PUBLICATION

Cross-species evidence for a developmental origin of adult hypersomnia with loss of synaptic adhesion molecules beat-Ia/CADM2

Authors
Mace, K., Zimmerman, A., Chesi, A., Doldur-Balli, F., Kim, H., Almeraya Del Valle, E., Rosa, J.B., Pack, A.I., Grant, S.F.A., Kayser, M.S.
ID
ZDB-PUB-260113-10
Date
2026
Source
Nature communications : (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Brain/metabolism
  • Cell Adhesion Molecules*/genetics
  • Cell Adhesion Molecules*/metabolism
  • Cell Adhesion Molecules, Neuronal*/genetics
  • Cell Adhesion Molecules, Neuronal*/metabolism
  • Connectome
  • Disorders of Excessive Somnolence*/genetics
  • Disorders of Excessive Somnolence*/metabolism
  • Drosophila Proteins*/genetics
  • Drosophila Proteins*/metabolism
  • Drosophila melanogaster/genetics
  • Female
  • Humans
  • Immunoglobulins*/genetics
  • Immunoglobulins*/metabolism
  • Male
  • Neurons/metabolism
  • Neuropeptides/genetics
  • Neuropeptides/metabolism
  • Sleep
  • Species Specificity
  • Synapses/metabolism
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
41526386 Full text @ Nat. Commun.
Abstract
Idiopathic hypersomnia (IH) is a poorly understood sleep disorder characterized by excessive daytime sleepiness despite normal nighttime sleep. Combining human genomics with behavioral and mechanistic studies in fish and flies, we uncover a role for beat-Ia/CADM2, synaptic adhesion molecules of the immunoglobulin superfamily, in excessive sleepiness. Neuronal knockdown of Drosophila beat-Ia results in sleepy flies and loss of the vertebrate ortholog of beat-Ia, CADM2, results in sleepy fish. We delineate a developmental function for beat-Ia in synaptic elaboration of neuropeptide F (NPF) neurites projecting to the suboesophageal zone (SEZ) of the fly brain. Brain connectome and experimental evidence demonstrate these NPF outputs synapse onto a subpopulation of SEZ GABAergic neurons to stabilize arousal. NPF is the Drosophila homolog of vertebrate neuropeptide Y (NPY), and an NPY receptor agonist restores sleep to normal levels in zebrafish lacking CADM2. These findings point towards NPY modulation as a treatment target for human hypersomnia.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping