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Enhancer-Driven OHC Targeting

NEW CELL TARGETING

Current cochlear gene therapies use ubiquitous promoters (CAG, CMV) that express in all cell types. The ARBITER workflow (Zhao et al. 2025) identified synthetic enhancers that drive expression exclusively in outer hair cells, with zero leakage into IHCs or vestibular cells.

The promoter problem

Ubiquitous promoter (CAG)
Expresses in OHCs, IHCs, and vestibular cells
Ectopic expression causes safety risks
Failed to restore hearing in Slc26a5-/- mice
B8 synthetic enhancer
OHC-specific: mimics native Slc26a5/prestin pattern
Zero expression in IHCs or vestibular cells
Fully restored hearing to wild-type levels

ARBITER: finding the right enhancer

ARBITER (AAV-Reporter-Based In vivo Transcriptional Enhancer Reconstruction) is a systematic workflow for identifying cell-type-specific enhancers. Starting from conserved non-coding elements (CNEs) near hearing loss genes, the pipeline tests reporter constructs in vivo, dissects critical modules, and reassembles them into optimized synthetic enhancers.

CNE screen
AAV-ie reporter
in vivo test
dissect elements
B8 synthetic enhancer

Key results (Slc26a5-/- rescue)

B8
Synthetic enhancer (reassembled from E1+E2 modules)
100%
ABR threshold restoration at 16 kHz (high dose)
0%
Ectopic expression (IHC/vestibular)

High-dose AAV-ie-B8-Slc26a5 (5e10 gc) restored prestin expression in OHCs to wild-type comparable levels, particularly in the apical cochlea.

ABR thresholds and wave 1 amplitudes/latencies at 16 kHz were completely rescued to wild-type levels.

Critically, no prestin mislocalization was observed in IHCs or vestibular hair cells, unlike the CAG promoter which caused ectopic expression in both.

Implications for STRC gene therapy

Stereocilin is an OHC-specific protein. Current STRC gene therapy research (Iranfar 2026) uses generic promoters. Applying the ARBITER workflow to find STRC-specific enhancers could improve targeting precision and potentially increase therapeutic expression levels.

The key question: do conserved non-coding elements near the STRC locus contain enhancer activity? Given that STRC (like Slc26a5) is OHC-specific, there is reason to expect dedicated regulatory elements exist.

Synergy with mini-STRC

A compact enhancer like B8 (~600 bp) combined with our recommended shorter mini-STRC (3,228 bp) fits comfortably within a single AAV vector: ~600 + 3,228 = 3,828 bp. This leaves 872 bp of headroom for UTRs, polyA, and optimized regulatory elements, enabling a single-vector, OHC-targeted STRC gene therapy.

Zhao et al. (2025) "Deciphering the enhancers of hearing loss genes enables targeted and effective gene therapy." Neuron.

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