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Related Concept Videos

Complementation Tests00:49

Complementation Tests

4.9K
A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
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Related Experiment Video

Updated: May 6, 2026

Author Spotlight: A Battery of Highly Reproducible Behavioral Tests to Validate an Angelman Syndrome Murine Model
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Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.

Benjamin A Kelvington1,2,3, Jaekyoon Kim1,2, Regan Fair1,2,4

  • 1Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa.

Biorxiv : the Preprint Server for Biology
|September 2, 2025
PubMed
Summary
This summary is machine-generated.

Elevated complement component 3 (C3) in the brain is linked to neurodevelopmental disorders (NDDs). Inhibiting the C3a receptor reduced hyperactivity in mouse models, suggesting complement system modulation for NDD treatment.

Keywords:
16p11.2complementhyperactivityinflammationmicroglianeurodevelopmental disordersstriatum

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Area of Science:

  • Neuroimmunology
  • Developmental Neuroscience

Background:

  • The complement system is crucial for innate immunity and immune surveillance.
  • Emerging evidence highlights its role in brain development and its dysregulation in neurodevelopmental disorders (NDDs).
  • Mechanisms linking complement to NDDs are not fully understood.

Purpose of the Study:

  • To investigate the role of the complement system, specifically complement component 3 (C3), in a mouse model of 16p11.2 deletion syndrome, a common genetic cause of NDDs.
  • To explore the therapeutic potential of targeting the complement system for NDD-related behavioral changes.

Main Methods:

  • Utilized a mouse model of 16p11.2 hemideletion (16p11.2 del).
  • Assessed C3 expression in the striatum.
  • Administered pharmacological inhibitors of the C3a receptor.
  • Analyzed the striatal cytokine environment.

Main Results:

  • C3 expression was upregulated in the striatum of 16p11.2 del mice.
  • Pharmacological inhibition of the C3a receptor significantly alleviated hyperactivity in these mice.
  • Several inflammatory factors were upregulated in the striatum of 16p11.2 del mice, indicating a pro-inflammatory state.

Conclusions:

  • Increased complement system activity, particularly C3, contributes to hyperactive behavior in the 16p11.2 del mouse model.
  • A pro-inflammatory environment in the striatum is associated with elevated complement.
  • Inhibiting the overactive complement system may be a viable strategy to treat NDD symptoms, including those linked to ADHD.