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Flickinger, Z.

Publications and source records attributed to Flickinger, Z..

2 recordsLinked to original sources

Muller glia mediated regeneration restores neuronal diversity and retinal circuit organization in the adult zebrafish

The ability to regenerate neurons with appropriate identities and circuit connectivity is a fundamental challenge in regenerative biology. Unlike mammals, adult zebrafish robustly regenerate retinal neurons after injury through the reprogramming of Muller glia. However, the extent to which regenerated neurons faithfully reconstruct molecular identity, cellular diversity, and circuit organization remains unclear. Here, we combined inducible lineage tracing, single-cell RNA sequencing and high-resolution morphological analysis to define the molecular identities and structural organization of regenerated neurons following photoreceptor-selective light lesion or NMDA-induced inner retinal injury. Both injury paradigms regenerated all major retinal cell classes, although the relative abundance of regenerated cell types reflected the pattern of neuronal loss. Across major neuronal classes and subtypes, regenerated neurons largely reestablished endogenous molecular identities, with the residual transcriptional differences primarily reflecting ongoing maturation. Regenerated amacrine and bipolar neurons recovered subtype diversity, characteristic dendritic morphologies, and laminar organization. Regenerated retinal ganglion cells likewise restored broad molecular diversity and appropriate retinotectal projections, while a subset underwent microglia-mediated refinement. Together, these findings demonstrate that Muller glia-mediated regeneration largely reconstructs neuronal identity, cellular diversity and key features of retinal circuit organization, providing insights into understanding how complex neuronal tissues are rebuilt after injury.

neuroscience↗

AAV-mediated regeneration of neurons in injury-induced and inherited retinal degeneration

Loss of retinal neurons is a leading cause of irreversible vision impairment, yet adult mammalian retinas lack the ability to regenerate these cells. In this study, we developed an adeno-associated virus (AAV)-based strategy to reprogram endogenous Muller glia into retinal neurons. Using stringent genetic lineage tracing, immunohistochemistry, electrophysiology and single-cell multiomic profiling, we show that AAV delivery of a stabilized, phospho-insensitive Neurogenin2 variant (Neurog2-9SA) efficiently converts Muller glia into multiple types of retinal neurons, including bipolar, starburst amacrine, and a small population of photoreceptor-like cells, in both injury-induced and inherited retinal degeneration models. The generated neurons exhibit electrical properties of retinal neurons, light-evoked responses and integrate into existing retinal circuitry. Single-cell multiomics analysis reveal that Neurog2-9SA induces reprogramming by remodeling chromatin accessibility, activating neurogenic transcriptional networks, and represses glial identity programs. Inhibiting Notch signaling markedly enhances reprogramming efficiency. Together, these findings establish Neurog2-9SA as a potent and clinically relevant factor for AAV-mediated reprogramming and provide a foundation for approaches to regenerate neuronal cells and restore function in retinal diseases.

neuroscience↗