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.

Uncx4.1 is required for the formation of the pedicles and proximal ribs and acts upstream of Pax9

Development ◽  
2000 ◽  
Vol 127 (11) ◽  
pp. 2251-2258 ◽  
Author(s):  
A. Mansouri ◽  
A.K. Voss ◽  
T. Thomas ◽  
Y. Yokota ◽  
P. Gruss
Keyword(s):  
Cell Adhesion ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Homeobox Gene ◽  
Axial Skeleton ◽  
Adhesion Properties ◽  
Marker Analysis ◽  
Targeted Mutation ◽  
Differential Cell

The expression of the homeobox gene Uncx4.1 in the somite is restricted to the caudal half of the newly formed somite and sclerotome. Here we show that mice with a targeted mutation of the Uncx4.1 gene exhibit defects in the axial skeleton and ribs. In the absence of Uncx4.1, pedicles of the neural arches and proximal ribs are not formed. In addition, dorsal root ganglia are disorganized. Histological and marker analysis revealed that Uncx4.1 is not necessary for somite segmentation. It is required to maintain the condensation of the caudal half-sclerotome, from which the missing skeletal elements are derived. The loss of proximal ribs in Pax1/Pax9 double mutants and the data presented here argue for a role of Uncx4.1 upstream of Pax9 in the caudolateral sclerotome. Our results further indicate that Uncx4.1 may be involved in the differential cell adhesion properties of the somite.

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 allocation of epiblast cells to the embryonic heart and other mesodermal lineages: the role of ingression and tissue movement during gastrulation

Development ◽  
1997 ◽  
Vol 124 (9) ◽  
pp. 1631-1642 ◽  
Author(s):  
P.P. Tam ◽  
M. Parameswaran ◽  
S.J. Kinder ◽  
R.P. Weinberger
Keyword(s):  
Cell Fate ◽  
Primitive Streak ◽  
Heart Cells ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Tissue Movement ◽  
Heart Field ◽  
Morphogenetic Event ◽  
Extraembryonic Mesoderm

The cardiogenic potency of cells in the epiblast of the early primitive-streak stage (early PS) embryo was tested by heterotopic transplantation. The results of this study show that cells in the anterior and posterior epiblast of the early PS-stage embryos have similar cardiogenic potency, and that they differentiated to heart cells after they were transplanted directly to the heart field of the late PS embryo. That the epiblast cells can acquire a cardiac fate without any prior act of ingression through the primitive streak or movement within the mesoderm suggests that neither morphogenetic event is critical for the specification of the cardiogenic fate. The mesodermal cells that have recently ingressed through the primitive streak can express a broad cell fate that is characteristic of the pre-ingressed cells in the host when they were returned to the epiblast. However, mesoderm cells that have ingressed through the primitive streak did not contribute to the lateral plate mesoderm after transplantation back to the epiblast, implying that some restriction of lineage potency may have occurred during ingression. Early PS stage epiblast cells that were transplanted to the epiblast of the mid PS host embryos colonised the embryonic mesoderm but not the extraembryonic mesoderm. This departure from the normal cell fate indicates that the allocation of epiblast cells to the mesodermal lineages is dependent on the timing of their recruitment to the primitive streak and the morphogenetic options that are available to the ingressing cells at that instance.

scholarly journals Enforced expression of the transcription factor HOXD3 under the control of the Wnt1 regulatory element modulates cell adhesion properties in the developing mouse neural tube

2011 ◽  
Vol 219 (5) ◽  
pp. 589-600 ◽  
Author(s):  
Yasushi Taniguchi ◽  
Osamu Tanaka ◽  
Masaki Sekiguchi ◽  
Susumu Takekoshi ◽  
Hideo Tsukamoto ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Adhesion ◽  
Neural Tube ◽  
Regulatory Element ◽  
Adhesion Properties

scholarly journals The migration of paraxial and lateral plate mesoderm cells emerging from the late primitive streak is controlled by different Wnt signals

2008 ◽  
Vol 8 (1) ◽  
pp. 63 ◽  
Author(s):  
Dylan Sweetman ◽  
Laura Wagstaff ◽  
Oliver Cooper ◽  
Cornelis Weijer ◽  
Andrea Münsterberg
Keyword(s):  
Primitive Streak ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate

scholarly journals Protocol for analysis of integrin-mediated cell adhesion of lateral plate mesoderm cells isolated from zebrafish embryos

2021 ◽  
Vol 2 (2) ◽  
pp. 100428
Author(s):  
Seung-Sik Rho ◽  
Eri Oguri-Nakamura ◽  
Koji Ando ◽  
Kiyotake Yamamoto ◽  
Yuki Takagi ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Zebrafish Embryos ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate

The bHLH transcription factor hand2 plays parallel roles in zebrafish heart and pectoral fin development

Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2573-2582 ◽  
Author(s):  
D. Yelon ◽  
B. Ticho ◽  
M.E. Halpern ◽  
I. Ruvinsky ◽  
R.K. Ho ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Early Stage ◽  
Bhlh Transcription Factor ◽  
Lateral Plate Mesoderm ◽  
Pectoral Fin ◽  
Lateral Plate ◽  
Anteroposterior Patterning ◽  
Cellular Processes ◽  
Myocardial Development ◽  
Tbx5 Expression

The precursors of several organs reside within the lateral plate mesoderm of vertebrate embryos. Here, we demonstrate that the zebrafish hands off locus is essential for the development of two structures derived from the lateral plate mesoderm - the heart and the pectoral fin. hands off mutant embryos have defects in myocardial development from an early stage: they produce a reduced number of myocardial precursors, and the myocardial tissue that does form is improperly patterned and fails to maintain tbx5 expression. A similar array of defects is observed in the differentiation of the pectoral fin mesenchyme: small fin buds form in a delayed fashion, anteroposterior patterning of the fin mesenchyme is absent and tbx5 expression is poorly maintained. Defects in these mesodermal structures are preceded by the aberrant morphogenesis of both the cardiogenic and forelimb-forming regions of the lateral plate mesoderm. Molecular analysis of two hands off alleles indicates that the hands off locus encodes the bHLH transcription factor Hand2, which is expressed in the lateral plate mesoderm starting at the completion of gastrulation. Thus, these studies reveal early functions for Hand2 in several cellular processes and highlight a genetic parallel between heart and forelimb development.

scholarly journals The Axenfeld–Rieger Syndrome Gene FOXC1 Contributes to Left–Right Patterning

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 170
Author(s):  
Paul W. Chrystal ◽  
Curtis R. French ◽  
Francesca Jean ◽  
Serhiy Havrylov ◽  
Suey van Baarle ◽  
...  
Keyword(s):  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Gene Dosage ◽  
Heart Defects ◽  
Lateral Plate Mesoderm ◽  
Forkhead Transcription Factor ◽  
Lateral Plate ◽  
Rieger Syndrome ◽  
And Function ◽  
System Disorder

Precise spatiotemporal expression of the Nodal-Lefty-Pitx2 cascade in the lateral plate mesoderm establishes the left–right axis, which provides vital cues for correct organ formation and function. Mutations of one cascade constituent PITX2 and, separately, the Forkhead transcription factor FOXC1 independently cause a multi-system disorder known as Axenfeld–Rieger syndrome (ARS). Since cardiac involvement is an established ARS phenotype and because disrupted left–right patterning can cause congenital heart defects, we investigated in zebrafish whether foxc1 contributes to organ laterality or situs. We demonstrate that CRISPR/Cas9-generated foxc1a and foxc1b mutants exhibit abnormal cardiac looping and that the prevalence of cardiac situs defects is increased in foxc1a−/−; foxc1b−/− homozygotes. Similarly, double homozygotes exhibit isomerism of the liver and pancreas, which are key features of abnormal gut situs. Placement of the asymmetric visceral organs relative to the midline was also perturbed by mRNA overexpression of foxc1a and foxc1b. In addition, an analysis of the left–right patterning components, identified in the lateral plate mesoderm of foxc1 mutants, reduced or abolished the expression of the NODAL antagonist lefty2. Together, these data reveal a novel contribution from foxc1 to left–right patterning, demonstrating that this role is sensitive to foxc1 gene dosage, and provide a plausible mechanism for the incidence of congenital heart defects in Axenfeld–Rieger syndrome patients.

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