scholarly journals Essential roles of zebrafish bmp2a, fgf10, and fgf24 in the specification of the ventral pancreas

2012 ◽  
Vol 23 (5) ◽  
pp. 945-954 ◽  
Author(s):  
François Naye ◽  
Marianne L. Voz ◽  
Nathalie Detry ◽  
Matthias Hammerschmidt ◽  
Bernard Peers ◽  
...  
Keyword(s):  
Fibroblast Growth ◽  
Lateral Plate Mesoderm ◽  
Loss Of Function ◽  
Lateral Plate ◽  
Bmp Pathway ◽  
Ventral Pancreas ◽  
Pancreas Agenesis ◽  
Gut Endoderm ◽  
Hepatic Markers

In vertebrates, pancreas and liver arise from bipotential progenitors located in the embryonic gut endoderm. Bone morphogenic protein (BMP) and fibroblast growth factor (FGF) signaling pathways have been shown to induce hepatic specification while repressing pancreatic fate. Here we show that BMP and FGF factors also play crucial function, at slightly later stages, in the specification of the ventral pancreas. By analyzing the pancreatic markers pdx1, ptf1a, and hlxb9la in different zebrafish models of BMP loss of function, we demonstrate that the BMP pathway is required between 20 and 24 h postfertilization to specify the ventral pancreatic bud. Knockdown experiments show that bmp2a, expressed in the lateral plate mesoderm at these stages, is essential for ventral pancreas specification. Bmp2a action is not restricted to the pancreatic domain and is also required for the proper expression of hepatic markers. By contrast, through the analysis of fgf10−/−; fgf24−/− embryos, we reveal the specific role of these two FGF ligands in the induction of the ventral pancreas and in the repression of the hepatic fate. These mutants display ventral pancreas agenesis and ectopic masses of hepatocytes. Overall, these data highlight the dynamic role of BMP and FGF in the patterning of the hepatopancreatic region.

scholarly journals Opposing RA and FGF signals control proximodistal vertebrate limb development through regulation of Meis genes

Development ◽  
2000 ◽  
Vol 127 (18) ◽  
pp. 3961-3970 ◽  
Author(s):  
N. Mercader ◽  
E. Leonardo ◽  
M.E. Piedra ◽  
C. Martinez-A ◽  
M.A. Ros ◽  
...  
Keyword(s):  
Limb Development ◽  
Fibroblast Growth ◽  
Specific Function ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Vertebrate Limb ◽  
Proximal Determinant ◽  
Vertebrate Limb Development ◽  
Limb Initiation

Vertebrate limbs develop in a temporal proximodistal sequence, with proximal regions specified and generated earlier than distal ones. Whereas considerable information is available on the mechanisms promoting limb growth, those involved in determining the proximodistal identity of limb parts remain largely unknown. We show here that retinoic acid (RA) is an upstream activator of the proximal determinant genes Meis1 and Meis2. RA promotes proximalization of limb cells and endogenous RA signaling is required to maintain the proximal Meis domain in the limb. RA synthesis and signaling range, which initially span the entire lateral plate mesoderm, become restricted to proximal limb domains by the apical ectodermal ridge (AER) activity following limb initiation. We identify fibroblast growth factor (FGF) as the main molecule responsible for this AER activity and propose a model integrating the role of FGF in limb cell proliferation, with a specific function in promoting distalization through inhibition of RA production and signaling.

Failure of ventral closure and axial rotation in embryos lacking the proprotein convertase Furin

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 4863-4876 ◽  
Author(s):  
A.J. Roebroek ◽  
L. Umans ◽  
I.G. Pauli ◽  
E.J. Robertson ◽  
F. van Leuven ◽  
...  
Keyword(s):  
Axial Rotation ◽  
Marker Genes ◽  
Loss Of Function ◽  
Heart Tube ◽  
Lateral Plate ◽  
Form Analysis ◽  
Left Right Asymmetry ◽  
Gut Endoderm ◽  
Endothelial Precursors

We have examined the role of Furin in postimplantation-stage mouse embryos by analyzing both the expression pattern of fur mRNA and the developmental consequences of a loss-of-function mutation at the fur locus. At early stages (day 7.5), fur mRNA is abundant in extraembryonic endoderm and mesoderm, anterior visceral endoderm, and in precardiac mesoderm. 1 day later fur is expressed throughout the heart tube and in the lateral plate mesoderm, notochordal plate and definitive gut endoderm. Embryos lacking Furin die between days 10.5 and 11.5, presumably due to hemodynamic insufficiency associated with severe ventral closure defects and the failure of the heart tube to fuse and undergo looping morphogenesis. Morphogenesis of the yolk sac vasculature is also abnormal, although blood islands and endothelial precursors form. Analysis of cardiac and endodermal marker genes shows that while both myocardial precursors and definitive endoderm cells are specified, their numbers and migratory properties are compromised. Notably, mutant embryos fail to undergo axial rotation, even though Nodal and eHand, two molecular markers of left-right asymmetry, are appropriately expressed. Overall, the present data identify Furin as an important activator of signals responsible for ventral closure and embryonic turning.

scholarly journals Gut endoderm is involved in the transfer of left-right asymmetry from the node to the lateral plate mesoderm in the mouse embryo

Development ◽  
2012 ◽  
Vol 139 (13) ◽  
pp. 2426-2435 ◽  
Author(s):  
R. S. Saund ◽  
M. Kanai-Azuma ◽  
Y. Kanai ◽  
I. Kim ◽  
M. T. Lucero ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Left Right Asymmetry ◽  
Gut Endoderm

scholarly journals Gdf3 is required for robust Nodal signaling during germ layer formation and left-right patterning

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jose L Pelliccia ◽  
Granton A Jindal ◽  
Rebecca D Burdine
Keyword(s):  
Embryonic Development ◽  
Nodal Signaling ◽  
Lateral Plate Mesoderm ◽  
Embryonic Patterning ◽  
Lateral Plate ◽  
Mesoderm Formation ◽  
Germ Layer Formation ◽  
Multiple Stages ◽  
Tgfβ Superfamily

Vertebrate embryonic patterning depends on signaling from Nodal, a TGFβ superfamily member. There are three Nodal orthologs in zebrafish; southpaw directs left-right asymmetries, while squint and cyclops function earlier to pattern mesendoderm. TGFβ member Vg1 is implicated in mesoderm formation but the role of the zebrafish ortholog, Growth differentiation factor 3 (Gdf3), has not been fully explored. We show that zygotic expression of gdf3 is dispensable for embryonic development, while maternally deposited gdf3 is required for mesendoderm formation and dorsal-ventral patterning. We further show that Gdf3 can affect left-right patterning at multiple stages, including proper development of regional cell morphology in Kupffer’s vesicle and the establishment of southpaw expression in the lateral plate mesoderm. Collectively, our data indicate that gdf3 is critical for robust Nodal signaling at multiple stages in zebrafish embryonic development.

Not Just Inductive: A Critical Mechanical Role for the Endoderm During Heart Tube Assembly

2012 ◽  
Author(s):  
Victor D. Varner ◽  
Larry A. Taber
Keyword(s):  
Close Contact ◽  
Ventral Side ◽  
Lateral Plate Mesoderm ◽  
Heart Tube ◽  
Lateral Plate ◽  
Cardiac Progenitors ◽  
Cardiac Specification ◽  
Tube Assembly ◽  
Heart Fields

The heart is the first functioning organ to form during development. Similar to other organ primordia, the embryonic heart forms as a simple tube — in this case, a straight muscle-wrapped tube situated on the ventral side of the embryo. During gastrulation, the cardiac progenitors reside in the lateral plate mesoderm but maintain close contact with the underlying endoderm. In amniotes, these bilateral heart fields are initially organized as a pair of flat epithelia that move toward the embryonic midline and fuse above the anterior intestinal portal (AIP) to form the heart tube. This medial motion is typically attributed to active mesodermal migration over the underlying endoderm. In this view, the role of the endoderm is two-fold: to serve as a mechanically passive substrate for the crawling mesoderm and to secrete various growth factors necessary for cardiac specification and differentiation.

The mesenchymal factor, FGF10, initiates and maintains the outgrowth of the chick limb bud through interaction with FGF8, an apical ectodermal factor

Development ◽  
1997 ◽  
Vol 124 (11) ◽  
pp. 2235-2244 ◽  
Author(s):  
H. Ohuchi ◽  
T. Nakagawa ◽  
A. Yamamoto ◽  
A. Araga ◽  
T. Ohata ◽  
...  
Keyword(s):  
Sonic Hedgehog ◽  
Limb Bud ◽  
Fibroblast Growth ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Bud Formation ◽  
Limb Mesenchyme ◽  
Vertebrate Limb ◽  
Fgf10 Expression ◽  
Zone Of Polarizing Activity

Vertebrate limb formation has been known to be initiated by a factor(s) secreted from the lateral plate mesoderm. In this report, we provide evidence that a member of the fibroblast growth factor (FGF) family, FGF10, emanates from the prospective limb mesoderm to serve as an endogenous initiator for limb bud formation. Fgf10 expression in the prospective limb mesenchyme precedes Fgf8 expression in the nascent apical ectoderm. Ectopic application of FGF10 to the chick embryonic flank can induce Fgf8 expression in the adjacent ectoderm, resulting in the formation of an additional complete limb. Expression of Fgf10 persists in the mesenchyme of the established limb bud and appears to interact with Fgf8 in the apical ectoderm and Sonic hedgehog in the zone of polarizing activity. These results suggest that FGF10 is a key mesenchymal factor involved in the initial budding as well as the continuous outgrowth of vertebrate limbs.

Hindlimb patterning and mandible development require the Ptx1 gene

Development ◽  
1999 ◽  
Vol 126 (9) ◽  
pp. 1805-1810 ◽  
Author(s):  
C. Lanctot ◽  
A. Moreau ◽  
M. Chamberland ◽  
M.L. Tremblay ◽  
J. Drouin
Keyword(s):  
Gene Knockout ◽  
Proximal Part ◽  
Branchial Arch ◽  
Dorsal Side ◽  
Lateral Plate Mesoderm ◽  
Lateral Plate ◽  
Similar Time ◽  
The Right ◽  
Tetrapod Evolution

The restricted expression of the Ptx1 (Pitx1) gene in the posterior half of the lateral plate mesoderm has suggested that it may play a role in specification of posterior structures, in particular, specification of hindlimb identity. Ptx1 is also expressed in the most anterior ectoderm, the stomodeum, and in the first branchial arch. Ptx1 expression overlaps with that of Ptx2 in stomodeum and in posterior left lateral plate mesoderm. We now show that targeted inactivation of the mouse Ptx1 gene severely impairs hindlimb development: the ilium and knee cartilage are absent and the long bones are underdeveloped. Greater reduction of the right femur size in Ptx1 null mice suggests partial compensation by Ptx2 on the left side. The similarly sized tibia and fibula of mutant hindlimbs may be taken to resemble forelimb bones: however, the mutant limb buds appear to have retained their molecular identity as assessed by forelimb expression of Tbx5 and by hindlimb expression of Tbx4, even though Tbx4 expression is decreased in Ptx1 null mice. The hindlimb defects appear to be, at least partly, due to abnormal chondrogenesis. Since the most affected structures derive from the dorsal side of hindlimb buds, the data suggest that Ptx1 is responsible for patterning of these dorsal structures and that as such it may control development of hindlimb-specific features. Ptx1 inactivation also leads to loss of bones derived from the proximal part of the mandibular mesenchyme. The dual role of Ptx1 revealed by the gene knockout may reflect features of the mammalian jaw and hindlimbs that were acquired at a similar time during tetrapod evolution.

scholarly journals Unexpected contribution of fibroblasts to muscle lineage as a mechanism for limb muscle patterning

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Joana Esteves de Lima ◽  
Cédrine Blavet ◽  
Marie-Ange Bonnin ◽  
Estelle Hirsinger ◽  
Glenda Comai ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Lineage Tracing ◽  
Myotendinous Junction ◽  
Genetic Lineage ◽  
Limb Muscle ◽  
Lateral Plate Mesoderm ◽  
Loss Of Function ◽  
Sequencing Data ◽  
Lateral Plate ◽  
Bmp Signalling

AbstractPositional information driving limb muscle patterning is contained in connective tissue fibroblasts but not in myogenic cells. Limb muscles originate from somites, while connective tissues originate from lateral plate mesoderm. With cell and genetic lineage tracing we challenge this model and identify an unexpected contribution of lateral plate-derived fibroblasts to the myogenic lineage, preferentially at the myotendinous junction. Analysis of single-cell RNA-sequencing data from whole limbs at successive developmental stages identifies a population displaying a dual muscle and connective tissue signature. BMP signalling is active in this dual population and at the tendon/muscle interface. In vivo and in vitro gain- and loss-of-function experiments show that BMP signalling regulates a fibroblast-to-myoblast conversion. These results suggest a scenario in which BMP signalling converts a subset of lateral plate mesoderm-derived cells to a myogenic fate in order to create a boundary of fibroblast-derived myonuclei at the myotendinous junction that controls limb muscle patterning.

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 Cohesin Components Stag1 and Stag2 Differentially Influence Haematopoietic Mesoderm Development in Zebrafish Embryos

2020 ◽  
Vol 8 ◽  
Author(s):  
Sarada Ketharnathan ◽  
Anastasia Labudina ◽  
Julia A. Horsfield
Keyword(s):  
Expression Patterns ◽  
Regulation Of Gene Expression ◽  
Three Dimensional ◽  
Genetic Dissection ◽  
Lateral Plate Mesoderm ◽  
Loss Of Function ◽  
Lateral Plate ◽  
Mesoderm Development ◽  
The Individual ◽  
Primitive Erythropoiesis

Cohesin is a multiprotein complex made up of core subunits Smc1, Smc3, and Rad21, and either Stag1 or Stag2. Normal haematopoietic development relies on crucial functions of cohesin in cell division and regulation of gene expression via three-dimensional chromatin organization. Cohesin subunit STAG2 is frequently mutated in myeloid malignancies, but the individual contributions of Stag variants to haematopoiesis or malignancy are not fully understood. Zebrafish have four Stag paralogues (Stag1a, Stag1b, Stag2a, and Stag2b), allowing detailed genetic dissection of the contribution of Stag1-cohesin and Stag2-cohesin to development. Here we characterize for the first time the expression patterns and functions of zebrafish stag genes during embryogenesis. Using loss-of-function CRISPR-Cas9 zebrafish mutants, we show that stag1a and stag2b contribute to primitive embryonic haematopoiesis. Both stag1a and stag2b mutants present with erythropenia by 24 h post-fertilization. Homozygous loss of either paralogue alters the number of haematopoietic/vascular progenitors in the lateral plate mesoderm. The lateral plate mesoderm zone of scl-positive cells is expanded in stag1a mutants with concomitant loss of kidney progenitors, and the number of spi1-positive cells are increased, consistent with skewing toward primitive myelopoiesis. In contrast, stag2b mutants have reduced haematopoietic/vascular mesoderm and downregulation of primitive erythropoiesis. Our results suggest that Stag1 and Stag2 proteins cooperate to balance the production of primitive haematopoietic/vascular progenitors from mesoderm.

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