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Related Experiment Video

Updated: Jun 2, 2026

Using Primary Neurosphere Cultures to Study Primary Cilia

Using Primary Neurosphere Cultures to Study Primary Cilia

Published on: April 14, 2017

Primary cilia control telencephalic patterning and morphogenesis via Gli3 proteolytic processing.

Laurianne Besse¹, Mariame Neti, Isabelle Anselme

¹CNRS UMR 7622, 9 Quai Saint Bernard, Boîte 24, F-75005, Paris, France.

Development (Cambridge, England)

|April 15, 2011

Summary

This summary is machine-generated.

Primary cilia are crucial for brain development. This study shows they control olfactory bulb formation by regulating Gli3 protein processing, offering insights into ciliopathies.

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Artificial Intelligence Approaches to Assessing Primary Cilia

Artificial Intelligence Approaches to Assessing Primary Cilia

Published on: May 1, 2021

Area of Science:

Developmental biology
Cell biology
Neuroscience

Background:

Primary cilia are vital for vertebrate development and signaling.
Cilia's role in brain morphogenesis and ciliopathies is poorly understood.

Purpose of the Study:

Investigate the function of primary cilia in telencephalic morphogenesis using a mouse model.
Determine the underlying mechanisms of olfactory bulb defects in ciliopathy.

Main Methods:

Analysis of a mouse mutant for the ciliopathy gene Ftm (Rpgrip1l).
Assessment of primary cilia presence and telencephalic patterning in mutant embryos.
Genetic rescue experiments using Gli3 mutant alleles.

Main Results:

Ftm(-/-) fetuses exhibit ectopic and underdeveloped olfactory bulbs.
Ftm(-/-) neuroepithelial cells lack primary cilia and show altered telencephalic patterning (subpallium expansion).
Genetic rescue with a Gli3 short-form allele restored telencephalic patterning and olfactory bulb development.

Conclusions:

Primary cilia are essential for olfactory bulb morphogenesis, acting via Gli3 processing.
This study demonstrates in vivo that primary cilia control development by producing the Gli3 repressor form.
Findings illuminate the origins of olfactory bulb agenesis and brain defects in human ciliopathies.