Expression pattern of the mouse T gene and its role in mesoderm formation

Wilkinson, David G.; Bhatt, Sangita; Herrmann, Bernhard G.

doi:10.1038/343657a0

Cited by 807 publications

(565 citation statements)

References 17 publications

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“…The transcription factor brachyury (T ) marked the posterior epiblast and the nascent primitive streak both in control and N1ICD epi littermates (n=3; Fig. 5G,G′) (Wilkinson et al, 1990). Cer1, encoding a NODAL antagonist expressed in AVE cells at the anterior pole of the embryo (Biben et al, 1998), was expressed normally in N1ICD epi embryos (n=4; Fig.…”

Section: Notch Activation Does Not Affect Anterior-posterior Polaritymentioning

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 Activation Does Not Affect Anterior-posterior Polaritymentioning

confidence: 99%

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

et al. 2015

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“…In brief, embryos were dissected and fixed overnight in 4% paraformaldehyde (PFA). The following probes were used: Nodal (Conlon et al, 1994), Cerberos-1 (Cer-1) (Thomas et al, 1997), Brachyury (T) (Wilkinson et al, 1990), Hex (Thomas et al, 1998), Sonic hedgehog (Shh) (Echelard et al, 1993), Lim1 (kind gift from M. Jakobson). For generating Bmp-4 probe primers, Bmp4-F 5 0 -TGATACCTGAGACGGGAAG-3 0 and Bmp4-R 5 0 -AACGATCGGCTGATTCT GAC-3 0 were used.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Nucleotide exchange factor RIC‐8 is indispensable in mammalian early development

Tõnissoo¹,

Lulla²,

Meier³

et al. 2010

Developmental Dynamics

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The guanine nucleotide exchange factor RIC-8 is a conserved protein essential for the asymmetric division in the early embryogenesis in different organisms. The function of RIC-8 in mammalian development is not characterized so far. In this study we map the expression of RIC-8 during the early development of mouse. To elucidate the RIC-8 function we used Ric-8 2/2 mutant embryos. The Ric-8 2/2 embryos reach the gastrulation stage but do not develop further and die at E6.5-E8.5. We characterized the Ric-8 2/2 embryonic phenotype by morphological and marker gene analyses. The gastrulation is initiated in Ric-8 2/2 embryos but their growth is retarded, epiblast and mesoderm disorganized. Additionally, the basement membrane is defective, amnion folding and the formation of allantois are interfered, also the cavitation. Furthermore, the orientation of the Ric-8 2/2 embryo in the uterus was abnormal. Our study reveals that the activity of RIC-8 protein is irreplaceable for the correct gastrulation of mouse embryo. Developmental Dynamics 239:3404-3415,

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“…Antisense riboprobes were synthesized using a DIG RNA labeling kit (Roche, #1 175 025) for the following genes: Bmp4 (Winnier et al, 1995), Cer1 (Belo et al, 1997), Fgf8 (Mahmood et al, 1995), Foxa2 ; Gbx2 (Wassarman et al, 1997), Hex (Bedford et al, 1993), Hesx1 (Thomas et al, 1995), Ebaf (previously Lefty2) (Meno et al, 1999), Lhx1 (Shawlot and Behringer, 1995), Lrp5 (Gong et al, 2001), Nodal (Meno et al, 1998), Pou5f1 (A. Smith), sprouty 2 (Minowada et al, 1999), Six3 (Oliver et al, 1995), Shh (Echelard et al, 1993), T (Wilkinson et al, 1990), Tbx6 (Image clone #599230) and Wnt3 (Roelink et al, 1990).…”

Section: Expression Analysis Of Whole-mount Embryosmentioning

confidence: 99%