Follistatin regulates the specification of the apical cochlea responsible for low-frequency hearing in mammals.
Level 5 - mechanism / opinion, no new human data
Preclinical animal genetic and developmental study
PubMed 36577057 · doi:10.1073/pnas.2213099120
What was done
Using mouse genetics and in vivo fate-mapping analysis in embryonic mice, researchers investigated the developmental roles of follistatin (FST) and sonic hedgehog (SHH) signaling in establishing cochlear regional identity and tonotopy.
What was found
The abstract reports no numerical data or effect sizes. Qualitatively, follistatin (FST) was found to be required for the maintenance of apical cochlear identity and apical cell expansion, but dispensable for initial induction. SHH was required for both induction and maintenance. Loss of either FST or SHH caused a shortened cochlea lacking the apical domain, loss of apex-specific molecular and anatomical features, and low-frequency hearing loss.
Why it matters
This work identifies FST as an essential developmental regulator of apical cochlear domain formation, establishing how early regional patterning underpins low-frequency hearing in mammals.
Limits
Animal study with no direct human data. The abstract provides no sample sizes, numerical auditory thresholds, or statistical values.
Cited by
- supports In the cochlea, high frequencies are tonotopically encoded at the base near the middle ear, whereas low frequencies are encoded at the apex.