Normal sleep requires the astrocyte brain-type fatty acid binding protein FABP7

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Abstract

The astrocyte brain-type fatty acid binding protein FABP7 regulates sleep consolidation across phylogeny.

Abstract

Sleep is found widely in the animal kingdom. Despite this, few conserved molecular pathways that govern sleep across phyla have been described. The mammalian brain-type fatty acid binding protein (Fabp7) is expressed in astrocytes, and its mRNA oscillates in tandem with the sleep-wake cycle. However, the role of FABP7 in regulating sleep remains poorly understood. We found that the missense mutation FABP7.T61M is associated with fragmented sleep in humans. This phenotype was recapitulated in mice and fruitflies bearing similar mutations: Fabp7-deficient mice and transgenic flies that express the FABP7.T61M missense mutation in astrocytes also show fragmented sleep. These results provide novel evidence for a distinct molecular pathway linking lipid-signaling cascades within astrocytes in sleep regulation among phylogenetically disparate species.

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Most cited references 26

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A SELF-RATING DEPRESSION SCALE.

W W Zung (1965)

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The homeostatic regulation of sleep need is under genetic control.

Paul Franken, Didier Chollet, Mehdi Tafti (2001)

Delta power, a measure of EEG activity in the 1-4 Hz range, in slow-wave sleep (SWS) is in a quantitative and predictive relationship with prior wakefulness. Thus, sleep loss evokes a proportional increase in delta power, and excess sleep a decrease. Therefore, delta power is thought to reflect SWS need and its underlying homeostatically regulated recovery process. The neurophysiological substrate of this process is unknown and forward genetics might help elucidate the nature of what is depleted during wakefulness and recovered during SWS. We applied a mathematical method that quantifies the relationship between the sleep-wake distribution and delta power to sleep data of six inbred mouse strains. The results demonstrated that the rate at which SWS need accumulated varied greatly with genotype. This conclusion was confirmed in a "dose-response" study of sleep loss and changes in delta power; delta power strongly depended on both the duration of prior wakefulness and genotype. We followed the segregation of the rebound of delta power after sleep deprivation in 25 BXD recombinant inbred strains by quantitative trait loci (QTL) analysis. One "significant" QTL was identified on chromosome 13 that accounted for 49% of the genetic variance in this trait. Interestingly, the rate at which SWS need decreases did not vary with genotype in any of the 31 inbred strains studied. These results demonstrate, for the first time, that the increase of SWS need is under a strong genetic control, and they provide a basis for identifying genes underlying SWS homeostasis.

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The emerging functions and mechanisms of mammalian fatty acid-binding proteins.

Judith Storch, Betina Córsico (2008)

Fatty acid-binding proteins (FABPs) are abundant intracellular proteins that bind long-chain fatty acids with high affinity. Nine separate mammalian FABPs have been identified, and their tertiary structures are highly conserved. The FABPs have unique tissue-specific distributions that have long suggested functional differences among them. In the last decade, considerable progress has been made in understanding the specific functions of the FABPs and, in some cases, their mechanisms of action at the molecular level. The FABPs appear to be involved in the extranuclear compartments of the cell by trafficking their ligands within the cytosol via interactions with organelle membranes and specific proteins. Several members of the FABP family have been shown to function directly in the regulation of cognate nuclear transcription factor activity via ligand-dependent translocation to the nucleus. This review will focus on these emerging functions and mechanisms of the FABPs, highlighting the unique functional properties of each as well as the similarities among them.

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Author and article information

Journal

Journal ID (nlm-ta): Sci Adv

Journal ID (iso-abbrev): Sci Adv

Journal ID (publisher-id): SciAdv

Journal ID (hwp): advances

Title: Science Advances

Publisher: American Association for the Advancement of Science

ISSN (Electronic): 2375-2548

Publication date Collection: April 2017

Publication date (Electronic): 05 April 2017

Volume: 3

Issue: 4

Electronic Location Identifier: e1602663

Affiliations

[1 ]Department of Biomedical Sciences, Elson S. Floyd College of Medicine, Washington State University, Spokane, WA 99202, USA.

[2 ]Sleep and Performance Research Center, Washington State University, Spokane, WA 99210, USA.

[3 ]Center for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

[4 ]Neuroscience Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

[5 ]RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan.

[6 ]Department of Sleep and Behavioral Sciences, Shiga University of Medical Science, Otsu City, Shiga 520-2192, Japan.

[7 ]Department of Organ Anatomy, Tohoku University Graduate School of Medicine, Sendai, Miyagi 980-8575, Japan.

[8 ]Department of Genetics, University of Wisconsin-Madison, Madison, WI 53706, USA.

Author notes

[* ]Corresponding author. Email: j.gerstner@ 123456wsu.edu

[†]

These authors contributed equally to this work.

Author information

Isaac J. Perron http://orcid.org/0000-0002-2080-6189

Hiroshi Kadotani http://orcid.org/0000-0001-7474-3315

Hans P. A. Van Dongen http://orcid.org/0000-0002-4678-2971

Raymond J. Galante http://orcid.org/0000-0001-7731-8648

Article

Publisher ID: 1602663

DOI: 10.1126/sciadv.1602663

PMC ID: 5381954

PubMed ID: 28435883

SO-VID: 7b9e60fe-d898-45f3-86c0-1fd0c5760701

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited.

History

Date received : 31 October 2016

Date accepted : 10 February 2017

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001700, Ministry of Education, Culture, Sports, Science, and Technology;

Award ID: ID0EVWAG13355

Award ID: MEXT KAKENHI 221S0002

Award Recipient : Hiroshi Kadotani

Funded by: FundRef http://dx.doi.org/10.13039/100000050, National Heart, Lung, and Blood Institute;

Award ID: ID0EU3AG13356

Award ID: HL007713

Award Recipient : Allan Pack

Funded by: FundRef http://dx.doi.org/10.13039/100000050, National Heart, Lung, and Blood Institute;

Award ID: ID0EE5AG13357

Award ID: HL111725

Award Recipient : Allan Pack

Funded by: FundRef http://dx.doi.org/10.13039/100000006, Office of Naval Research;

Award ID: ID0EU6AG13358

Award ID: N00014-13-1-0302

Award Recipient : Hans Van Dongen

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Copyeditor Ken Marvin Ortega

Keywords: sleep,gene,evolution,astrocyte,glia,sleep fragmentation,blbp,b-fabp,missense,polymorphism

Data availability:

Keywords: sleep, gene, evolution, astrocyte, glia, sleep fragmentation, blbp, b-fabp, missense, polymorphism

Normal sleep requires the astrocyte brain-type fatty acid binding protein FABP7

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Most cited references 26

A SELF-RATING DEPRESSION SCALE.

The homeostatic regulation of sleep need is under genetic control.

The emerging functions and mechanisms of mammalian fatty acid-binding proteins.

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