Abstract

Blind mole rats (Nannospalax) are subterranean mammals noted for their longevity and cancerresistance. It is known that these animals' vestigial eyes, particularly the Harder gland around the eyes, maygenerate considerable amounts of melatonin. Furthermore, the melatonin production mechanism in thecircadian rhythm cycle of blind mole rats is regarded to be different from that of other living beings. Themelatonin and Clock genes are hypothesized to be linked to the formation, development, and spread ofcancer, but the researchers still cannot explain their extraordinary cancer resistance.In this study, we hypothesized that the melatonin production mechanism in the circadian rhythm cycle ofblind mole rats, which have been shown in the literature to be cancer-resistant, may differ from that of otherliving species due to the difference in their amino acid variations. Differences in the DNA of the Clockgenes (Cry1 and Per1) involved in melatonin biosynthesis in blind mole rats were studied compared toother model species (Spalax galili, Mus musculus, Heterocephalus glaber, Rattus norvegicus, and Homosapiens). As a result, while no variations were found in the Cry1 gene; only p.G7R variation was found inthe Per1 gene. The SNAP2 software had demonstrated that the human analogs of this variation harmfuleffects. It was suggested that more or full exon sites, more samples and genes should be studied to observemore variants in Nannospalax species. Thereby, the cancer resistance of blind mole rats may be explainedbetter by these variations and the functions of protein domains where these variants are located in.

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