Breaking constraint of mammalian axial formulae [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA660395 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12551256_1.fastq.gz | Fastqsanger.gz | |||
| SRR12551256_2.fastq.gz | Fastqsanger.gz | |||
| SRR12551257_1.fastq.gz | Fastqsanger.gz | |||
| SRR12551257_2.fastq.gz | Fastqsanger.gz | |||
| SRR12551258_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Breaking constraint of mammalian axial formulae
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Project description:Breaking constraint of mammalian axial formulae [RNA-Seq]
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Project description:The axial skeleton of individual mammalian species exhibits remarkable robustness in the number and identity of vertebral elements that form(Owen 1853; Owen 1866; Narita and Kuratani 2005). Between mammalian species however, a great diversity in axial formulae has arisen due to natural selection(Narita and Kuratani 2005; Thewissen et al. 2006; Buchholtz 2007; Matsubara et al. 2017; Kingsley et al. 2017). The genetic mechanism(s) by which axial formulae in mammals is canalised, or manipulated to drive this diversity, remains a major question in biology. Here, we reveal three regulatory pathways essential in constraining total vertebral number and regional axial identity in the mouse. Specifically, the manipulation of Gdf11, Retinoic acid and microRNA-196 activity, individually and cumulatively, led to increasing total vertebral number and allowed us to understand the molecular logic constraining each major division of the vertebral column, from cervical through to tail vertebrae. All three pathways had differing control over Hox cluster expression, with heterochronic and quantitative changes in Hox expression found to parallel changes in axial identity. However, our work revealed an additional, and highly unexpected, role for Hox genes in supporting axial elongation within the tail region. This provides important support for an emerging view that mammalian Hox gene function is not limited to imparting positional identity as the mammalian body plan is laid down, and more broadly, this work provides a molecular framework with which to interrogate mechanisms of evolutionary change.
2023-08-31 | GSE157172 | GEO
Project description:The axial skeleton of individual mammalian species exhibits remarkable robustness in the number and identity of vertebral elements that form(Owen 1853; Owen 1866; Narita and Kuratani 2005). Between mammalian species however, a great diversity in axial formulae has arisen due to natural selection(Narita and Kuratani 2005; Thewissen et al. 2006; Buchholtz 2007; Matsubara et al. 2017; Kingsley et al. 2017). The genetic mechanism(s) by which axial formulae in mammals is canalised, or manipulated to drive this diversity, remains a major question in biology. Here, we reveal three regulatory pathways essential in constraining total vertebral number and regional axial identity in the mouse. Specifically, the manipulation of Gdf11, Retinoic acid and microRNA-196 activity, individually and cumulatively, led to increasing total vertebral number and allowed us to understand the molecular logic constraining each major division of the vertebral column, from cervical through to tail vertebrae. All three pathways had differing control over Hox cluster expression, with heterochronic and quantitative changes in Hox expression found to parallel changes in axial identity. However, our work revealed an additional, and highly unexpected, role for Hox genes in supporting axial elongation within the tail region. This provides important support for an emerging view that mammalian Hox gene function is not limited to imparting positional identity as the mammalian body plan is laid down, and more broadly, this work provides a molecular framework with which to interrogate mechanisms of evolutionary change.
2023-08-31 | GSE157171 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-31 | GSE157173 | GEO
Project description:The vertebral column of individual mammalian species often exhibits remarkable robustness in the number and identity of vertebral elements that form (known as axial formulae). The genetic mechanism(s) underlying this constraint however remain ill-defined. Here, we reveal the interplay of three regulatory pathways (Gdf11, miR-196 and Retinoic acid) is essential in constraining total vertebral number and regional axial identity in the mouse, from cervical through to tail vertebrae. All three pathways have differing control over Hox cluster expression, with heterochronic and quantitative changes found to parallel changes in axial identity. However, our work reveals an additional role for Hox genes in supporting axial elongation within the tail region, providing important support for an emerging view that mammalian Hox function is not limited to imparting positional identity as the mammalian body plan is laid down. More broadly, this work provides a molecular framework to interrogate mechanisms of evolutionary change and congenital anomalies of the vertebral column.
| S-EPMC8752674 | biostudies-literature
Project description:The human embryo breaks symmetry to form the anterior-posterior axis of the body. As the embryo elongates along this axis, progenitors in the tailbud give rise to tissues that generate the spinal cord, skeleton, and musculature. This raises the question of how the embryo achieves axial elongation and patterning. While ethics necessitate in vitro studies, the variability of organoid systems has hindered mechanistic insights. Here we developed a bioengineering and machine learning framework that optimizes symmetry breaking by tuning the spatial coupling between human stem cell-derived organoids. This framework enabled the reproducible generation of axially elongating organoids, each possessing a tailbud and neural tube. We discovered that an excitable system composed of WNT/FGF signaling drives elongation through induction of a neuromesodermal progenitor (NMP)-like signaling center. We discovered that instabilities in the excitable system are suppressed by secreted WNT inhibitors. Absence of these inhibitors led to ectopic tailbuds and branches. Our results identify mechanisms governing stable human axial elongation.
2022-12-12 | GSE220472 | GEO
Project description:Controlling organoid symmetry breaking uncovers an excitable system underlying human axial elongation
| PRJNA909820 | ENA
Project description:Axial development of mammals is a dynamic process involving several coordinated morphogenetic events, including axial elongation, somitogenesis, and neural tube formation. To gain insight into the signals control the dynamics of human axial morphogenesis, we generated hundreds of axially elongating organoids by inducing anteroposterior symmetry breaking of spatially coupled epithelial cysts derived from human pluripotent stem cells. Each organoid was composed of a neural tube flanked by presomitic mesoderm sequentially segmented into somites. Periodic activation of the somite differentiation gene MESP2 coincided in space and time with anteriorly traveling segmentation clock waves in the presomitic mesoderm of the organoids, recapitulating critical aspects of somitogenesis. Through timed perturbations of organoids, we demonstrated that FGF and WNT signaling play distinct roles in axial elongation and somitogenesis and that FGF signaling gradients drive the segmentation clock waves. By generating and perturbing organoids that robustly recapitulate the architecture and dynamics of multiple axial tissues in human embryos, this work offers a means to dissect complex mechanisms underlying human embryogenesis.
2022-12-12 | GSE220563 | GEO
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.
2009-10-19 | GSE17660 | GEO