Rebound sleep in Drosophila melanogaster
Lead Research Organisation:
Imperial College London
Department Name: Life Sciences
Abstract
Sleep is a highly conserved process throughout the animal kingdom; for both vertebrates and
invertebrates, sleep has an important function. Creatures take a risk by sleeping, as during this state
they are unable to protect themselves from the external environment. This suggests that sleep
confers a vital benefit that outweighs the risk. Why is this? What happens when we sleep that has
caused us to, throughout evolution, negate the risks? A universally accepted sleep theory is that it is
regulated through circadian and homeostatic mechanisms (Borbély et al., 1982). However, the
underlying biological functions of these mechanisms are still relatively unknown. Sleep rebound is an
important part of the homeostatic regulation of sleep, which proposes that a period of sleep
deprivation (SD) creates a sleep debt that must be repaid via a period of sleep post-deprivation.
Although this rebound is known to be an important consolidation process for the loss of sleep, the
environment can be seen to have some impact on whether rebound occurs, and therefore also on the
homeostatic process. For example, recent studies in Drosophila melanogaster showed that when SD
is due to sexual arousal, rebound sleep does not occur (Beckwith et al., 2017). This highlights
animals' abilities to overcome the requirement of sleep based on external stimuli.
Drosophila melanogaster has been commonly used in genetic studies over the past decades and is a
useful tool for studying highly conserved neurological processes. Fruit flies have a short generation
time of 10 days and a relatively small genome which can be easily manipulated. Genetic mutations
frequently have a strong phenotype, allowing researchers to investigate the genetic factors that
underpin behaviours.
Over the course of my research project, I will be using this model organism to study sleep rebound
using the bioinformatic hardware and software developed within the Gilestro Lab (Geissman et al.,
2017). I will be looking at the different environmental factors which can impact sleep rebound with
the aim that this work will shed light on how the phenomenon works but also on the homeostatic
regulation of sleep. This behavioural phenomenon will be modelled biologically and computationally.
References
Beckwith, E.J et al. (2017) Regulation of sleep homeostasis by sexual arousal, Elife. 6
Borbély et al. (1983) A two process model of sleep regulation, Human Neurobiology. 1(3)
Geissmann, Q et al. (2017) Ethoscopes: An open platform for high-throughput ethomics, PLoS
Biology. 15(10): e2003026
invertebrates, sleep has an important function. Creatures take a risk by sleeping, as during this state
they are unable to protect themselves from the external environment. This suggests that sleep
confers a vital benefit that outweighs the risk. Why is this? What happens when we sleep that has
caused us to, throughout evolution, negate the risks? A universally accepted sleep theory is that it is
regulated through circadian and homeostatic mechanisms (Borbély et al., 1982). However, the
underlying biological functions of these mechanisms are still relatively unknown. Sleep rebound is an
important part of the homeostatic regulation of sleep, which proposes that a period of sleep
deprivation (SD) creates a sleep debt that must be repaid via a period of sleep post-deprivation.
Although this rebound is known to be an important consolidation process for the loss of sleep, the
environment can be seen to have some impact on whether rebound occurs, and therefore also on the
homeostatic process. For example, recent studies in Drosophila melanogaster showed that when SD
is due to sexual arousal, rebound sleep does not occur (Beckwith et al., 2017). This highlights
animals' abilities to overcome the requirement of sleep based on external stimuli.
Drosophila melanogaster has been commonly used in genetic studies over the past decades and is a
useful tool for studying highly conserved neurological processes. Fruit flies have a short generation
time of 10 days and a relatively small genome which can be easily manipulated. Genetic mutations
frequently have a strong phenotype, allowing researchers to investigate the genetic factors that
underpin behaviours.
Over the course of my research project, I will be using this model organism to study sleep rebound
using the bioinformatic hardware and software developed within the Gilestro Lab (Geissman et al.,
2017). I will be looking at the different environmental factors which can impact sleep rebound with
the aim that this work will shed light on how the phenomenon works but also on the homeostatic
regulation of sleep. This behavioural phenomenon will be modelled biologically and computationally.
References
Beckwith, E.J et al. (2017) Regulation of sleep homeostasis by sexual arousal, Elife. 6
Borbély et al. (1983) A two process model of sleep regulation, Human Neurobiology. 1(3)
Geissmann, Q et al. (2017) Ethoscopes: An open platform for high-throughput ethomics, PLoS
Biology. 15(10): e2003026
Organisations
People |
ORCID iD |
| Michaela Joyce (Student) |
Studentship Projects
| Project Reference | Relationship | Related To | Start | End | Student Name |
|---|---|---|---|---|---|
| EP/R513052/1 | 30/09/2018 | 29/09/2023 | |||
| 2133211 | Studentship | EP/R513052/1 | 28/09/2018 | 29/09/2022 | Michaela Joyce |
| NE/W503198/1 | 31/03/2021 | 30/03/2022 | |||
| 2133211 | Studentship | NE/W503198/1 | 28/09/2018 | 29/09/2022 | Michaela Joyce |