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How does Foxj1 build smell-sensing cilia?

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In zebrafish and mice, Foxj1 is required for olfactory epithelium formation and OSN differentiation; mutants lose olfactory cilia programs and show diminished bile-acid odor responses.

Source

The forkhead transcription factor Foxj1 controls vertebrate olfactory cilia biogenesis and sensory neuron differentiation

Rayamajhi D, Ege M, Ukhanov K, et al. · PLoS biology · 2024

doi.org/10.1371/journal.pbio.3002468Read the full paper ↗28 citationscc by

What they did

Examined Foxj1 expression and loss-of-function phenotypes in zebrafish and mouse OSNs, including transcriptomic and odor-response readouts, and compared motility-gene repression across zebrafish, mouse, and human OSNs.

What they found

Foxj1, classically a motile-cilia factor, is expressed in OSNs and required for OE formation. Motility genes are repressed in OSNs across species. Foxj1 also controls OSN differentiation genes such as omp; foxj1 mutant zebrafish have significantly diminished bile-acid responses.

The limits

What it doesn't show

Animal genetics do not by themselves map all human anosmia syndromes to Foxj1; exact downstream circuitry beyond highlighted targets remains incompletely charted.

Key terms

Foxj1
Forkhead transcription factor classically programming motile cilia.
OSN
Olfactory sensory neuron detecting odors via cilia.
Olfactory cilia
Immotile cilia on OSN dendritic knobs housing receptors.
omp
Olfactory marker protein gene tied to odor-evoked transduction.
Anosmia
Loss of smell, often linked to ciliary dysfunction.

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Foxj1’s classic textbook role is in:

Common questions

Models?

Zebrafish and mice (plus human OSN expression comparisons).

Classic Foxj1 role?

Motile cilia biogenesis — here repurposed for immotile olfactory cilia.

Beyond cilia?

Also controls OSN differentiation genes such as omp.

Functional readout?

Reduced bile-acid odor responses in foxj1 mutant zebrafish.

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