GNAT3, also known as gustducin, is the α subunit of a G protein that governs sweet, savory, and bitter taste transduction [3]. It is involved in the gustatory signaling pathway and plays a significant role in taste perception, which is crucial for animals to detect and respond to various food-related stimuli [3,4,5,6]. Genetic models, such as gene knockout mice, have been valuable in studying its functions.

In pancreatic cancer, Gnat3-null (Gnat3-/-) mice crossed with KC or KCERT mice showed that ablation of Gnat3 in KC organoids increased the release of tumor-promoting cytokines like CXCL1 and CXCL2. In Gnat3-/-;KCERT pancreata, there were altered immunomodulatory gene expressions in Cxcr2-expressing myeloid-derived suppressor cells (MDSCs) and an increased number of granulocytic MDSCs. Aged Gnat3-/-;KC mice progressed more rapidly to metastatic carcinoma compared with KC controls, indicating that Gnat3 suppresses pancreatic cancer progression [1]. In periodontitis, Ga-gustducin-null (Gnat3-/-) mice were used to validate that salicin, which activates Tas2r143-mediated bitter taste signaling via Gnat3, alleviates periodontitis. The anti-inflammatory effects of salicin, such as inhibiting periodontal bone loss, were abolished in Gnat3-/-mice, suggesting that Gnat3 in gingival fibroblasts is critical for maintaining periodontal homeostasis [2].

In conclusion, GNAT3 is essential for taste perception. Its study through gene-knockout mouse models has revealed its significant role in suppressing pancreatic cancer progression and maintaining periodontal homeostasis. Understanding GNAT3 functions can potentially provide new insights into the mechanisms of these diseases and may lead to novel therapeutic strategies.