Single-cell analysis identifies a key role for Hhip in murine coronal suture development

Greg Holmes (), Ana S. Gonzalez-Reiche, Madrikha Saturne, Susan M. Motch Perrine, Xianxiao Zhou, Ana C. Borges, Bhavana Shewale, Joan T. Richtsmeier, Bin Zhang, Harm Bakel and Ethylin Wang Jabs
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Greg Holmes: Icahn School of Medicine at Mount Sinai
Ana S. Gonzalez-Reiche: Icahn School of Medicine at Mount Sinai
Madrikha Saturne: Icahn School of Medicine at Mount Sinai
Susan M. Motch Perrine: Pennsylvania State University
Xianxiao Zhou: Icahn School of Medicine at Mount Sinai
Ana C. Borges: Icahn School of Medicine at Mount Sinai
Bhavana Shewale: Icahn School of Medicine at Mount Sinai
Joan T. Richtsmeier: Pennsylvania State University
Bin Zhang: Icahn School of Medicine at Mount Sinai
Harm Bakel: Icahn School of Medicine at Mount Sinai
Ethylin Wang Jabs: Icahn School of Medicine at Mount Sinai

Nature Communications, 2021, vol. 12, issue 1, 1-16

Abstract: Abstract Craniofacial development depends on formation and maintenance of sutures between bones of the skull. In sutures, growth occurs at osteogenic fronts along the edge of each bone, and suture mesenchyme separates adjacent bones. Here, we perform single-cell RNA-seq analysis of the embryonic, wild type murine coronal suture to define its population structure. Seven populations at E16.5 and nine at E18.5 comprise the suture mesenchyme, osteogenic cells, and associated populations. Expression of Hhip, an inhibitor of hedgehog signaling, marks a mesenchymal population distinct from those of other neurocranial sutures. Tracing of the neonatal Hhip-expressing population shows that descendant cells persist in the coronal suture and contribute to calvarial bone growth. In Hhip−/− coronal sutures at E18.5, the osteogenic fronts are closely apposed and the suture mesenchyme is depleted with increased hedgehog signaling compared to those of the wild type. Collectively, these data demonstrate that Hhip is required for normal coronal suture development.

Date: 2021
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DOI: 10.1038/s41467-021-27402-5

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