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Intellectual disability-causing mutations in KIF11 impair microtubule dynamics and dendritic arborization.

Jenna L Wingfield¹, Lukas Niese², Yosef Avchalumov³

¹Department of Neuroscience, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, FL, USA.

Nature Communications

|March 18, 2026

Summary

Microcephaly with intellectual disabilities (MCLID) is linked to KIF11 mutations. This study shows KIF11 regulates microtubule dynamics and neuronal growth, revealing key mechanisms behind MCLID.

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Area of Science:

Neuroscience
Cell Biology
Genetics

Background:

Microcephaly with intellectual disabilities (MCLID) is a rare genetic disorder.
Mutations in the KIF11 gene are implicated in MCLID.
The precise neuronal roles of KIF11 and the impact of MCLID mutations are not well understood.

Purpose of the Study:

To investigate the function of KIF11 in mature neurons.
To elucidate KIF11's mechanisms of microtubule (MT) regulation.
To determine how MCLID-associated mutations affect KIF11 function and neuronal development.

Main Methods:

Live-imaging of KIF11 function in postmitotic neurons.
Analysis of KIF11 mutations (KIF11^Y82F and KIF11^ΔCterm) in neurons.
Biochemical assays to assess KIF11's interaction with microtubules.
Temporal KIF11 inhibition using photo-controllable KIF11.

Main Results:

KIF11 depletion increases MT dynamics in axons and dendrites.
MCLID-associated KIF11 mutations reduce MT dynamics, impair dendritic arborization, and decrease mEPSC frequency.
KIF11^ΔCterm disrupts tetramer formation and MT crosslinking; KIF11^Y82F reduces MT sliding velocity and ATP affinity.
Temporal KIF11 inhibition enhances MT dynamics and dendritic growth.

Conclusions:

KIF11 acts as a rheostat controlling MT dynamics in mature neurons.
KIF11 is crucial for regulating dendritic arborization.
These findings provide insights into the molecular basis of MCLID.