scholarly journals MouseAlx3:Anaristaless-like Homeobox Gene Expressed during Embryogenesis in Ectomesenchyme and Lateral Plate Mesoderm

1998 ◽  
Vol 199 (1) ◽  
pp. 11-25 ◽  
Author(s):  
Derk ten Berge ◽  
Antje Brouwer ◽  
Sophia El Bahi ◽  
Jean-Louis Guénet ◽  
Benoı̂t Robert ◽  
...  
Keyword(s):  
Homeobox Gene ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate

The Xenopus homeobox gene pitx3 impinges upon somitogenesis and laterality

2013 ◽  
Vol 91 (2) ◽  
pp. 79-87 ◽  
Author(s):  
Cristine Smoczer ◽  
Lara Hooker ◽  
Sarah Brode ◽  
Marian Wolanski ◽  
Farhad KhosrowShahian ◽  
...  
Keyword(s):  
Anterior Segment ◽  
Homeobox Gene ◽  
The Other ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Anterior Segment Dysgenesis ◽  
Cellular Changes ◽  
Causative Locus ◽  
Dorsal Axis ◽  
Vertebral Anomalies

Pitx3 has been identified as the causative locus in a developmental eye mutation associated with mammalian anterior segment dysgenesis, congenital cataracts, and aphakia. In recent studies of frog eye development we discovered that pitx3 expresses symmetrically in the somites and lateral plate mesoderm and asymmetrically during cardiac and gut looping. We report that disruption of pitx3 activity on one side of an embryo relative to the other, either by over- or underexpression of pitx3, elicits a crooked dorsal axis in embryos that is a consequence of a retarded progression through somitogenesis. Unlike in amniotes, Xenopus somites form as cohorts of presomitic cells that rotate perpendicular to the dorsal axis. Since no vertebral anomalies have been reported in mouse and human Pitx3 mutants, we attempt to distinguish whether the segmentation clock is uniquely affected in frog or if the pitx3 perturbation inhibits the cellular changes that are necessary to rotation of presomitic cells. In Xenopus, pitx3 appears to inhibit the rotation of presomitic cell cohorts and to be necessary to the bilaterally symmetric expression of pitx2 in somites.

The homeobox gene Pitx2: mediator of asymmetric left-right signaling in vertebrate heart and gut looping

Development ◽  
1999 ◽  
Vol 126 (6) ◽  
pp. 1225-1234 ◽  
Author(s):  
M. Campione ◽  
H. Steinbeisser ◽  
A. Schweickert ◽  
K. Deissler ◽  
F. van Bebber ◽  
...  
Keyword(s):  
Ectopic Expression ◽  
Homeobox Gene ◽  
Zebrafish Embryos ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Left Right Asymmetry ◽  
The Right ◽  
Pitx2 Expression

Left-right asymmetry in vertebrates is controlled by activities emanating from the left lateral plate. How these signals get transmitted to the forming organs is not known. A candidate mediator in mouse, frog and zebrafish embryos is the homeobox gene Pitx2. It is asymmetrically expressed in the left lateral plate mesoderm, tubular heart and early gut tube. Localized Pitx2 expression continues when these organs undergo asymmetric looping morphogenesis. Ectopic expression of Xnr1 in the right lateral plate induces Pitx2 transcription in Xenopus. Misexpression of Pitx2 affects situs and morphology of organs. These experiments suggest a role for Pitx2 in promoting looping of the linear heart and gut.

The forkhead transcription factor Foxf1 is required for differentiation of extra-embryonic and lateral plate mesoderm

Development ◽  
2001 ◽  
Vol 128 (2) ◽  
pp. 155-166 ◽  
Author(s):  
M. Mahlapuu ◽  
M. Ormestad ◽  
S. Enerback ◽  
P. Carlsson
Keyword(s):  
Transcription Factor ◽  
Cell Adhesion ◽  
Posterior Part ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Yolk Sac ◽  
Lateral Plate Mesoderm ◽  
Forkhead Transcription Factor ◽  
Lateral Plate ◽  
Adhesion Properties

The murine Foxf1 gene encodes a forkhead transcription factor expressed in extra-embryonic and lateral plate mesoderm and later in splanchnic mesenchyme surrounding the gut and its derivatives. We have disrupted Foxf1 and show that mutant embryos die at midgestation due to defects in mesodermal differentiation and cell adhesion. The embryos do not turn and become deformed by the constraints of a small, inflexible amnion. Extra-embryonic structures exhibit a number of differentiation defects: no vasculogenesis occurs in yolk sac or allantois; chorioallantoic fusion fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers. Separation of the bulk of yolk sac mesoderm from the endodermal layer and adherence between mesoderm of yolk sac and amnion, indicate altered cell adhesion properties and enhanced intramesodermal cohesion. A possible cause of this is misexpression of the cell-adhesion protein VCAM1 in Foxf1-deficient extra-embryonic mesoderm, which leads to co-expression of VCAM with its receptor, alpha(4)-integrin. The expression level of Bmp4 is decreased in the posterior part of the embryo proper. Consistent with this, mesodermal proliferation in the primitive streak is reduced and somite formation is retarded. Expression of Foxf1 and the homeobox gene Irx3 defines the splanchnic and somatic mesodermal layers, respectively. In Foxf1-deficient embryos incomplete separation of splanchnic and somatic mesoderm is accompanied by misexpression of Irx3 in the splanchnopleure, which implicates Foxf1 as a repressor of Irx3 and as a factor involved in coelom formation.

scholarly journals FZD4 Marks Lateral Plate Mesoderm and Signals with NORRIN to Increase Cardiomyocyte Induction from Pluripotent Stem Cell-Derived Cardiac Progenitors

2018 ◽  
Vol 10 (1) ◽  
pp. 87-100 ◽  
Author(s):  
Charles Yoon ◽  
Hannah Song ◽  
Ting Yin ◽  
Damaris Bausch-Fluck ◽  
Andreas P. Frei ◽  
...  
Keyword(s):  
Stem Cell ◽  
Pluripotent Stem Cell ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Cardiac Progenitors

scholarly journals Loss of Abdominal Muscle in Pitx2 Mutants Associated with Altered Axial Specification of Lateral Plate Mesoderm

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e42228 ◽  
Author(s):  
Diana Eng ◽  
Hsiao-Yen Ma ◽  
Jun Xu ◽  
Hung-Ping Shih ◽  
Michael K. Gross ◽  
...  
Keyword(s):  
Abdominal Muscle ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Axial Specification

scholarly journals Charting cell migration dynamics during lateral plate mesoderm patterning in zebrafish using lightsheet microscopy

2017 ◽  
Vol 145 ◽  
pp. S79-S80
Author(s):  
Karin Dorien Prummel ◽  
Christopher Hess ◽  
Eline Brombacher ◽  
Anastasia Felker ◽  
Christian Mosimann
Keyword(s):  
Cell Migration ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Migration Dynamics ◽  
Mesoderm Patterning

scholarly journals Antagonistic interactions in the zebrafish midline prior to the emergence of asymmetric gene expression are important for left–right patterning

2016 ◽  
Vol 371 (1710) ◽  
pp. 20150402 ◽  
Author(s):  
Rebecca D. Burdine ◽  
Daniel T. Grimes
Keyword(s):  
Gene Expression ◽  
Lateral Plate Mesoderm ◽  
Internal Organs ◽  
Lateral Plate ◽  
Left Right Asymmetry ◽  
Antagonistic Interactions

Left–right (L-R) asymmetry of the internal organs of vertebrates is presaged by domains of asymmetric gene expression in the lateral plate mesoderm (LPM) during somitogenesis. Ciliated L-R coordinators (LRCs) are critical for biasing the initiation of asymmetrically expressed genes, such as nodal and pitx2 , to the left LPM. Other midline structures, including the notochord and floorplate, are then required to maintain these asymmetries. Here we report an unexpected role for the zebrafish EGF-CFC gene one-eyed pinhead ( oep ) in the midline to promote pitx2 expression in the LPM. Late zygotic oep (LZ oep ) mutants have strongly reduced or absent pitx2 expression in the LPM, but this expression can be rescued to strong levels by restoring oep in midline structures only. Furthermore, removing midline structures from LZ oep embryos can rescue pitx2 expression in the LPM, suggesting the midline is a source of an LPM pitx2 repressor that is itself inhibited by oep . Reducing lefty1 activity in LZ oep embryos mimics removal of the midline, implicating lefty1 in the midline-derived repression. Together, this suggests a model where Oep in the midline functions to overcome a midline-derived repressor, involving lefty1 , to allow for the expression of left side-specific genes in the LPM. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.

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