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Hox gene activity directs physical forces to differentially shape chick small and large intestinal epithelia

ABSTRACT: Hox genes are highly conserved, master regulators of spatial patterning in the embryo, but how these factors trigger regional morphogenesis has largely remained a mystery. In the developing gut, Hox genes help demarcate identities of the small and large intestines early in embryogenesis, which ultimately leads to their specialization in both form and function. While the midgut forms villi, the hindgut develops flat, brain-like sulci that resolve into heterogeneous outgrowths. Combining mechanical measurements and mathematical modeling, we demonstrate that the posterior Hox gene Hoxd13 regulates biophysical phenomena that shape the hindgut lumen. We further show that Hoxd13 acts through the TGFβ pathway to thicken, stiffen, and promote isotropic growth of the subepithelial mesenchyme; together, these features lead to hindgut surface buckling. TGFβ, in turn, promotes collagen deposition to affect mesenchymal geometry and growth. We thus identify a cascade of events downstream of positional genetic identity that direct posterior intestinal morphogenesis.

ORGANISM(S): Gallus gallus

PROVIDER: GSE236181 | GEO | 2023/07/06

REPOSITORIES: GEO

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Hox gene activity directs physical forces to differentially shape chick small and large intestinal epithelia

Project description:Hox genes are highly conserved, master regulators of spatial patterning in the embryo, but how these factors trigger regional morphogenesis has largely remained a mystery. In the developing gut, Hox genes help demarcate identities of the small and large intestines early in embryogenesis, which ultimately leads to their specialization in both form and function. While the midgut forms villi, the hindgut develops flat, brain-like sulci that resolve into heterogeneous outgrowths. Combining mechanical measurements of the embryonic chick intestine and mathematical modeling, we demonstrate that the posterior Hox gene HOXD13 regulates biophysical phenomena that shape the hindgut lumen. We further show that HOXD13 acts through the TGFβ pathway to thicken, stiffen, and promote isotropic growth of the subepithelial mesenchyme; together, these features lead to hindgut surface buckling. TGFβ, in turn, promotes collagen deposition to affect mesenchymal geometry and growth. We thus identify a cascade of events downstream of positional genetic identity that direct posterior intestinal morphogenesis.

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Hox gene activity directs physical forces to differentially shape chick small and large intestinal epithelia

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Cdx and Hox genes differentially regulate posterior axial growth in mammalian embryos -13 somites embryonic stage

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Transcription profiling of mouse Cdx2+/-Cdx4-/- mutant embryos versus wild type embryos at the 13 somite stage

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Protogenin Facilitates Trunk-to-Tail HOX Code Transition via Modulating GDF11/SMAD2 Signaling in Mammalian Embryos

Project description:Vertebral axial patterning is determined during embryogenesis via complicated regulation involving multiple signaling networks. This study revealed that protogenin (Prtg), a member of the immunoglobulin superfamily, is involved in controlling vertebral patterning. Prtg knockout (Prtg-/-) mice exhibited anterior homeotic transformations in their vertebral columns accompanied by significant alternations in the expression of numerous homeobox (Hox) genes. Transcriptomic profiling of Prtg-/- embryos revealed that genes regulated by Prtg play a pivotal role in modulating axial development, displaying prominent associations with the transforming growth factor beta (TGFβ) signaling pathway. Additionally, we observed a pronounced reduction in TGFβ signaling activity in Prtg-/- embryos, as evidenced by decreased phosphorylated Smad2 (pSmad2) levels within the developing tail region. Furthermore, we introduced human induced pluripotent stem cell-derived presomitic mesoderm-like (hiPSC-PSM) cells as an in vitro model to explore the role of PRTG in somitogenesis, specifically focusing on the collinear expression of HOX genes. Our findings indicate that PRTG knockout in hiPSC-PSM cells results in delayed posterior HOX gene expression. Intriguingly, supplementation with growth differentiation factor 11 (GDF11) successfully rescued the abnormal expression of posterior HOX genes, providing compelling evidence that PRTG’s regulation of HOX genes is mediated by the GDF11/SMAD2 signaling pathway.

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