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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 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.

ORGANISM(S): Gallus gallus

PROVIDER: GSE258895 | GEO | 2024/07/06

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 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.

2023-07-06 | GSE236181 | GEO

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.

2024-07-06 | GSE260533 | GEO

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

2009-10-19 | GSE17660 | GEO

Cdx and Hox genes differentially regulate posterior axial growth in mammalian embryos - 5/6 somites embryonic stage

2009-10-19 | GSE17658 | GEO

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

Project description:Hox and Cdx transcription factors regulate embryonic positional identities. Cdx mutant mice display posterior body truncations of the axial skeleton, neuraxis, and caudal uro-rectal structures. We show that trunk Hox genes stimulate axial extension as they can largely rescue these Cdx mutant phenotypes. Conversely, posterior (paralog group 13) Hox genes can prematurely arrest posterior axial growth when precociously expressed. Our data suggest that the transition from trunk to tail Hox gene expression successively regulates construction and termination of axial structures in the mouse embryo. Thus, Hox genes seem to differentially orchestrate posterior expansion of embryonic tissues during axial morphogenesis as an integral part of their function in specifying head-to-tail identity. In addition, we present evidence that Cdx and Hox transcription factors exert these effects by controlling Wnt signaling. Concomitant regulation of Cyp26a1 expression, restraining retinoic acid signaling in the posterior growth zone, may likewise play a role in timing the trunk-tail transition. Experiment Overall Design: A micro-array screen of down regulated and upregulated genes in Cdx2+/-Cdx4-/- mutant embryos versus wildtype embryos was performed at the embryonic stage of 13 somites. RNA was isolated from the posterior part of the embryos dissected at the same axial level using the last somite boundary as a landmark. Posterior tissues from pools of 7 embryos of each genotype were pooled. The labeled cRNAs were hybridized on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in a dye swap experiment, resulting in two individual microarrays.

2009-10-23 | E-GEOD-17660 | biostudies-arrayexpress

Transcription profiling of mouse Cdx2+/-Cdx4-/- mutant embryos versus wild type embryos at the 5/6 somite stage

Project description:Hox and Cdx transcription factors regulate embryonic positional identities. Cdx mutant mice display posterior body truncations of the axial skeleton, neuraxis, and caudal uro-rectal structures. We show that trunk Hox genes stimulate axial extension as they can largely rescue these Cdx mutant phenotypes. Conversely, posterior (paralog group 13) Hox genes can prematurely arrest posterior axial growth when precociously expressed. Our data suggest that the transition from trunk to tail Hox gene expression successively regulates construction and termination of axial structures in the mouse embryo. Thus, Hox genes seem to differentially orchestrate posterior expansion of embryonic tissues during axial morphogenesis as an integral part of their function in specifying head-to-tail identity. In addition, we present evidence that Cdx and Hox transcription factors exert these effects by controlling Wnt signaling. Concomitant regulation of Cyp26a1 expression, restraining retinoic acid signaling in the posterior growth zone, may likewise play a role in timing the trunk-tail transition. Experiment Overall Design: A micro-array screen of down regulated and upregulated genes in Cdx2+/-Cdx4-/- mutant embryos versus wildtype embryos was performed at the embryonic stage of 5/6 somites. RNA was isolated from the posterior part of the embryos dissected at the same axial level using the last somite boundary as a landmark. Posterior tissues from pools of 10 embryos of each genotype were pooled. The labeled cRNAs were hybridized on 4X44K Agilent Whole Mouse Genome dual colour Microarrays (G4122F) in two dye swap experiments, resulting in four individual microarrays.

2009-10-23 | E-GEOD-17658 | biostudies-arrayexpress

EWS-FLI1 and HOXD13 control tumor cell plasticity in Ewing sarcoma [CUT&RUN]

2022-06-28 | GSE182512 | GEO

EWS-FLI1 and HOXD13 control tumor cell plasticity in Ewing sarcoma [RNA-seq]

Project description:Posterior homeobox D genes, in particular HOXD13, are over-expressed by Ewing sarcoma, a tumor driven by the oncogenic fusion protein EWS-FLI1. Here, we have found that EWS-FLI1 maintains HOXD13 expression through a GGAA microsatellite enhancer in the developmental posterior HOXD regulatory domain. Activation of this enhancer is EWS-FLI1 dependent and epigenomic silencing of this region leads to loss of HOXD13 expression in Ewing sarcoma cells, but not in unrelated cells. To determine the function of HOXD13 activation in Ewing sarcoma we performed nascent RNA sequencing or RNA sequencing upon HOXD13 knockdown.

2022-06-28 | GSE148494 | GEO

EWS-FLI1 and HOXD13 control tumor cell plasticity in Ewing sarcoma [CITE-seq]

2022-06-28 | GSE165973 | GEO

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.

2024-11-13 | GSE256393 | GEO

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