| dc.description.abstracteng | Abstract: Sleep is vital for living organisms. Disruption of sleep is a hallmark of natural
aging. A growing body of evidence suggests that sleep serves roles in nervous
system-specific functions as well as general cell physiological functions related
to aging. However, the molecular mechanisms underlying the connection
between sleep and aging are still poorly understood.
In this study, I have focused on starvation-induced sleep in larval C. elegans, and
aimed to figure out the sleep functions and the mechanism that connect sleep,
starvation, survival, and aging. First, I found that the sleep-promoting neuron RIS
is activated by starvation through sirtuin signaling and PTEN by further
activating the longevity regulators AMP kinase and FoxO, respectively. Next, I
discovered that the potential functions of sleep are involved in several
fundamental physiological mechanisms such as proteostasis, apoptotic cell death,
and autophagy as well as the aging process in starved larval C. elegans. Lastly, I
identified a novel protective anti-aging mechanism of sleep in arrested L1 larval
worms, which interacts with the mitochondrial respiratory chain, TOR signaling
and the unfolded protein response in regulating survival and aging during food
deprivation.
The discoveries in this study suggest that sleep is required to ensure the survival
by counteracting aging processes of larval C. elegans during prolonged
starvation, and sleep acts as a predictor for the longevity of the starvation-induced
developmental arrest. As a fundamental process, sleep presents a
beneficial strategy to protect living organisms against aging and starvation in the
larval period. These findings indicate that the functions of sleep have been
selected for early in evolution and might be conserved in humans. | de |