The transcription factor FoxH1 (FAST) mediates Nodal signaling during anterior-posterior patterning and node formation in the mouse

Yamamoto, Masamichi; Meno, Chikara; Sakai, Yasuo; Shiratori, Hidetaka; Mochida, Kyoko; Ikawa, Yayoi; Saijoh, Yukio; Hamada, Hiroshi

doi:10.1101/gad.883901

Cited by 205 publications

(162 citation statements)

References 63 publications

(67 reference statements)

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“…6B,B′). Gsc and Lefty1 expression in the APS and AVE respectively require high levels of NODAL signalling in the epiblast (Hoodless et al, 2001;Takaoka et al, 2006;Vincent et al, 2003;Yamamoto et al, 2001). We found that Nodal expression was reduced in the epiblast, the primitive streak and the VE of N1ICD epi embryos (n=4/5; Fig.…”

Section: Notch Activation Impairs Axial Mesoderm Formation and Perturmentioning

confidence: 67%

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 Activation Impairs Axial Mesoderm Formation and Perturmentioning

confidence: 67%

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

et al. 2015

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“…As Cer1 and Leftb are Nodal antagonists, and Drap1 is probably a transcriptional corepressor for Nodal, these defects appear to be a consequence of increased levels of Nodal signaling. In support of this idea, mutant embryos with the loss-of-function of two Nodal signaling modulators, Foxh1 and arkadia (Rnf111 -Mouse Genome Informatics), fail to establish an anterior primitive streak/node and its derivatives (Hoodless et al, 2001;Yamamoto et al, 2001;Episkopou et al, 2001). Finally, either conditional loss-of-function of Smad2, a Nodal effector, in the epiblast or decreased Nodal signals in the primitive streak results in a specific loss of the ADE and prechordal mesoderm (Vincent et al, 2003).…”

Section: Lrp5 and Lrp6 Have Redundant Functions During Embryonic Devementioning

confidence: 86%

The Wnt co-receptors Lrp5 and Lrp6 are essential for gastrulation in mice

2004

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“…Fluorescein-, Cy3-and Cy5-conjugated secondary antibodies were obtained from Jackson ImmunoResearch, reconstituted in 50% glycerol according to the manufacturer's recommendation, and used at 1:100, 1:500 and 1:250 dilution, respectively, in the blocking solution. Whole-mount in situ hybridisation was performed by a standard method using digoxigenin-labelled probes 57 . Embryos were staged according to the dissection time (noon of the vaginal plug as E0.5) and morphology.…”

Section: Methodsmentioning

confidence: 99%

Delivery of endosomes to lysosomes via microautophagy in the visceral endoderm of mouse embryos

et al. 2012

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The differentiation and patterning of murine early embryos are sustained by the visceral endoderm, an epithelial layer of polarised cells that has critical roles in multiple signalling pathways and nutrient uptake. Both nutritional and signalling functions rely upon the endocytosis of various molecules from the cell surface via the endocytic pathway. However, endocytic membrane dynamics in this embryonic tissue remain poorly understood. Here we show that the functions of rab7, a small GTP-binding protein regulating the late endocytic pathway, are essential for embryonic patterning during gastrulation. The endosomes of visceral endoderm cells are delivered via a unique microautophagy-like process to the apical vacuole, a large compartment exhibiting lysosomal characteristics. Loss of rab7 function results in severe inhibition of this endocytic pathway. our results indicate that the microautophagic process and flow of the endocytic membrane have essential roles in early embryonic development.

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The transcription factor FoxH1 (FAST) mediates Nodal signaling during anterior-posterior patterning and node formation in the mouse

Abstract: FoxH1 (FAST) is a transcription factor that mediates

Cited by 205 publications

References 63 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 Wnt co-receptors Lrp5 and Lrp6 are essential for gastrulation in mice

Delivery of endosomes to lysosomes via microautophagy in the visceral endoderm of mouse embryos

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