ArticleDevelopment (Cambridge, England)2014
Hox proteins drive cell segregation and non-autonomous apical remodelling during hindbrain segmentation.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Hoxb genes determine the timing of cell ingression by regulating cell surface fluctuations during zebrafish gastrulation.Development (Cambridge, England) · 2025Article
- Developmental patterns of extracellular matrix molecules in the embryonic and postnatal mouse hindbrain.Frontiers in neuroanatomy · 2024Article
- A single-cell transcriptional timelapse of mouse embryonic development, from gastrula to pup.bioRxiv : the preprint server for biology · 2023Article
- Hox genes in development and beyond.Development (Cambridge, England) · 2023Article
- Prognostic significance of HOXD4 protein expression in human ovarian cancers.Iranian journal of basic medical sciences · 2021Article
- Segmentation and patterning of the vertebrate hindbrain.Development (Cambridge, England) · 2021Review
- Mutually Repulsive EphA7-EfnA5 Organize Region-to-Region Corticopontine Projection by Inhibiting Collateral Extension.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Regulating Retinoic Acid Availability during Development and Regeneration: The Role of the CYP26 Enzymes.Journal of developmental biology · 2020Review
- An atlas of anterior hox gene expression in the embryonic sea lamprey head: Hox-code evolution in vertebrates.Developmental biology · 2019Article
- Getting direction(s): The Eph/ephrin signaling system in cell positioning.Developmental biology · 2019Review
- Cell segregation in the vertebrate hindbrain: a matter of boundaries.Cellular and molecular life sciences : CMLS · 2015Review
- A Simple Predictive Enhancer Syntax for Hindbrain Patterning Is Conserved in Vertebrate Genomes.PloS one · 2015Article
- Ephrin-Eph signaling in embryonic tissue separation.Cell adhesion & migration · 2014Review
- Hox proteins as regulators of extracellular matrix interactions during neural crest migration.Differentiation; research in biological diversityReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hox genes encode a conserved family of homeodomain transcription factors regulating development along the major body axis. During embryogenesis, Hox proteins are expressed in segment-specific patterns and control numerous different segment-specific cell fates. It has been unclear, however, whether Hox proteins drive the epithelial cell segregation mechanism that is thought to initiate the segmentation process. Here, we investigate the role of vertebrate Hox proteins during the partitioning of the developing hindbrain into lineage-restricted units called rhombomeres. Loss-of-function mutants and ectopic expression assays reveal that Hoxb4 and its paralogue Hoxd4 are necessary and sufficient for cell segregation, and for the most caudal rhombomere boundary (r6/r7). Hox4 proteins regulate Eph/ephrins and other cell-surface proteins, and can function in a non-cell-autonomous manner to induce apical cell enlargement on both sides of their expression border. Similarly, other Hox proteins expressed at more rostral rhombomere interfaces can also regulate Eph/ephrins, induce apical remodelling and drive cell segregation in ectopic expression assays. However, Krox20, a key segmentation factor expressed in odd rhombomeres (r3 and r5), can largely override Hox proteins at the level of regulation of a cell surface target, Epha4. This study suggests that most, if not all, Hox proteins share a common potential to induce cell segregation but in some contexts this is masked or modulated by other transcription factors.
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