in diseases such as primary aldosteronism, Salmonella infection, and potentially in melanoma and neural-crest-derived organ development [1,3,4,5]. These findings enhance our understanding of the role of zinc in biological processes and associated disease mechanisms.