Key result
Deleting Drosophila Zasp52 exon 15e causes flightlessness and structural muscle defects by disrupting thin filament stability.
The intrinsically disordered region of Zasp52 is required for maintaining thin filament stability at the Z-disc in Drosophila muscle.
Highlights IDR necessity for force-resistant Z-discs in flies; leaves open whether analogous regions stabilize vertebrate cardiac sarcomeres.
The Drosophila scaffolding protein Zasp52 is required to maintain structure at the muscle Z-disc which experiences strong forces during contraction. It is alternatively spliced into many isoforms, some of which contain a long intrinsically disordered region (IDR). We show that this region is primarily expressed in the indirect flight muscle (IFM) and is required for maintaining integrity of the Z-disc. Deleting the IDR-encoding exon 15e results in flightlessness and structural IFM defects, including sarcomere bending at the Z-disc and an inability to de-contract. These defects are indicative of a lack of proper thin filament anchoring to the Z-disc. This is further supported by a genetic interaction between exon 15e and actin. Fluorescence recovery after photobleaching of an isoform lacking exon 15e shows that the IDR is required for maintaining Zasp52 at the Z-disc and thereby stabilizing Z-discs. Lastly, we can rescue these phenotypes by restricting IFM use. Together, these results suggest that Zasp52’s IDR confers thin filament stability at the Z-disc of IFM.
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Ho et al. (2026) studied Drosophila muscle structure. Deletion of IDR-encoding exon 15e vs. Wild-type / Isoform with exon 15e was evaluated on Flightlessness and structural IFM defects. Deleting the IDR-encoding exon 15e of Zasp52 in Drosophila resulted in flightlessness and structural indirect flight muscle defects, indicating its requirement for thin filament stability.
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