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Peer-reviewedCC BY 4.0Development (Cambridge, England)

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

  • Nicole Pannullo1
  • Debarpita Datta1
  • Clayton P. Santiago2
  • Jared A. Tangeman1
  • Lizhi Jiang1
  • Leighton H. Duncan1
  • Taqdees Gohar1
  • Megan Gimmen1
  • Seth Blackshaw1,3,4,5,6
6 affiliations
  1. 1Solomon H. Snyder Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15219, USA
  2. 2Department of Ophthalmology, University of Pittsburgh, Pittsburgh, PA 15219, USA
  3. 3Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
  4. 4Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
  5. 5Kavli Neuroscience Discovery Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
  6. 6Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
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Abstract

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 have employed gain- and loss-of-function approaches, single-cell multiomic profiling, and injury models to investigate Sox8 and Sox9 function. Overexpression of human SOX8 and SOX9 in early-stage mouse retinal progenitor cells both suppressed generation of early-born cells, consistent with a role in late-stage temporal identity, and induced ectopic generation of oligodendrocyte lineage-like cells. Conversely, conditional deletion of Sox8 and/or Sox9 in late-stage progenitors did not impair Müller glia specification, but caused radial displacement of glial nuclei into the outer retina and reduced expression of multiple markers of mature Müller glia. Loss of Sox8 and/or Sox9 in mature Müller glia modestly increased proliferation post-injury without inducing neurogenic competence. These findings suggest that Sox8 and Sox9 are dispensable for gliogenesis and repression of neurogenic competence, but are essential for proper laminar positioning and full terminal differentiation of retinal Müller glia.

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Cite

BibTeXRIS
BibTeX
@article{pannullo2026sox8,
  title = {{Sox8 and Sox9 regulate differentiation and nuclear positioning of retinal Müller glia}},
  author = {Nicole Pannullo and Debarpita Datta and Clayton P. Santiago and Jared A. Tangeman and Lizhi Jiang and Leighton H. Duncan and Taqdees Gohar and Megan Gimmen and Seth Blackshaw},
  journal = {Development (Cambridge, England)},
  year = {2026},
  month = oct,
  doi = {10.1242/dev.205508},
  url = {https://doi.org/10.1242/dev.205508},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Sox8 and Sox9 regulate differentiation and nuclear positioning of retinal Müller glia
AU  - Nicole Pannullo
AU  - Debarpita Datta
AU  - Clayton P. Santiago
AU  - Jared A. Tangeman
AU  - Lizhi Jiang
AU  - Leighton H. Duncan
AU  - Taqdees Gohar
AU  - Megan Gimmen
AU  - Seth Blackshaw
PY  - 2026
DA  - 2026/10/13
JO  - Development (Cambridge, England)
DO  - 10.1242/dev.205508
UR  - https://doi.org/10.1242/dev.205508
AB  - 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 have employed gain- and loss-of-function approaches, single-cell multiomic profiling, and injury models to investigate Sox8 and Sox9 function. Overexpression of human SOX8 and SOX9 in early-stage mouse retinal progenitor cells both suppressed generation of early-born cells, consistent with a role in late-stage temporal identity, and induced ectopic generation of oligodendrocyte lineage-like cells. Conversely, conditional deletion of Sox8 and/or Sox9 in late-stage progenitors did not impair Müller glia specification, but caused radial displacement of glial nuclei into the outer retina and reduced expression of multiple markers of mature Müller glia. Loss of Sox8 and/or Sox9 in mature Müller glia modestly increased proliferation post-injury without inducing neurogenic competence. These findings suggest that Sox8 and Sox9 are dispensable for gliogenesis and repression of neurogenic competence, but are essential for proper laminar positioning and full terminal differentiation of retinal Müller glia.
SN  - 0950-1991
SN  - 1477-9129
ER  -