Notch signalling regulates the contribution of progenitor cells from the chick Hensen's node to the floor plate and notochord

Gray, Shona; Dale, J. Kim

doi:10.1242/dev.041608

Cited by 20 publications

(26 citation statements)

References 76 publications

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“…NOTCH signalling regulates the formation of organiserderived midline structures in other vertebrates. In Xenopus and chick embryos, overexpression of NICD leads to an expansion of the floor plate at the expense of the notochord, suggesting that NOTCH signalling regulates a binary cell fate choice between these two derivatives of the organiser (Gray and Dale, 2010;López et al, 2003). In N1ICD epi embryos, the notochord is similarly absent.…”

Section: Discussionmentioning

confidence: 99%

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

et al. 2015

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NOTCH signalling is an evolutionarily conserved pathway involved in intercellular communication essential for cell fate choices during development. Although dispensable for early aspects of mouse development, canonical RBPJ-dependent NOTCH signalling has been shown to influence lineage commitment during embryonic stem cell (ESC) differentiation. NOTCH activation in ESCs promotes the acquisition of a neural fate, whereas its suppression favours their differentiation into cardiomyocytes. This suggests that NOTCH signalling is implicated in the acquisition of distinct embryonic fates at early stages of mammalian development. In order to investigate in vivo such a role for NOTCH signalling in shaping cell fate specification, we use genetic approaches to constitutively activate the NOTCH pathway in the mouse embryo. Early embryonic development, including the establishment of anterior-posterior polarity, is not perturbed by forced NOTCH activation. By contrast, widespread NOTCH activity in the epiblast triggers dramatic gastrulation defects. These are fully rescued in a RBPJ-deficient background. Epiblast-specific NOTCH activation induces acquisition of neurectoderm identity and disrupts the formation of specific mesodermal precursors including the derivatives of the anterior primitive streak, the mouse organiser. In addition, we show that forced NOTCH activation results in misregulation of NODAL signalling, a major determinant of early embryonic patterning. Our study reveals a previously unidentified role for canonical NOTCH signalling during mammalian gastrulation. It also exemplifies how in vivo studies can shed light on the mechanisms underlying cell fate specification during in vitro directed differentiation.

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Section: Discussionmentioning

confidence: 99%

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

et al. 2015

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“…There is strong evidence for a conserved role of Notch signaling in regulating hypochord allocation during gastrulation, but the signals regulating medial floor plate allocation are less clear (Appel et al, 1999;Latimer and Appel, 2006;Latimer et al, 2002;Peyrot et al, 2011). Speciesspecific roles for Notch and Midkine signaling have been identified, but a conserved pathway regulating this process across all species has yet to be identified (Gray and Dale, 2010;Lopez et al, 2003Lopez et al, , 2005Peyrot et al, 2011;Schafer et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

The zebrafish tailbud contains two independent populations of midline progenitor cells that maintain long-term germ layer plasticity and differentiate based on local signaling cues

et al. 2015

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Vertebrate body axis formation depends on a population of bipotential neuromesodermal cells along the posterior wall of the tailbud that make a germ layer decision after gastrulation to form spinal cord and mesoderm. Despite exhibiting germ layer plasticity, these cells never give rise to midline tissues of the notochord, floor plate and dorsal endoderm, raising the question of whether midline tissues also arise from basal posterior progenitors after gastrulation. We show in zebrafish that local posterior signals specify germ layer fate in two basal tailbud midline progenitor populations. Wnt signaling induces notochord within a population of notochord/floor plate bipotential cells through negative transcriptional regulation of sox2. Notch signaling, required for hypochord induction during gastrulation, continues to act in the tailbud to specify hypochord from a notochord/hypochord bipotential cell population. Our results lend strong support to a continuous allocation model of midline tissue formation in zebrafish, and provide an embryological basis for zebrafish and mouse bifurcated notochord phenotypes as well as the rare human congenital split notochord syndrome. We demonstrate developmental equivalency between the tailbud progenitor cell populations. Midline progenitors can be transfated from notochord to somite fate after gastrulation by ectopic expression of msgn1, a master regulator of paraxial mesoderm fate, or if transplanted into the bipotential progenitors that normally give rise to somites. Our results indicate that the entire non-epidermal posterior body is derived from discrete, basal tailbud cell populations. These cells remain receptive to extracellular cues after gastrulation and continue to make basic germ layer decisions.

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“…Interestingly, there are two genes of the Hairy family of Notch effectors expressed in the dorsal midline. Hairy2a , implicated in choices between FP and notochord (Gray and Dale, 2010; Lopez et al, 2005), is expressed during gastrula stages, but has not been tested for a role in hypochord development. XHRT1 is expressed in FP and hypochord domains beginning at early neurula, but has not been tested for a requirement in either of these tissues (Pichon et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…In chick, Notch signaling regulates allocation of cells in Hensen’s node to FP and notochord, in a manner analogous to its role in fish and frog (Gray and Dale, 2010). There is also evidence that Notch signaling is required to maintain FP identity during neurogenesis in chick (le Roux et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…However, little functional analysis has been performed to ascertain what signaling pathways influence the allocation of these cells to midline tissues. Because Notch signaling regulates cell fate choices in the midline in zebrafish (Appel et al, 1999) and chick, (Gray and Dale, 2010), we initially chose to focus on this pathway to test the allocation model in frog. Previous findings on Notch in Xenopus midline development (Lopez et al, 2003; Lopez et al, 2005) mostly conform to the allocation model proposed by original work on the zebrafish deltaA mutant, indicating a high degree of conservation in this process.…”

Section: Introductionmentioning

confidence: 99%

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A revised model of Xenopus dorsal midline development: Differential and separable requirements for Notch and Shh signaling

Peyrot

Wallingford

Harland

2011

Developmental Biology

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The development of the vertebrate dorsal midline (floor plate, notochord, and hypochord) has been an area of classical research and debate. Previous studies in vertebrates have led to contrasting models for the roles of Shh and Notch signaling in specification of the floor plate, by late inductive or early allocation mechanisms, respectively. Here, we show that Notch signaling plays an integral role in cell fate decisions in the dorsal midline of Xenopus laevis, similar to that observed in zebrafish and chick. Notch signaling promotes floor plate and hypochord fates over notochord, but has variable effects on Shh expression in the midline. In contrast to previous reports in frog, we find that Shh signaling is not required for floor plate vs. notochord decisions and plays a minor role in floor plate specification, where it acts in parallel to Notch signaling. As in zebrafish, Shh signaling is required for specification of the lateral floor plate in the frog. We also find that the medial floor plate in Xenopus comprises two distinct populations of cells, each dependent upon different signals for its specification. Using expression analysis of several midline markers, and dissection of functional relationships, we propose a revised allocation mechanism of dorsal midline specification in Xenopus. Our model is distinct from those proposed to date, and may serve as a guide for future studies in frog and other vertebrate organisms.

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Notch signalling regulates the contribution of progenitor cells from the chick Hensen's node to the floor plate and notochord

Cited by 20 publications

References 76 publications

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

NOTCH activation interferes with cell fate specification in the gastrulating mouse embryo

The zebrafish tailbud contains two independent populations of midline progenitor cells that maintain long-term germ layer plasticity and differentiate based on local signaling cues

A revised model of Xenopus dorsal midline development: Differential and separable requirements for Notch and Shh signaling

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