Investigation of Clock Gene Variations in Nannospalax Cytotypes

Abstract

Blind mole rats (Nannospalax) are subterranean mammals noted for their longevity and cancer resistance. It is known that these animals' vestigial eyes, particularly the Harder gland around the eyes, may generate considerable amounts of melatonin. Furthermore, the melatonin production mechanism in the circadian rhythm cycle of blind mole rats is regarded to be different from that of other living beings. The melatonin and Clock genes are hypothesized to be linked to the formation, development, and spread of cancer, 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 of blind mole rats, which have been shown in the literature to be cancer-resistant, may differ from that of other living species due to the difference in their amino acid variations. Differences in the DNA of the Clock genes (Cry1 and Per1) involved in melatonin biosynthesis in blind mole rats were studied compared to other model species (Spalax galili, Mus musculus, Heterocephalus glaber, Rattus norvegicus, and Homo sapiens). As a result, while no variations were found in the Cry1 gene; only p.G7R variation was found in the Per1 gene. The SNAP2 software had demonstrated that the human analogs of this variation harmful effects. It was suggested that more or full exon sites, more samples and genes should be studied to observe more variants in Nannospalax species. Thereby, the cancer resistance of blind mole rats may be explained better by these variations and the functions of protein domains where these variants are located in.