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Ift43 Controls the Ciliary Levels of Gli2 and Gli3
Biorxiv : the Preprint Server for Biology
|February 6, 2026
Summary
The study reveals that Ift43 is crucial for Hedgehog signaling, linking cilia assembly to Gli protein regulation. Its absence causes developmental defects and disrupts the balance of Gli activator and repressor forms.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Intraflagellar transport (IFT) is essential for cilia function and Hedgehog signaling.
- The IFT-A complex is involved in IFT, but the Ift43 subunit is poorly understood.
- Ift43's absence in some species suggests specialized roles beyond core ciliogenesis.
Purpose of the Study:
- To investigate the function of the IFT-A subunit, Ift43, in mammalian development and Hedgehog signaling.
- To determine the role of Ift43 in cilia assembly and the regulation of Gli transcription factors.
Main Methods:
- Generation and analysis of Ift43-deficient mice.
- Assessment of embryonic lethality and developmental defects.
- Cellular analysis of cilia structure and Hedgehog pathway activity, including Gli protein localization and processing.
Main Results:
- Loss of Ift43 leads to mid-gestation lethality with severe craniofacial and developmental abnormalities.
- Ift43 deficiency impairs cilia formation and length, and blocks Gli1 induction.
- Mutants exhibit abnormal Gli2 and Gli3 accumulation at ciliary tips and altered repressor form generation.
- Ift43 regulates Gli2 cleavage, impacting the balance of Gli activator and repressor forms.
Conclusions:
- Ift43 is a critical IFT-A component essential for mammalian development.
- Ift43 plays a dual role in linking cilia assembly to Hedgehog signal transduction.
- Ift43 regulates Gli processing, influencing the balance of Gli activator/repressor forms in Hedgehog signaling.
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