<i>Snail</i> genes at the crossroads of symmetric and asymmetric processes in the developing mesoderm

Morales, Aixa V.; Acloque, Hervé; Ocaña, Oscar H.; Frutos, Cristina A. de; Gold, Veronica; Nieto, M. Ángela

doi:10.1038/sj.embor.7400867

Cited by 26 publications

(32 citation statements)

References 27 publications

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“…EMT-based escape involves 5 steps: (1) a post-mitotic cell breaking tight junction connections with its neighbors, (2) losing epithelial adherence (E-cadherin downregulation), (3) transiently acquiring motility and other mesenchymal characteristics, (4) epithelial exit, and (5) the re-formation of tight junctions between remaining cells across the space vacated (Morales et al, 2007). Despite the release of pro-endocrine cells from the trunk epithelium being proposed to involve EMT, concrete evidence of the actual process or components involved has yet to be provided.…”

Section: Delamination Of Pro-endocrine Cells and Isletogenesismentioning

confidence: 99%

Pancreas organogenesis: From bud to plexus to gland

Pan

Wright

2011

Developmental Dynamics

525

594

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Pancreas oganogenesis comprises a coordinated and highly complex interplay of signaling events and transcriptional networks that guide a step-wise process of organ development from early bud specification all the way to the final mature organ state. Extensive research on pancreas development over the last few years, largely driven by a translational potential for pancreatic diseases (diabetes, pancreatic cancer, and so on), is markedly advancing our knowledge of these processes. It is a tenable goal that we will one day have a clear, complete picture of the transcriptional and signaling codes that control the entire organogenetic process, allowing us to apply this knowledge in a therapeutic context, by generating replacement cells in vitro, or perhaps one day to the whole organ in vivo. This review summarizes findings in the past 5 years that we feel are amongst the most significant in contributing to the deeper understanding of pancreas development. Rather than try to cover all aspects comprehensively, we have chosen to highlight interesting new concepts, and to discuss provocatively some of the more controversial findings or proposals. At the end of the review, we include a perspective section on how the whole pancreas differentiation process might be able to be unwound in a regulated fashion, or redirected, and suggest linkages to the possible reprogramming of other pancreatic cell-types in vivo, and to the optimization of the forward-directed-differentiation of human embryonic stem cells (hESC), or induced pluripotential cells (iPSC), towards mature b-cells. Developmental Dynamics 240:530-565,

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Section: Delamination Of Pro-endocrine Cells and Isletogenesismentioning

confidence: 99%

Pancreas organogenesis: From bud to plexus to gland

Pan

Wright

2011

Developmental Dynamics

525

594

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“…After being washed with PBS, embryos were transferred to an EC culture plate and incubated until HH stage 12/13 (omeprazole) or HH stage 15 (Z-VAD-FMK). Cells within the primitive streak were electroporated with Pitx2a-RCAS (45) or a chick Snail1-pcDNA3 construct (46). To visualize the electroporated cells, an eGFP reporter construct (pCAGGS-GFP) was used (47).…”

Section: Methodsmentioning

confidence: 99%

“…Whole mount in situ hybridization was performed as previously described (48). Antisense RNA probes for chicken Tbx18, Nodal, Wt1, Snai1, and Pitx2 were generated from full-length cDNA clones (8,23,46,49). Double color whole mount in situ hybridization was performed as previously described (50).…”

Section: Methodsmentioning

confidence: 99%

A right-sided pathway involving FGF8 / Snai1 controls asymmetric development of the proepicardium in the chick embryo

Schlueter

Brand

2009

Proc. Natl. Acad. Sci. U.S.A.

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The proepicardium (PE) is a transient structure that forms at the venous pole of the embryonic vertebrate heart. This cardiac progenitor cell population gives rise to the epicardium, coronary vasculature, and fibroblasts. In the chicken embryo, the PE displays left-right (L-R) asymmetry and develops only on the right side, while on the left only a vestigial PE is formed, which subsequently gets lost by apoptosis. In this study, we analyzed how the L-R asymmetry pathway affects PE formation. Experimental manipulation of left-side determinants such as Shh, Nodal, and Cfc as well as forced expression of Pitx2 had no effect on the sidedness of PE development. In contrast, inhibition of early-acting regulators of L-R axis formation such as H ؉ /K ؉ -ATPase or primitive streak apoptosis affected the sidedness of PE development. Experimental interference with the right-side determinants Fgf8 or Snai1 prevented PE formation, whereas ectopic left-sided expression of Fgf8 or Snai1 resulted in bilateral PE development. These data provide novel insight into the molecular control of asymmetric morphogenesis suggesting that also the right side harbors an instructive signaling pathway that is involved in the control of PE development. This pathway might be of general relevance for setting up L-R asymmetries at the venous pole of the heart. left-right asymmetry ͉ Tbx18 ͉ Pitx2 ͉ venous pole morphogenesis T he left-right (L-R) axis controls asymmetric organogenesis in vertebrates (1-3). In lower chordates, Xenopus, and chick, breaking of the initial bilateral body symmetry involves the asymmetric distribution of ion channels and transporters, resulting in the development of membrane potential differences between the left and right body side, which may drive an asymmetric transport of small molecules through gap junctions (4, 5). In mammals, Xenopus, and zebrafish, ciliated cells in the organizer generate a fluid flow to the left that transports L-R determinants (6). In mammals, this nodal flow is believed to be the sole mechanism by which L-R asymmetry is initiated (7). In the chicken embryo, asymmetric gene expression in Hensen's node of gastrula stage embryos is an important intermediate step of establishing L-R asymmetry (2). Shh, for example, is asymmetrically expressed on the left side of Hensen's node and induces Nodal expression in a small left-sided domain adjacent to Hensen's node (8). Nodal establishes a large expression domain in the left lateral plate mesoderm (LPM) and induces the expression of Pitx2, a homeobox gene of the bicoid class (7). Pitx2 determines morphological L-R asymmetries in most organ systems (9-12) via modulation of cell-cell adhesion, cell morphology, extracellular matrix composition, spindle orientation, and cell proliferation (13-15).A right-sided regulatory cascade of gene expression is also initiated in Hensen's node including Bmp4 that induces asymmetric expression of Fgf18 and Fgf8 on the right side (16-18). It is believed that the right side does not initiate its own sidespecific morphogene...

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“…Indeed, in the chick it was shown that in the absence of RA signaling, snail1 expression is not affected in the LPM but starts to be asymmetrically expressed in the right anterior PSM. This asymmetric PSM expression of snail1 results in asymmetric expression of the cyclic genes snail2 and lfng and later leads to asynchronous somitogenesis [99]. In mouse, asymmetric somite formation seen in the absence of RA signaling [94] may be due to a misregulation of snail1 expression in the PSM, since it has been shown that in mice mutants for Rere there is an asymmetric snail1 expression in the PSM [95].…”

Section: Retinoic Acid Buffers the Psm From The Influence Of Lr Signalsmentioning

confidence: 99%

“…In both chick and mouse embryos, snail1 is transiently asymmetrically expressed in the right LPM and plays a role in organ lateralization [97,98]. Furthermore, it was shown that the period of asymmetric snail1 expression in the LPM coincides with the time window during which RA is necessary to protect the PSM from asymmetric signals [99]. Indeed, in the chick it was shown that in the absence of RA signaling, snail1 expression is not affected in the LPM but starts to be asymmetrically expressed in the right anterior PSM.…”

Section: Retinoic Acid Buffers the Psm From The Influence Of Lr Signalsmentioning

confidence: 99%

Symmetry OUT, Asymmetry IN

Lourenço

Saúde

2010

Symmetry

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Abstract:The formation of a perfect vertebrate body plan poses many questions that thrill developmental biologists. Special attention has been given to the symmetric segmental patterning that allows the formation of the vertebrae and skeletal muscles. These segmented structures derive from bilaterally symmetric units called somites, which are formed under the control of a segmentation clock. At the same time that these symmetric units are being formed, asymmetric signals are establishing laterality in nearby embryonic tissues, allowing the asymmetric placement of the internal organs. More recently, a "shield" that protects symmetric segmentation from the influence of laterality cues was uncovered. Here we review the mechanisms that control symmetric versus asymmetric development along the left-right axis among vertebrates. We also discuss the impact that these studies might have in the understanding of human congenital disorders characterized by congenital vertebral malformations and abnormal laterality phenotypes.

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Snail genes at the crossroads of symmetric and asymmetric processes in the developing mesoderm

Cited by 26 publications

References 27 publications

Pancreas organogenesis: From bud to plexus to gland

Pancreas organogenesis: From bud to plexus to gland

A right-sided pathway involving FGF8 / Snai1 controls asymmetric development of the proepicardium in the chick embryo

Symmetry OUT, Asymmetry IN

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