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Related Concept Videos

Complementation Tests00:49

Complementation Tests

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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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Complement contributes to hyperactive behavior in the 16p11.2 hemideletion mouse model.

Benjamin A Kelvington1, Jaekyoon Kim2, Regan Fair3

  • 1Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, United States; Iowa Neuroscience Institute, University of Iowa, United States; Pharmacology Graduate Program, Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, United States.

Brain, Behavior, and Immunity
|March 25, 2026
PubMed
Summary
This summary is machine-generated.

The complement system, particularly C3a receptor (C3aR), is upregulated in a mouse model of 16p11.2 deletion, a common cause of neurodevelopmental disorders. Inhibiting C3aR reduced hyperactivity, suggesting complement system modulation as a potential ADHD treatment.

Keywords:
16p11.2ComplementHyperactivityInflammationInterferonMicrogliaNeurodevelopmental disordersStriatum

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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • The complement system is crucial for innate immunity and immune surveillance.
  • Emerging evidence links complement system dysregulation to neurodevelopmental disorders (NDDs).
  • Mechanisms connecting complement to NDDs, like 16p11.2 hemideletion, are not fully understood.

Purpose of the Study:

  • Investigate the role of the complement system in the 16p11.2 deletion mouse model.
  • Determine if complement C3a receptor (C3aR) signaling contributes to NDD-related behaviors.
  • Explore potential therapeutic strategies targeting the complement system for NDDs.

Main Methods:

  • Analyzed gene and protein expression in the striatum of 16p11.2 deletion mice.
  • Utilized pharmacological inhibition of C3aR to assess behavioral changes.
  • Examined microglial morphology and gene expression, including interferon-stimulated genes.

Main Results:

  • Complement components, including C3aR, and cytokines were upregulated in the 16p11.2 deletion mouse striatum.
  • Pharmacological C3aR inhibition significantly reduced hyperactivity in these mice.
  • C3aR inhibition decreased elevated interferon-stimulated gene expression and normalized microglial responses.

Conclusions:

  • Upregulated complement system activity, specifically C3aR signaling, exacerbates hyperactive behavior in 16p11.2 deletion mice.
  • These findings highlight a link between complement, interferon signaling, and microglial activation in NDDs.
  • Targeting the complement system, particularly C3aR, may offer a therapeutic avenue for NDD symptoms associated with 16p11.2 hemideletion, including ADHD.