Reprogramming lineage-traced Müller glia for robust proliferation and neurogenesis in adult mammalian retinas: Cell Reports https://t.co/Eqwz4mrVWO
Once again, we would like to share this exciting finding. “Two-step strategy” to reprogram Muller glia in adult mouse retina.
Last, microglia and neurotoxicity injury modulate the proliferative and neurogenic capacities of FAR-treated MG. This approach provides a two-step strategy for inducing MG-derived neurogenesis, which may represent a potent avenue toward retinal regeneration.
AAV-mediated one-step glia-to-neuron conversions have been challenged by rigorous lineage-tracing.
Here, we demonstrate a two-step strategy that reprograms lineage-traced Muller glia for robust proliferation and neurogenesis in adult mouse retinas.
https://t.co/QLz1qXaoO2
We are excited to announce that a majority of Senior Researchers at Mount Sinai have signed authorization cards in support of forming our union, Researchers Organizing Committee at Sinai-UAW!
The RReSTORe Consortium has published a White Paper comprehensively describing the questions and challenges that need to be addressed to develop translational therapies capable of restoring vision for patients with optic neuropathy. https://t.co/6jZQe1quvF
Whether the controversial reprogramming factor Neurod1 alone is sufficient to efficiently convert resident muller glia or astrocytes into functional neurons? Our newly developed AAV systems with high glia-specificity indicate the answer is No! https://t.co/ZWdGd0lONt
@theawely Hi, we tested Neurog2 in this study in mouse retina, a single factor Neurog2 is insufficient to trigger muller glia-to-neuron conversion. As we have more expertise on muller glia than astrocytes, we then currently have no plan testing this gene in astrocytes.
Interested in single cell genomics but need help getting started? Check out the full agenda for our Single Cell Genomics Day next Friday (4/7). All talks will be live-streamed (no registration required) at https://t.co/mkkGb2p91d
We also interestingly find that lowering viral titers cannot eliminate the leakage but significantly reduce the transduction efficiency. Using different AAV serotypes, injection routes and regions could also alter the patterns and levels of neuronal leakage.
The second strategy is using AAV-FLEX constructs combined with lineage tracing techniques, such as Glast-CreERT;Sun1-GFP muller glia cells in retina, to restrict the expression of transgene, i.e., Neurod1-P2A, Math5-P2A-mCherry, in resident glia cells.
By developing two new AAV systems with high-glia specificity, we find Neurod1 alone is insufficient to convert muller glia cells into retinal neurons. The first strategy is to positioning the reporter mCherry before the factor, i.e., mCherry-P2A-Neurod1, mCherry-P2A-Math5.