It seems likely that the next century will see the engineering of new humans to have genetic alterations that have been identified as wholly beneficial. It is a lot easier to edit the genomes in an embryo than it is to adjust all of the cells in an adult in the same way, due to the issues of delivery of suitable genetic medicine to all cells in all tissues. One interesting class of beneficial gene variants are those associated with what is known as natural short sleep, a phenomenon in which a rare few human lineages need very little sleep, as little as a few hours a night. More time spent awake in a lifetime is somewhat analogous to living for longer. So far ADRB1 variants and DEC2 variants have been identified. Here, researchers show that SIK3 is another gene in which variants can produce the need for very little sleep.
Sleep is an essential component of our daily life. A mutation in human salt induced kinase 3 (hSIK3), which is critical for regulating sleep duration and depth in rodents, is associated with natural short sleep (NSS), a condition characterized by reduced daily sleep duration in human subjects. This NSS hSIK3-N783Y mutation results in diminished kinase activity in vitro.
In a mouse model, the presence of the NSS hSIK3-N783Y mutation leads to a decrease in sleep time and an increase in electroencephalogram delta power. At the phosphoproteomic level, the SIK3-N783Y mutation induces substantial changes predominantly at synaptic sites. Bioinformatic analysis has identified several sleep-related kinase alterations triggered by the SIK3-N783Y mutation, including changes in protein kinase A and mitogen-activated protein kinase. These findings underscore the conserved function of SIK3 as a critical gene in human sleep regulation and provide insights into the kinase regulatory network governing sleep.
Link: https://doi.org/10.1073/pnas.2500356122
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