Cripto promotes A–P axis specification independently of its stimulatory effect on Nodal autoinduction

D'Andrea, Daniela; Liguori, Giovanna L.; Good, J. Ann Le; Lonardo, Enza; Andersson, Olov; Constam, Daniel; Persico, M. Graziella; Minchiotti, Gabriella

doi:10.1083/jcb.200709090

Cited by 29 publications

(24 citation statements)

References 63 publications

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“…Finally, using murine knock out models, Liguori and colleagues recently demonstrated that Nodal can signal extensively and control axis specification in the absence of Cripto, if its inhibitor Cerberus is also inhibited [44]. More recent evidence also supports a role for Cripto-1 during anterior-posterior axis specification independently of canonical Nodal signaling pathway [45].…”

Section: Cripto-1mentioning

confidence: 85%

Emerging Roles of Nodal and Cripto-1: From Embryogenesis to Breast Cancer Progression

Strizzi

Postovit

Margaryan

et al. 2008

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Breast carcinoma cells and embryonic progenitors similarly implement stem cell-associated signaling pathways to sustain continued growth and plasticity. Indeed, recent studies have implicated signaling pathways, including those associated with the Notch, and Transforming Growth Factor-Beta (TGF-β) superfamilies, as instrumental to both embryological development and breast cancer progression. In particular, Nodal, an embryonic morphogen belonging to the TGF-β superfamily, and its co-receptor, Cripto-1, are requisite to both embryogenesis and mammary gland maturation. Moreover, these developmental proteins have been shown to promote breast cancer progression. Here, we review the role of Nodal and its co-receptor Cripto-1 during development and we describe how this signaling pathway may be involved in breast cancer tumorigenesis. Moreover, we emphasize the potential utility of this signaling pathway as a novel target for the treatment and diagnosis of breast cancer.

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Section: Cripto-1mentioning

confidence: 85%

Emerging Roles of Nodal and Cripto-1: From Embryogenesis to Breast Cancer Progression

Strizzi

Postovit

Margaryan

et al. 2008

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“…Experimentally, cells in the visceral endoderm may be directed to move from regions of high (where there is elevated cell proliferation) to low Nodal activity (Fig. 5B) (Yamamoto et al, 2004) and, consistent with Nodal having such a role, DVE cells do not move when Cripto activity is lost (Ding et al, 1998 ;Criptonull), allows the formation and translocation of the DVE to become the AVE D'Andrea et al, 2008). AVE formation may therefore be accomplished, at least in part, by a Cripto-independent Nodal pathway that is sensitive to Cer1 inhibition.…”

Section: Cellular and Molecular Mechanisms Of Dve Translocationmentioning

confidence: 99%

Blastocyst lineage formation, early embryonic asymmetries and axis patterning in the mouse

2009

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The investigation into lineage allocation and early asymmetries in the pre-and peri-implantation mouse embryo is gaining momentum. As we review here, new insights have been gained into the cellular and molecular events that lead to the establishment of the three lineages of the blastocyst, to the determination of the origin and the fates of the visceral endoderm in the peri-implantation mouse embryo, and to the generation of cellular and molecular activities that accompany the emergence of asymmetries in the pre-gastrulation embryo. We also discuss the continuing debate that surrounds the relative impacts of early lineage bias versus the stochastic allocation of cells with respect to the events that pattern the blastocyst and initiate its later asymmetries. IntroductionThe progression of the mammalian embryo from fertilization to gastrulation involves an ordered series of lineage specifications and axial asymmetries (Fig. 1) that result, first, in the development of the blastocyst (see Glossary, Box 1), with its embryonic-abembryonic axis ( Fig. 1; Box 2), and, later, in the formation of the embryo itself, with its anterior-posterior (AP), dorsal-ventral (DV) and left-right (LR) axes. In many invertebrates and vertebrates, asymmetries that are established in the egg correlate with the segregation of determinants that influence later lineage formation and axis development. However, in the mouse egg, the morphological asymmetries that exist, such as the position of the second polar body (see Glossary, Box 1) and the sperm entry point, do not clearly demarcate an asymmetric domain of, for example, signaling activity or of cell fate determinants in the fertilized mouse egg. Whether there is any instructive relationship between the asymmetry of the egg and the later asymmetry of the blastocyst and lineage allocation remains a controversial issue. It is well known that the pre-implantation mammalian embryo is highly regulative and resistant to the loss or addition of cells brought about by experimental manipulations. However, this does not preclude the existence of an, as yet, uncharacterized property that could bias developmental outcomes in the intact embryo.Whether any early asymmetries in the mouse egg and/or blastocyst relate to the orientation of the definitive body axes is even less certain. It is now clear that the AP patterning of the gastrulating embryo is initiated prior to gastrulation by spatially localized signals that emanate from regionally patterned extra-embryonic tissues. Some of these asymmetries may be set up as early as the blastocyst stage, linking pre-implantation patterning to post-implantation morphogenesis.Here, we review recent experiments that define the molecular components of lineage specification in the mouse blastocyst. We also review the ongoing uncertainty and debate that surrounds the relative importance of early cleavage patterns at the two-to four-cell stage and of symmetric versus asymmetric divisions at the eight-to 16-and 16-to 32-cell stage, and the importance of final cell po...

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“…Compound mutant mouse embryos lacking both Cripto and Cryptic phenocopy Nodal Ϫ/Ϫ null mutants (17). In addition, analysis of Cripto Ϫ/Ϫ and Cryptic Ϫ/Ϫ single mutants revealed unique functions in different tissues: Cripto expression in the epiblast enables Nodal autoinduction and thereby promotes germ layer formation (14,18). By contrast, Cryptic is primarily required after gastrulation to mediate paracrine Nodal signaling from the ventral node to the left lateral plate mesoderm during leftright axis formation (19,20).…”

mentioning

confidence: 99%

Nodal·Gdf1 Heterodimers with Bound Prodomains Enable Serum-independent Nodal Signaling and Endoderm Differentiation

Fuerer

Nostro

Constam

2014

Journal of Biological Chemistry

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Background: To generate active Nodal suited for directed stem cell differentiation, we purified it as a heterodimer with Gdf1. Results: Heterodimeric Nodal⅐Gdf1 copurified with their cleaved prodomains, potentiated receptor activation and endoderm differentiation, and enabled paracrine signaling in serum-free conditions. Conclusion: Cell-non-autonomous high Nodal signaling thresholds depend on low molecular weight heterodimers. Significance: Nodal⅐Gdf1 is a new reagent to differentiate endoderm.

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Cripto promotes A–P axis specification independently of its stimulatory effect on Nodal autoinduction

Cited by 29 publications

References 63 publications

Emerging Roles of Nodal and Cripto-1: From Embryogenesis to Breast Cancer Progression

Emerging Roles of Nodal and Cripto-1: From Embryogenesis to Breast Cancer Progression

Blastocyst lineage formation, early embryonic asymmetries and axis patterning in the mouse

Nodal·Gdf1 Heterodimers with Bound Prodomains Enable Serum-independent Nodal Signaling and Endoderm Differentiation

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