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Related Experiment Video

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Chemogenetic Regulation in Reprogrammed Stem Cell-derived Precursor Cells in Treating Neurodegenerative Diseases
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The Complement Regulator Susd4 Influences Nervous-System Function and Neuronal Morphology in Mice.

Hongling Zhu1, Laura E Meissner2, Colleen Byrnes1

  • 1Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892, USA.

Iscience
|March 18, 2020
PubMed
Summary

Sushi domain-containing protein 4 (SUSD4) deletion causes neurological defects in mice, including motor and anxiety impairments. This suggests SUSD4 is vital for nervous system function, potentially through complement inhibition.

Keywords:
Behavioral NeuroscienceCellular NeuroscienceComponents of the Immune SystemNeuroscience

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Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Sushi domain-containing protein 4 (SUSD4) is a complement inhibitor.
  • SUSD4 deletion is linked to 1q41q42 microdeletion syndrome, causing neurodevelopmental issues.
  • The precise role of SUSD4 in the mammalian nervous system remains unclear.

Purpose of the Study:

  • To investigate the function of SUSD4 in the mammalian nervous system.
  • To determine the impact of SUSD4 deficiency on neuronal structure and behavior.

Main Methods:

  • Analysis of Susd4 knockout (KO) mice.
  • Assessment of motor performance and anxiety-like behaviors.
  • Histological examination of cerebellar and hippocampal neuronal morphology.
  • Analysis of Susd4 mRNA and C1q protein expression in the brain.

Main Results:

  • Susd4 KO mice displayed significant motor deficits and increased anxiety-like behaviors.
  • Cerebellar basket cells were abnormal, and hippocampal dendritic spine density was reduced in KO mice.
  • Susd4 mRNA was detected in neurons and oligodendrocyte lineage cells.
  • Increased C1q protein levels were observed in the brains of Susd4 KO mice.

Conclusions:

  • SUSD4 plays a crucial role in mammalian nervous system function.
  • SUSD4 may regulate neuronal integrity and behavior through the complement pathway.
  • SUSD4 deficiency could contribute to the neurological abnormalities seen in 1q41q42 microdeletion syndrome.