According to the study's results, it may be particularly important in situations where sleep is critical, including recovering from illness, and its two-pronged activity demonstrates a link between sleep and immune function. Despite spending a large portion of our lives sleeping, why we sleep and the mechanisms underlying what makes us sleepy are largely unknown. Previous research has suggested that being awake promotes a buildup of sleep-promoting signals in the nervous system, cumulatively increasing our drive to fall asleep. This drive has also been found to increase during sickness. However, whether there is a relationship between being tired from a lack of sleep and being under the weather, remains unknown.
Hirofumi Toda and colleagues performed a genetic screen of over 12,000 Drosophila and found a single gene that constantly increased the amount of sleep when overexpressed. According to Toda et al., the nemuri (nur) gene, which encodes the sleep-promoting NUR peptide, is involved in the flies' innate homeostatic need for sleep. Overexpression of the gene created sleepier flies; by contrast, flies in which nur was mutated woke easily and had difficulty falling asleep. What's more, in addition to increasing sleep, nur was also shown to increase the ability of the flies to survive bacterial infection. The study revealed that the NUR peptide, secreted by neurons in the brain, serves a dual purpose - to promote sleep and kill bacteria. This suggests that NUR is relevant in driving sickness- or stress-induced sleep. Since sleep during illness promotes survival, the sleep promotion of NUR is likely closely linked to its immune function, according to the authors.