scholarly journals Specification of cell fate along the proximal-distal axis in the developing chick limb bud

Development ◽  
2007 ◽  
Vol 134 (7) ◽  
pp. 1397-1406 ◽  
Author(s):  
K. Sato ◽  
Y. Koizumi ◽  
M. Takahashi ◽  
A. Kuroiwa ◽  
K. Tamura
Keyword(s):  
Cell Fate ◽  
Limb Bud

scholarly journals Plasticity of proximal–distal cell fate in the mammalian limb bud

2008 ◽  
Vol 313 (1) ◽  
pp. 225-233 ◽  
Author(s):  
Laurie A. Wyngaarden ◽  
Sevan Hopyan
Keyword(s):  
Cell Fate ◽  
Limb Bud ◽  
Distal Cell

Retinoic acid induces a pattern of digits in anterior half wing buds that lack the zone of polarizing activity

Development ◽  
1989 ◽  
Vol 107 (4) ◽  
pp. 863-867 ◽  
Author(s):  
G. Eichele
Keyword(s):  
Retinoic Acid ◽  
Cell Fate ◽  
Anterior Margin ◽  
Limb Bud ◽  
Posterior Half ◽  
Anterior Half ◽  
Zone Of Polarizing Activity

Wing buds whose posterior half is excised, develop into wings lacking distal structures. However, such experimentally generated preaxial half wing buds can be rescued by implanting a retinoic-acid-releasing bead at their anterior margin. The polarity of the pattern that originates from preaxial half wing buds is reversed. For example, instead of a 234 digit pattern typical for normal wings, the order of digits is 432. This result implies that retinoic acid has the capacity to reprogram anterior limb bud tissue, and that the resulting change in cell fate does not depend on the presence of posterior tissue regions such as the zone of polarizing activity (ZPA).

scholarly journals SOXC proteins amplify canonical WNT signaling to secure nonchondrocytic fates in skeletogenesis

2014 ◽  
Vol 207 (5) ◽  
pp. 657-671 ◽  
Author(s):  
Pallavi Bhattaram ◽  
Alfredo Penzo-Méndez ◽  
Kenji Kato ◽  
Kaustav Bandyopadhyay ◽  
Abhilash Gadi ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Wnt Signaling ◽  
Cell Fate ◽  
Mouse Embryo ◽  
Limb Bud ◽  
Adenomatous Polyposis ◽  
Polyposis Coli ◽  
Canonical Wnt Signaling ◽  
Limiting Step ◽  
Canonical Wnt

Canonical WNT signaling stabilizes β-catenin to determine cell fate in many processes from development onwards. One of its main roles in skeletogenesis is to antagonize the chondrogenic transcription factor SOX9. We here identify the SOXC proteins as potent amplifiers of this pathway. The SOXC genes, i.e., Sox4, Sox11, and Sox12, are coexpressed in skeletogenic mesenchyme, including presumptive joints and perichondrium, but not in cartilage. Their inactivation in mouse embryo limb bud caused massive cartilage fusions, as joint and perichondrium cells underwent chondrogenesis. SOXC proteins govern these cells cell autonomously. They replace SOX9 in the adenomatous polyposis coli–Axin destruction complex and therein inhibit phosphorylation of β-catenin by GSK3. This inhibition, a crucial, limiting step in canonical WNT signaling, thus becomes a constitutive event. The resulting SOXC/canonical WNT-mediated synergistic stabilization of β-catenin contributes to efficient repression of Sox9 in presumptive joint and perichondrium cells and thereby ensures proper delineation and articulation of skeletal primordia. This synergy may determine cell fate in many processes besides skeletogenesis.

Dorso-ventral ectodermal compartments and origin of apical ectodermal ridge in developing chick limb

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4547-4556 ◽  
Author(s):  
M. Altabef ◽  
J.D. Clarke ◽  
C. Tickle
Keyword(s):  
Cell Fate ◽  
Apical Ectodermal Ridge ◽  
The Body ◽  
Limb Bud ◽  
Mesodermal Cell ◽  
Cell Lineages ◽  
Compartment Boundary ◽  
Dorsal Ectoderm ◽  
Neural Ectoderm ◽  
Vertebrate Embryos

We wish to understand how limbs are positioned with respect to the dorso-ventral axis of the body in vertebrate embryos, and how different regions of limb bud ectoderm, i.e. dorsal ectoderm, apical ridge and ventral ectoderm, originate. Signals from dorsal and ventral ectoderm control dorso-ventral patterning while the apical ectodermal ridge (AER) controls bud outgrowth and patterning along the proximo-distal axis. We show, using cell-fate tracers, the existence of two distinct ectodermal compartments, dorsal versus ventral, in both presumptive limb and flank of early chick embryos. This organisation of limb ectoderm is the first direct evidence, in vertebrates, of compartments in non-neural ectoderm. Since the apical ridge appears to be confined to this compartment boundary, this positions the limb. The mesoderm, unlike the ectoderm, does not contain two separate dorsal and ventral cell lineages, suggesting that dorsal and ventral ectoderm compartments may be important to ensure appropriate control of mesodermal cell fate. Surprisingly, we also show that cells which form the apical ridge are initially scattered in a wide region of early ectoderm and that both dorsal and ventral ectoderm cells contribute to the apical ridge, intermingling to some extent within it.

scholarly journals Cell fate in the chick limb bud and relationship to gene expression

Development ◽  
1997 ◽  
Vol 124 (10) ◽  
pp. 1909-1918 ◽  
Author(s):  
N. Vargesson ◽  
J.D. Clarke ◽  
K. Vincent ◽  
C. Coles ◽  
L. Wolpert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Posterior Margin ◽  
Cell Lineage ◽  
Limb Bud ◽  
Cell Populations ◽  
Apical Region ◽  
Vertebrate Limb ◽  
Wing Bud ◽  
The Relationship

We have produced detailed fate maps for mesenchyme and apical ridge of a stage 20 chick wing bud. The fate maps of the mesenchyme show that most of the wing arises from the posterior half of the bud. Subapical mesenchyme gives rise to digits. Cell populations beneath the ridge in the mid apical region fan out into the anterior tip of the handplate, while posterior cell populations extend right along the posterior margin. Subapical mesenchyme of the leg bud behaves similarly. The absence of anterior bending of posterior cell populations has implications when considering models of vertebrate limb evolution. The fatemaps of the apical ridge show that there is also a marked anterior expansion and cells that were in anterior apical ridge later become incorporated into non-ridge ectoderm along the margin of the bud. Mesenchyme and apical ridge do not expand in concert--the apical ridge extends more anteriorly. We used the fatemaps to investigate the relationship between cell lineage and elaboration of Hoxd-13 and Fgf-4 domains. Hoxd-13 and Fgf-4 are initially expressed posteriorly until about the mid-point of the early wing bud in mesenchyme and apical ridge respectively. Later in development, the genes come to be expressed throughout most of the handplate and apical ridge respectively. We found that at the proximal edge of the Hoxd-13 domain, cell populations stopped expressing the gene as development proceeded and found no evidence that the changes in extent of the domains were due to initiation of gene expression in anterior cells. Instead the changes in extent of expression fit with the fate maps and can be attributed to expansion and fanning out of cell populations initially expressing the genes.

scholarly journals SCA-1/Ly6A Mesodermal Skeletal Progenitor Subpopulations Reveal Differential Commitment of Early Limb Bud Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Jessica Cristina Marín-Llera ◽  
Carlos Ignacio Lorda-Diez ◽  
Juan Mario Hurle ◽  
Jesús Chimal-Monroy
Keyword(s):  
Cell Fate ◽  
Limb Development ◽  
Developmental Stages ◽  
Limb Bud ◽  
Its Gene ◽  
Undifferentiated Cells ◽  
Advanced Stages ◽  
Cell Subpopulations ◽  
Inductive Signals

At early developmental stages, limb bud mesodermal undifferentiated cells are morphologically indistinguishable. Although the identification of several mesodermal skeletal progenitor cell populations has been recognized, in advanced stages of limb development here we identified and characterized the differentiation hierarchy of two new early limb bud subpopulations of skeletal progenitors defined by the differential expression of the SCA-1 marker. Based on tissue localization of the mesenchymal stromal cell-associated markers (MSC-am) CD29, Sca-1, CD44, CD105, CD90, and CD73, we identified, by multiparametric analysis, the presence of cell subpopulations in the limb bud capable of responding to inductive signals differentially, namely, sSca+ and sSca– cells. In concordance with its gene expression profile, cell cultures of the sSca+ subpopulation showed higher osteogenic but lower chondrogenic capacity than those of sSca–. Interestingly, under high-density conditions, fibroblast-like cells in the sSca+ subpopulation were abundant. Gain-of-function employing micromass cultures and the recombinant limb assay showed that SCA-1 expression promoted tenogenic differentiation, whereas chondrogenesis is delayed. This model represents a system to determine cell differentiation and morphogenesis of different cell subpopulations in similar conditions like in vivo. Our results suggest that the limb bud is composed of a heterogeneous population of progenitors that respond differently to local differentiation inductive signals in the early stages of development, where SCA-1 expression may play a permissive role during cell fate.

Analysis of the tendon cell fate using Scleraxis, a specific marker for tendons and ligaments

Development ◽  
2001 ◽  
Vol 128 (19) ◽  
pp. 3855-3866 ◽  
Author(s):  
Ronen Schweitzer ◽  
Jay H. Chyung ◽  
Lewis C. Murtaugh ◽  
Ava E. Brent ◽  
Vicki Rosen ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Bmp Signaling ◽  
Limb Bud ◽  
Bhlh Transcription Factor ◽  
Specific Marker ◽  
Connective Tissues ◽  
Endogenous Expression ◽  
Morphogenetic Protein ◽  
Early Markers

Little is known about the genesis and patterning of tendons and other connective tissues, mostly owing to the absence of early markers. We have found that Scleraxis, a bHLH transcription factor, is a highly specific marker for all the connective tissues that mediate attachment of muscle to bone in chick and mouse, including the limb tendons, and show that early scleraxis expression marks the progenitor cell populations for these tissues. In the early limb bud, the tendon progenitor population is found in the superficial proximomedial mesenchyme. Using the scleraxis gene as a marker we show that these progenitors are induced by ectodermal signals and restricted by bone morphogenetic protein (BMP) signaling within the mesenchyme. Application of Noggin protein antagonizes this endogenous BMP activity and induces ectopic scleraxis expression. However, the presence of excess tendon progenitors does not lead to the production of additional or longer tendons, indicating that additional signals are required for the final formation of a tendon. Finally, we show that the endogenous expression of noggin within the condensing digit cartilage contributes to the induction of distal tendons.

scholarly journals Cell lineage specification during development of the anterior lateral plate mesoderm and forelimb field

2022 ◽  
Author(s):  
Axel H Newton ◽  
Sarah M Williams ◽  
Andrew T Major ◽  
Craig A Smith
Keyword(s):  
Cell Fate ◽  
Cell Lineage ◽  
Cell Types ◽  
Limb Bud ◽  
Signalling Pathways ◽  
Urogenital System ◽  
Lateral Plate Mesoderm ◽  
Mature Cell ◽  
Lineage Specification ◽  
Lateral Plate

The lateral plate mesoderm (LPM) is a transient embryonic tissue that gives rise to a diverse range of mature cell types, including the cardiovascular system, the urogenital system, endoskeleton of the limbs, and mesenchyme of the gut. While the genetic processes that drive development of these tissues are well defined, the early cell fate choices underlying LPM development and specification are poorly understood. In this study, we utilize single-cell transcriptomics to define cell lineage specification during development of the anterior LPM and the forelimb field in the chicken embryo. We identify the molecular pathways directing differentiation of the aLPM towards a somatic or splanchnic cell fate, and subsequent emergence of the forelimb mesenchyme. We establish the first transcriptional atlas of progenitor, transitional and mature cell types throughout the early forelimb field and uncover the global signalling pathways which are active during LPM differentiation and forelimb initiation. Specification of the somatic and splanchnic LPM from undifferentiated mesoderm utilizes distinct signalling pathways and involves shared repression of early mesodermal markers, followed by activation of lineage-specific gene modules. We identify rapid activation of the transcription factor TWIST1 in the somatic LPM preceding activation of known limb initiation genes, such as TBX5, which plays a likely role in epithelial-to-mesenchyme transition of the limb bud mesenchyme. Furthermore, development of the somatic LPM and limb is dependent on ectodermal BMP signalling, where BMP antagonism reduces expression of key somatic LPM and limb genes to inhibit formation of the limb bud mesenchyme. Together, these findings provide new insights into molecular mechanisms that drive fate cell choices during specification of the aLPM and forelimb initiation.

Centrosome Aurora A gradient ensures single polarity axis in C. elegans embryos

2020 ◽  
Vol 48 (3) ◽  
pp. 1243-1253 ◽  
Author(s):  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Symmetry Breaking ◽  
Cell Fate ◽  
Cell Cortex ◽  
Axis Formation ◽  
Aurora A Kinase ◽  
Aurora A ◽  
C Elegans ◽  
Cell Embryo ◽  
Polarity Establishment

Cellular asymmetries are vital for generating cell fate diversity during development and in stem cells. In the newly fertilized Caenorhabditis elegans embryo, centrosomes are responsible for polarity establishment, i.e. anterior–posterior body axis formation. The signal for polarity originates from the centrosomes and is transmitted to the cell cortex, where it disassembles the actomyosin network. This event leads to symmetry breaking and the establishment of distinct domains of evolutionarily conserved PAR proteins. However, the identity of an essential component that localizes to the centrosomes and promotes symmetry breaking was unknown. Recent work has uncovered that the loss of Aurora A kinase (AIR-1 in C. elegans and hereafter referred to as Aurora A) in the one-cell embryo disrupts stereotypical actomyosin-based cortical flows that occur at the time of polarity establishment. This misregulation of actomyosin flow dynamics results in the occurrence of two polarity axes. Notably, the role of Aurora A in ensuring a single polarity axis is independent of its well-established function in centrosome maturation. The mechanism by which Aurora A directs symmetry breaking is likely through direct regulation of Rho-dependent contractility. In this mini-review, we will discuss the unconventional role of Aurora A kinase in polarity establishment in C. elegans embryos and propose a refined model of centrosome-dependent symmetry breaking.

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