Proud to have been part of this work.

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.

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/...

Indeed.

Resolving forebrain developmental organisation by analysis of differential growth patterns - Nature Communications Experiments on the embryonic chick brain reveal distinct directional growth patterns and a tripartite hypothalamus, challenging the classic segmented prosomere model and offering an updated view of ho...

Excited to finally share the final/final.doc version of our paper. It's been a journey, but very proud of the result. Well done to all involved, especially @elsieplace.bsky.social

@kchinnaiya.bsky.social , @thomasdwkim.bsky.social, @sethblackshaw.bsky.social 👏👏

www.nature.com/articles/s41...

Second paper is a collaboration with Jim Handa's lab at Hopkins. Cigarette smoke exposure induces aging-related molecular changes in both mouse and human retinal pigment epithelium.
www.pnas.org/doi/10.1073/...

I'd like to close by thanking lead author Nicole Pannullo, who recently defended her thesis, who with Debarpita Datta, @claytonsantiago.bsky.social, Jared Hangman, Lizhi Jiang, and Leighton Duncan -- and support from NIH -- made this possible./end

One reason why the Sox8/9 mutant phenotype is so much less dramatic than that of Nfia/b/x mutants may be persistent compensatory expression of other Sox family members, most notably Sox2, which might compensate for the loss of Sox8/9./11

So what's going on here? While Sox8/9 suppress early-born cell type generation when misexpressed, and directly regulate transcription of NFI family genes, they are not required for maintaining late-stage temporal identity, being required for glial differentiation rather than specification./10

What about Sox8/9 function in mature Muller glia, where we previously showed that Nfia/b/x actively suppress neurogenic competence? As with Nfia/b/x mutants, we observe a modest induction of injury-induced proliferation, but no glial-derived neurogenesis or induction of Ascl1./9

scATAC-Seq and CUT&TAG data show that Sox8/9 predominantly function as transcriptional activators, in combination with other late-stage progenitor-specific factors such as NFIs. However, Sox8/9 mutants show no change in retinal cell fate specification or clear disruptions of temporal identity./8

Single-cell multiomic analysis of Sox8/9 double mutant glia show reduced Notch signaling and altered expression of many genes known to regulate cell adhesion and migration, as well as mature glial markers./7

Both Sox8 and Sox9 mutants resulted in progressive radial displacement of Muller glial cell nuclei towards the photoreceptor layer. This was enhanced in Sox8/9 double mutants./6

Early retinal progenitor-specific loss of function of Sox9 did not affect neurogenesis or cell fate specification, and despite much effort, we were unable to generate early progenitor-specific Sox8 or Sox8/9 double mutants. We shifted instead to selectively deleting these genes in neonates./5

When over expressed in early-stage E14 progenitors, both Sox8 and Sox9 repress generation of early-born retinal ganglion and amacrine cells and promote formation of later-born photoreceptors. This matches what we previously observed with NFI factors./4

Gene regulatory networks controlling temporal patterning, neurogenesis, and cell-fate specification in mammalian retina Gene regulatory networks (GRNs), consisting of transcription factors and their target sites, control neurogenesis and cell-fate specification in the d…

Overexpression, conditional loss of function, and biochemical analysis all confirmed that this was the case for Nfia/b/x in retina. We asked if this was also the case for Sox8/9./3

www.sciencedirect.com/science/arti...

Sox8/9 play an important role in regulating brain and spinal cord astrocyte and oligodendrocyte differentiation, often acting cooperatively with Nfia. Our multiomic analysis of retinal progenitors identified NFI and SoxE factor as more broadly promoting late-stage temporal identity, however./2

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...

We’re thrilled to share that CSHL Associate Professor Jeremy Borniger (@jborniger.bsky.social) has received the 2026 Bakewell Emerging Leader Award from The Mark Foundation. His lab is exploring synthetic torpor—a hibernation-like state—as a novel way to slow cancer growth. #ScienceMakesLifeBetter

Several stages of brain development in a chick embryo

New featured article!

Resolving forebrain developmental organisation by analysis of differential growth patterns

@emmanning.bsky.social @elsieplace.bsky.social @kchinnaiya.bsky.social @sethblackshaw.bsky.social @thomasdwkim.bsky.social

http://dlvr.it/TQLWh5

Congratulation!

How ground squirrels enhanced their retinas - Scientific editing and writing experts - Life Science Editors Scientific editing and writing experts for manuscripts and grants

Nice summary on our paper on mechanisms controlling development and evolution of the cone-dominant ground squirrel retina, which is now in final form at eLife.
www.lifescienceeditors.com/2026/01/06/h...

rdcu.be/eX8JD

DRN new publication alert:

Manning et al., 2025, @emmanning.bsky.social, co-led by Marysia Placzek and Elsie Place @elsieplace.bsky.social, in collaboration with Seth Blackshaw @sethblackshaw.bsky.social

ipRGC properties prevent light from shifting the SCN clock during daytime Nature - The inability of intrinsically photosensitive retinal ganglion cells to shift the circadian clock in the suprachiasmatic nucleus during daytime is caused by light-dependent depolarization...

A new paper from my lab. I will have a full description soon. rdcu.be/eX1Ld

I want to give my deepest thanks to Tomomi Shimogori -- with whom this all started nearly 20 years ago -- and more recently Marysia and Elsie. It has been an honor and privilege to work with you all.

I have no illusions that this will stop the ongoing trickle of prosomere-promoting single-color in situ hybridization studies in one Frontiers journal or another. I hope this will lead the Allen Brain Atlas to finally revise their developmental mouse reference atlas, however.

Decoding gene networks controlling hypothalamic and prethalamic neuron development Kim et al. map gene regulatory networks of the developing mouse hypothalamus and prethalamus using single-cell multiomics, identifying regulators of regionalization and neurogenesis. They further show...

And finally combining multiomic-based gene regulatory network and genetic analysis in mouse earlier this year:
www.cell.com/cell-reports...

Single-cell analysis of early chick hypothalamic development reveals that hypothalamic cells are induced from prethalamic-like progenitors Using scRNA-seq in the developing chick hypothalamus, Kim et al. identify progenitors during hypothalamic specification, regionalization, and early neurogenesis and demonstrate evolutionary conservati...

Moving to chick here:
www.cell.com/cell-reports...

The cellular and molecular landscape of hypothalamic patterning and differentiation from embryonic to late postnatal development - Nature Communications The cellular and molecular mechanisms regulating hypothalamic patterning and differentiation are unclear. Here, the authors profiled the transcriptome of the developing hypothalamus at single cell lev...

Moving to single-cell analysis in mouse:
www.nature.com/articles/s41...

A genomic atlas of mouse hypothalamic development - Nature Neuroscience This Resource chronicles dynamic gene expression patterns in the developing hypothalamus from embryonic day 10.5 through maturity. The authors find that Shh must be expressed in the hypothalamic basal...

Starting here: www.nature.com/articles/nn....

Contrast with the prosomere model, which puts that telencephalon and hypothalamus as dorsal and ventral halves of the "secondary prosencephalon". The data here match the conclusions drawn from what's now a long series of molecular studies of both mouse and chick hypothalamic development.