Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis

Yoder, Michael; Gumbiner, Barry M.

doi:10.1002/dvdy.22754

Cited by 11 publications

(8 citation statements)

References 69 publications

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“…embryos, and its knockdown using morpholinos results in the loss of notochord formation (Yoder and Gumbiner, 2011). Intriguingly, the authors of that study could not detect any alterations in the adhesion-related behavior of cells, such as cell sorting, when AXPC expression was manipulated in embryos.…”

Section: Developmental Roles Of D1-protocadherinsmentioning

confidence: 92%

Emerging roles of protocadherins: from self-avoidance to enhancement of motility

Hayashi

Takeichi

2015

Journal of Cell Science

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Protocadherins are a group of transmembrane proteins belonging to the cadherin superfamily that are subgrouped into 'clustered' and 'nonclustered' protocadherins. Although cadherin superfamily members are known to regulate various forms of cell-cell interactions, including cell-cell adhesion, the functions of protocadherins have long been elusive. Recent studies are, however, uncovering their unique roles. The clustered protocadherins regulate neuronal survival, as well as dendrite self-avoidance. Combinatorial expression of clustered protocadherin isoforms creates a great diversity of adhesive specificity for cells, and this process is likely to underlie the dendritic selfavoidance. Non-clustered protocadherins promote cell motility rather than the stabilization of cell adhesion, unlike the classic cadherins, and mediate dynamic cellular processes, such as growth cone migration. Protocadherin dysfunction in humans is implicated in neurological disorders, such as epilepsy and mental retardation. This Commentary provides an overview of recent findings regarding protocadherin functions, as well as a discussion of the molecular basis underlying these functions.

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Section: Developmental Roles Of D1-protocadherinsmentioning

confidence: 92%

Emerging roles of protocadherins: from self-avoidance to enhancement of motility

Hayashi

Takeichi

2015

Journal of Cell Science

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“…Indeed, in Xenopus laevis embryo, the cell adhesion molecule Axial protocadherin (AXPC), an orthologue of mammalian Protocadherin-1 (PCDH1), is expressed in notochord precursor cells and plays an important role in the assembly of notochord cells [ 18 , 19 ]. In axpc knockdown Xenopus embryos, the notochord is not properly formed, and the elongation of the embryonic body axis is inhibited [ 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Protocadherin-1 is expressed in the notochord of mouse embryo but is dispensable for its formation

Fukunaga

Tanji

Hanzawa

et al. 2021

Biochemistry and Biophysics Reports

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Notochord is an embryonic midline structure that serves as mechanical support for axis elongation and the signaling center for the surrounding tissues. Precursors of notochord are initially induced in the dorsal most mesoderm region in gastrulating embryo and separate from the surrounding mesoderm/endoderm tissue to form an elongated rod-like structure, suggesting that cell adhesion molecules may play an important role in this step. In Xenopus embryo, axial protocadherin (AXPC), an orthologue of mammalian Protocadherin-1 (PCDH1), is indispensable for the assembly and separation from the surrounding tissue of the notochord cells. However, the role of PCDH1 in mammalian notochord remains unknown. We herein report that PCDH1 is expressed in the notochord of mouse embryo and that PCDH1-deficient mice form notochord normally. First, we examined the temporal expression pattern of pcdh1 and found that pcdh1 mRNA was expressed from embryonic day (E) 7.5, prior to the stage when notochord cells detach from the surrounding endoderm tissue. Second, we found that PCDH1 protein is expressed in the notochord of mouse embryos in addition to the previously reported expression in endothelial cells. To further investigate the role of PCDH1 in embryonic development, we generated PCDH1-deficient mice using the CRISPR-Cas9 system. In PCDH1-deficient embryos, notochord formation and separation from the surrounding tissue were normal. Structure and marker gene expression of notochord were also unaffected by loss of PCDH1. Major vascular patterns in PCDH1-deficient embryo were essentially normal. These results suggest that PCDH1 is dispensable for notochord formation, including the tissue separation process, in mammalian embryos. We successfully identified the evolutionary conserved expression of PCDH1 in notochord, but its function may differ among species.

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“…Cell-cell contact formation is thought to be important for cell-fate specification in both vertebrate and invertebrate development (Babb and Marrs, 2004;Goldstein, 1992;Guisoni et al, 2017;Larue et al, 1996;Michel et al, 2011;Shaya et al, 2017;Stephenson et al, 2010;Tassy et al, 2006;Yoder and Gumbiner, 2011). In mouse embryogenesis, for instance, cell-cell contact formation is required for the induction of the pluripotent inner cell mass giving rise to the embryo proper (Stephenson et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

An Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling Determines Cell Fate

et al. 2017

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Cell-cell contact formation constitutes an essential step in evolution, leading to the differentiation of specialized cell types. However, remarkably little is known about whether and how the interplay between contact formation and fate specification affects development. Here, we identify a positive feedback loop between cell-cell contact duration, morphogen signaling, and mesendoderm cell-fate specification during zebrafish gastrulation. We show that long-lasting cell-cell contacts enhance the competence of prechordal plate (ppl) progenitor cells to respond to Nodal signaling, required for ppl cell-fate specification. We further show that Nodal signaling promotes ppl cell-cell contact duration, generating a positive feedback loop between ppl cell-cell contact duration and cell-fate specification. Finally, by combining mathematical modeling and experimentation, we show that this feedback determines whether anterior axial mesendoderm cells become ppl or, instead, turn into endoderm. Thus, the interdependent activities of cell-cell signaling and contact formation control fate diversification within the developing embryo.

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Axial protocadherin (AXPC) regulates cell fate during notochordal morphogenesis

Cited by 11 publications

References 69 publications

Emerging roles of protocadherins: from self-avoidance to enhancement of motility

Emerging roles of protocadherins: from self-avoidance to enhancement of motility

Protocadherin-1 is expressed in the notochord of mouse embryo but is dispensable for its formation

An Effective Feedback Loop between Cell-Cell Contact Duration and Morphogen Signaling Determines Cell Fate

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