dc.contributor.advisor | Bringmann, Henrik Dr. | |
dc.contributor.author | Koutsoumparis, Anastasios | |
dc.date.accessioned | 2020-11-24T16:30:35Z | |
dc.date.available | 2021-11-07T00:50:10Z | |
dc.date.issued | 2020-11-24 | |
dc.identifier.uri | http://hdl.handle.net/21.11130/00-1735-0000-0005-14FA-B | |
dc.identifier.uri | http://dx.doi.org/10.53846/goediss-8314 | |
dc.identifier.uri | http://dx.doi.org/10.53846/goediss-8314 | |
dc.language.iso | eng | de |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | |
dc.subject.ddc | 570 | de |
dc.title | An omics analysis of genetic sleep loss in C. elegans | de |
dc.type | doctoralThesis | de |
dc.contributor.referee | Heinrich, Ralf Prof. Dr. | |
dc.date.examination | 2020-11-09 | |
dc.description.abstracteng | Sleep is a state of consciousness that has persisted through evolution and has become a necessity
for animal welfare. In humans sleep loss has been shown to be inextricably intertwined with
poor health. The prevalence of sleep defects in elderly people not only associates sleep quality
with aging, but also draws attention to an underrated problem that will continue to affect the
life quality of the increasingly aging population of the western world.
Sleep regulates energy metabolism and higher brain functions. Little is known about the precise
molecular mechanisms that control and are controlled by sleep, even though it has been
extensively studied, due to its complex nature. In this thesis, I used the nematode C. elegans,
which is a simple, yet complex enough model organism in order to discover the downstream
processes that are regulated by sleep.
Although sleep is connected to development in C. elegans, I used sleep loss in L1 arrested
worms, as a model that couples sleep, metabolism and aging phenotypes. This is more relevant
to mammal physiology than developmental sleep. By genetically ablating the sleep-active
neuron RIS and recruiting powerful omics techniques, I was able to identify those components
of C. elegans physiology that are affected by sleep loss. I complemented the omics experiments
with extensive genetic screening for sleep alterations in animals with defects in metabolic
pathways, lifespan, egg-laying and other assays.
I was able to discover that sleep loss causes tissue-specific changes, reduces body size and
increases the basal metabolic rate. Furthermore, I discovered that sleep loss upregulates the
unfolded protein response in the endoplasmic reticulum by upregulating relevant transcription
factors. Finally, I discovered that sleep loss causes oxidative stress and I characterized
components of the life-prolonging antioxidant pathways that are directly regulated by the sleepactive neuron RIS. | de |
dc.contributor.coReferee | Urlaub, Henning Prof. Dr. | |
dc.subject.eng | C. elegans | de |
dc.subject.eng | Sleep | de |
dc.identifier.urn | urn:nbn:de:gbv:7-21.11130/00-1735-0000-0005-14FA-B-5 | |
dc.affiliation.institute | Göttinger Graduiertenschule für Neurowissenschaften, Biophysik und molekulare Biowissenschaften (GGNB) | de |
dc.subject.gokfull | Biologie (PPN619462639) | de |
dc.description.embargoed | 2021-11-07 | |
dc.identifier.ppn | 1740978773 | |