The murine allantois: emerging paradigms in development of the mammalian umbilical cord and its relation to the fetus

Inman, Kimberly E.; Downs, Karen M.

doi:10.1002/dvg.20281

Cited by 73 publications

(100 citation statements)

References 199 publications

(207 reference statements)

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“…The most prominent Flk1 expression observed in N1ICD epi embryos was found in extra-embryonic mesoderm cells that accumulated proximal to the primitive streak, suggesting that it corresponds to allantois precursors that failed to organise into an elongated allantois bud (Fig. 7C,C′) (Inman and Downs, 2007). By contrast, Flk1 expression was severely reduced in the cardiac and the yolk sac regions of N1ICD epi embryos at E7.5 and E8.5, indicating that endothelial cell specification and blood island formation are impaired (n=6; Fig.…”

Section: Notch Signalling Regulates the Acquisition Of Distinct Mesodmentioning

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: Notch Signalling Regulates the Acquisition Of Distinct Mesodmentioning

confidence: 99%

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

et al. 2015

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“…The vasculature of the labyrinth originates from the allantois (Inman and Downs, 2007;Rossant and Cross, 2001), a mesoderm derivative of the posterior primitive streak (Downs et al, 2004;Kinder et al, 1999;Lawson, 1999). Allantoic vascularization occurs de novo similarly to the embryo and yolk sac vascularization (Downs et al, 1998;Drake and Fleming, 2000).…”

Section: Hoxa10 and Hoxa11 Together With Hoxa13mentioning

confidence: 99%

“…Following the initiation of vasculogenesis, the distal tip of the allantois fuses to the chorion and subsequent expansion of the distal allantoic vascular plexus within the chorionic plate gives rise to the fetal vasculature of the labyrinth (Inman and Downs, 2007;Rossant and Cross, 2001). To establish which Hoxa genes are involved in the development of the labyrinthine vasculature, we analyzed the…”

Section: Hoxa10 and Hoxa11 Together With Hoxa13mentioning

confidence: 99%

Recruitment of 5′ Hoxa genes in the allantois is essential for proper extra-embryonic function in placental mammals

Scotti

Kmita

2012

Development

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SUMMARYThe Hox gene family is well known for its functions in establishing morphological diversity along the anterior-posterior axis of developing embryos. In mammals, one of these genes, Hoxa13, is crucial for embryonic survival, as its function is required for the proper expansion of the fetal vasculature in the placenta. Thus, it appears that the developmental strategy specific to placental mammals is linked, at least in part, to the recruitment of Hoxa13 function in developing extra-embryonic tissues. Yet, the mechanism underlying this extra-embryonic recruitment is unknown. Here, we provide evidence that this functional novelty is not exclusive to Hoxa13 but is shared with its neighboring Hoxa11 and Hoxa10 genes. We show that the extra-embryonic function of these three Hoxa genes stems from their specific expression in the allantois, an extra-embryonic hallmark of amniote vertebrates. Interestingly, Hoxa10-13 expression in the allantois is conserved in chick embryos, which are non-placental amniotes, suggesting that the extra-embryonic recruitment of Hoxa10, Hoxa11 and Hoxa13 most likely arose in amniotes, i.e. prior to the emergence of placental mammals. Finally, using a series of targeted recombination and transgenic assays, we provide evidence that the regulatory mechanism underlying Hoxa expression in the allantois is extremely complex and relies on several cis-regulatory sequences.

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“…The key idea on this genetic mouse is that the mouse will express a full-length FAK protein but lacks its kinase activity. The KD FAK mouse is early embryonic lethal at E9.5 due to a number of defects, demonstrating that the kinase activity is essential in early embryo developmental processes including vessel formation and chorio-allantois fusion (Inman and Downs, 2007;Lim et al, 2010b;.…”

Section: Introductionmentioning

confidence: 99%

Nuclear FAK: a New Mode of Gene Regulation from Cellular Adhesions

Lim

2013

Molecules and Cells

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Focal adhesion kinase (FAK) is a protein tyrosine kinase (PTK) crucial in regulation of cell migration and proliferation. In addition to its canonical roles as a cytoplasmic kinase downstream of integrin and growth factor receptor signaling, recent studies revealed new aspects of FAK action in the nucleus. Nuclear FAK promotes p53 and GATA4 degradation via ubiquitination, resulting in enhanced cell proliferation and reduced inflammatory responses. FAK can also serve as a co-transcriptional regulator that alters a gene transcriptional activity. These findings established a new paradigm of FAK signaling from cellular adhesions to the nucleus. Although physiological stimuli for controlling FAK nuclear localization have not been completely characterized, FAK shuttles from focal adhesions to the nucleus to directly convey extracellular signals. Interestingly, nuclear translocation of FAK becomes prominent in kinase-inhibited conditions such as in de-adhesion and pharmacological FAK inhibition, while a small fraction of nuclear FAK is observed a normal growth condition. In this review, roles of nuclear FAK in regulating transcription factors will be discussed. Furthermore, a potential use of a pharmacological FAK inhibitor to target nuclear FAK function in diseases such as inflammation will be emphasized.

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The murine allantois: emerging paradigms in development of the mammalian umbilical cord and its relation to the fetus

Cited by 73 publications

References 199 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

Recruitment of 5′ Hoxa genes in the allantois is essential for proper extra-embryonic function in placental mammals

Nuclear FAK: a New Mode of Gene Regulation from Cellular Adhesions

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