The TUB bipartite transcription factor (TUB) gene encodes a member of the Tubby family of proteins that play a role in obesity and sensory degeneration. The four members of the Tubby protein family in vertebrates share similar structural domains, including a highly conserved C-terminal domain that mediates DNA binding and a divergent N-terminal region containing nuclear localization signals and transcriptional activation structural domains, which are associated with interprotein binding^[1]. TUB can function by binding to the intraciliary transport A protein (IFTAP) in the eye, and similar to other members of the Tubby family, TUB is also involved in controlling the initiation of phagocytosis and facilitating the clearance of apoptotic cells or cellular debris by retinal pigment epithelial cells (RPE) and macrophages. Diseases associated with TUB mutations and functional abnormalities include retinal dystrophy (RD), retinitis pigmentosa (RP), and obesity^[2-3]. Mice carrying a spontaneous mutation in the Tub gene (Tubby mice) present a phenotype of obesity at maturity, retinal degeneration, and progressive hearing loss, and the phenotype in this mouse is associated with a deficiency in Tub protein function due to abnormal splicing of the Tub gene^[4].

This strain is a mouse Tub knockout model that uses gene editing technology to knock out the homolog of the human TUB gene in mice. The Tub knockout mouse model has been reported to have the same phenotype as Tubby mice carrying spontaneous mutations in the Tub gene, and the deletion of Tub gene expression in mice leads to abnormalities of photoreceptors in the retina through apoptosis, which subsequently causes defects in the retina^[5], and this model can be used for the study of retinal degeneration and related diseases. The homozygous Tub-KO mice are viable and fertile, but the phenomenon of filial cannibalism is more pronounced in homozygotes.