New research explores role of sleep in protein repair
In a culture of over-extended students and ever-expanding to-do lists, it is no wonder that a full night’s rest has no place among the end-of-semester priorities. Still, new research exploring the role of rest in protein repair might encourage students to abandon cold cubicles and oversized coffees once-and-for-all.
Of course, the decision to forego sleep is not unfounded. Forbes magazine, faithful watchdogs for the up-and-coming, suggest the leaders of today have already boasted a full day’s activities before 8 a.m. Guelph’s own former President Summerlee was rumored to have required merely a few hours of sleep each night, not unlike the cohort of successful musicians, politicians, and artists who lay claim to similar, unconventional sleep habits. And of course, who can forget that wise bit about the early bird and his coveted worm.
Still, though science has previously struggled to identify the role for sleep, recent research has outlined a pertinent role for restful moments in repairing and replacing damaged proteins.
In particular, researchers have focused on the ability stressful and damaging environments on activating a sleep-like state in C. elegans, which in turn is connected with signals for protein repair.
It was found that intense heat, and the associated cellular damage, activated the ALA neuron, a nerve cell responsible for relaying sensory and mechanical information within a particular area of the brain. In response to the heat damage, the activated ALA neuron releases signaling proteins, FLP-13-encoded-neuropeptides. Together, this signaling cascade initiates a sleep-state in the C. elegan, characterized by both decreased locomotion and feeding.
In addition to heat stress, other environmental stressors causing cellular damage, such as severe cold and toxin exposure, activated the ALA neuron, and promoted the sleep-state suggesting a role for this restful phase in facilitating cellular recovery from stress.
Following heat stress, cells are capable of clearing damaged proteins using heat-shock proteins. Researchers found that the ability to induce sleep following stress and cellular damage promoted recovery by heat-shock proteins. When the ALA neuron was mutated, and the sleep state could not be entered, heat-shock proteins remained active longer, suggesting a more robust cleanup effort. Similarly, when restful states were entered more frequently, the heat-shock protein response was quicker, suggesting a more efficient clean up of damaged proteins under sleep-like conditions.
While further research is needed to tease apart the roles of sleep in maintaining health and wellbeing, the researchers are optimistic that the role of rest in protein repair is only the beginning of a larger understanding of the benefits of sleep.