Seth Blackshaw

@sethblackshaw.bsky.social

Professor of Neuroscience. Studying neural development, regeneration, and control of innate behaviors at Johns Hopkins.

This perspective piece reviews new omics, developmental genetic, and cell lineage studies to critically review current models of developing forebrain organization. Spoiler: there are _serious_ problems with the prosomere model.

Elizabeth Manning@emmanning.bsky.social · 2mo ago

Well done to @elsieplace.bsky.social, Marysia Placzek and @sethblackshaw.bsky.social for this beautifully clear overview of a very complex history of brain developmental models www.sciencedirect.com/science/arti...

Happy to announce that our latest paper is now out! Have you ever wondered how neural tissues control their size? In this paper, we show that cell division orientation is critical in both the cortex and retina. www.science.org/doi/10.1126/...

Oriented cell divisions induce basal progenitors and regulate neural expansion across tissues and species

A fundamental role for division orientation in progenitor output driving cortical and retinal growth is revealed.

science.org

The lab's first paper of the new year is out. In it, we investigate the role of the late stage retinal progenitor-enriched SoxE family factors Sox8 and Sox9 in controlling retinal development./1 www.biorxiv.org/content/10.6...

Sox8 and Sox9 regulate differentiation and nuclear positioning of retinal Müller glia

Temporal patterning of retinal progenitor cells governs the sequential generation of retinal cell types, with gliogenesis occurring late in development. Sox8 and Sox9, members of the SoxE transcription factor family, are highly expressed in late-stage retinal progenitor cells and mature Müller glia, yet their functional roles remain incompletely defined. Here we employed gain- and loss-of-function approaches, single-cell multiomic profiling, and injury models to investigate Sox8/9 function. Overexpression of SOX8 and/or SOX9 in early-stage retinal progenitor cells suppressed early-born cell fates and promoted photoreceptor generation, consistent with a role in late-stage temporal identity. Conversely, conditional deletion of Sox8 and/or Sox9 in late-stage progenitors did not impair Müller glia specification, but caused radial displacement of Müller glia nuclei into the outer retina and modest changes in glial gene expression. Loss of Sox8/9 in mature Müller glia modestly increased proliferation post-injury without inducing neurogenic competence. These findings suggest that Sox8/9 are dispensable for gliogenesis and repression of neurogenic competence, but are essential for proper laminar positioning and maturation of retinal Müller glia. ### Competing Interest Statement S.B. is a cofounder, shareholder, and scientific advisory board member of CDI Labs LLC, and receives research support from Genentech. National Eye Institute, https://ror.org/03wkg3b53, R01EY036173

biorxiv.org

👁️The retina — strikingly conserved across vertebrates, but an oddity among bilaterians! So how did it evolve? With @mikebok.bsky.social, @neurofishh.bsky.social and @denilsson.bsky.social, we argue that retinal complexity may 𝑝𝑟𝑒𝑑𝑎𝑡𝑒 𝑡ℎ𝑒 𝑒𝑦𝑒 𝑖𝑡𝑠𝑒𝑙𝑓. www.biorxiv.org/content/10.1... 1/n

a black and white dog is sitting on a couch with its tongue sticking out .

ALT: a black and white dog is sitting on a couch with its tongue sticking out .

media.tenor.com

Now up, positively our lab's last word on Ptbp1. Developmental loss of function Ptbp1 turns out not to regulate neurogenesis or cell fate specification at all, but does alter splicing patterns and slightly accelerates expression of photoreceptor-specific genes./1 www.biorxiv.org/content/10.1...

Ptbp1 is not required for retinal neurogenesis and cell fate specification.

The RNA-binding protein Ptbp1 has been proposed as a master regulator of neuronal fate, repressing neurogenesis through its effects on alternative splicing and miRNA maturation. While prior studies us...

biorxiv.org