scholarly journals Successive specification of Drosophila neuroblasts NB 6-4 and NB 7-3 depends on interaction of the segment polarity genes wingless, gooseberry and naked cuticle

Development ◽  
2001 ◽  
Vol 128 (17) ◽  
pp. 3253-3261 ◽  
Author(s):  
Nirupama Deshpande ◽  
Rainer Dittrich ◽  
Gerhard M. Technau ◽  
Joachim Urban
Keyword(s):  
Cell Fate ◽  
Cell Lineage ◽  
Positional Information ◽  
Dorsoventral Patterning ◽  
Expression Domain ◽  
Direct Role ◽  
Segment Polarity Genes ◽  
Segment Polarity ◽  
Unique Identity

The Drosophila central nervous system derives from neural precursor cells, the neuroblasts (NBs), which are born from the neuroectoderm by the process of delamination. Each NB has a unique identity, which is revealed by the production of a characteristic cell lineage and a specific set of molecular markers it expresses. These NBs delaminate at different but reproducible time points during neurogenesis (S1-S5) and it has been shown for early delaminating NBs (S1/S2) that their identities depend on positional information conferred by segment polarity genes and dorsoventral patterning genes. We have studied mechanisms leading to the fate specification of a set of late delaminating neuroblasts, NB 6-4 and NB 7-3, both of which arise from the engrailed (en) expression domain, with NB 6-4 delaminating first. In contrast to former reports, we did not find any evidence for a direct role of hedgehog in the process of NB 7-3 specification. Instead, we present evidence to show that the interplay of the segmentation genes naked cuticle (nkd) and gooseberry (gsb), both of which are targets of wingless (wg) activity, leads to differential commitment to NB 6-4 and NB 7-3 cell fate. In the absence of either nkd or gsb, one NB fate is replaced by the other. However, the temporal sequence of delamination is maintained, suggesting that formation and specification of these two NBs are under independent control.

An axial domain of HOM/Hox gene expression is formed by morphogenetic alignment of independently specified cell lineages in the leech Helobdella

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1839-1849 ◽  
Author(s):  
D. Nardelli-Haefliger ◽  
A.E. Bruce ◽  
M. Shankland
Keyword(s):  
Embryonic Stem ◽  
Cell Lineage ◽  
Homeobox Gene ◽  
Positional Information ◽  
The Other ◽  
Expression Domain ◽  
Hox Gene ◽  
Cell Lineages ◽  
High Level

The homeobox gene Lox2, a member of the HOM/Hox gene class, is expressed in a restricted domain along the anteroposterior (A-P) body axis of the leech Helobdella. The segmental tissues of the leech embryo arise from the parallel merger of five distinct and bilaterally paired cell lineages generated by embryonic stem cells or teloblasts. Injection of cell lineage tracers coupled with anti-LOX2 immunochemistry reveals that all five teloblast lineages generate central nervous system neurons that express the LOX2 protein, and that each lineage expresses LOX2 within a similar domain of body segments. Some lineally identified neurons display anti-LOX2 immunoreactivity over the entire expression domain, but the OM7 neuron has a distinctively high level of LOX2 expression, which is restricted to the seventh midbody ganglion. To ascertain the role of positional information in the axial patterning of LOX2 expression, we performed focal cell ablations that displaced one or another of the teloblast lineages out of segmental register with the other axial tissues. Such displacements brought about a corresponding shift in the LOX2 expression of the perturbed lineage, and had little or no effect on the LOX2 expression of the other, unperturbed lineages. This result indicates that the axial domain of LOX2 expression is not specified by positional cues acting coordinately across the various teloblast lineages, nor would it seem that the expression domain is imprinted from one lineage to the others. Rather, the different teloblast lineages acquire their axial patterns independently, and secondarily bring these patterns into alignment along the A-P axis through a process of morphogenetic assembly.

Role of segment polarity genes in the definition and maintenance of cell states in the Drosophila embryo

Development ◽  
1988 ◽  
Vol 103 (1) ◽  
pp. 157-170 ◽  
Author(s):  
A. Martinez Arias ◽  
N.E. Baker ◽  
P.W. Ingham
Keyword(s):  
Positional Information ◽  
Drosophila Embryo ◽  
Gene Products ◽  
Segment Polarity Genes ◽  
Restricted Domains ◽  
Segment Polarity ◽  
Mutant Phenotypes ◽  
Segment Polarity Gene ◽  
Polarity Gene

Segment polarity genes are expressed and required in restricted domains within each metameric unit of the Drosophila embryo. We have used the expression of two segment polarity genes engrailed (en) and wingless (wg) to monitor the effects of segment polarity mutants on the basic metameric pattern. Absence of patched (ptc) or naked (nkd) functions triggers a novel sequence of en and wg patterns. In addition, although wg and en are not expressed on the same cells absence of either one has effects on the expression of the other. These observations, together with an analysis of mutant phenotypes during development, lead us to suggest that positional information is encoded in cell states defined and maintained by the activity of segment polarity gene products.

scholarly journals EBF1 is expressed in pericytes and contributes to pericyte cell commitment

2021 ◽  
Author(s):  
Francesca Pagani ◽  
Elisa Tratta ◽  
Patrizia Dell’Era ◽  
Manuela Cominelli ◽  
Pietro Luigi Poliani
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Mesenchymal Stem Cells ◽  
B Cell ◽  
Cell Fate ◽  
Early Stage ◽  
Cell Lineage ◽  
Cell Maturation ◽  
Cell Commitment

AbstractEarly B-cell factor-1 (EBF1) is a transcription factor with an important role in cell lineage specification and commitment during the early stage of cell maturation. Originally described during B-cell maturation, EBF1 was subsequently identified as a crucial molecule for proper cell fate commitment of mesenchymal stem cells into adipocytes, osteoblasts and muscle cells. In vessels, EBF1 expression and function have never been documented. Our data indicate that EBF1 is highly expressed in peri-endothelial cells in both tumor vessels and in physiological conditions. Immunohistochemistry, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and fluorescence-activated cell sorting (FACS) analysis suggest that EBF1-expressing peri-endothelial cells represent bona fide pericytes and selectively express well-recognized markers employed in the identification of the pericyte phenotype (SMA, PDGFRβ, CD146, NG2). This observation was also confirmed in vitro in human placenta-derived pericytes and in human brain vascular pericytes (HBVP). Of note, in accord with the key role of EBF1 in the cell lineage commitment of mesenchymal stem cells, EBF1-silenced HBVP cells showed a significant reduction in PDGFRβ and CD146, but not CD90, a marker mostly associated with a prominent mesenchymal phenotype. Moreover, the expression levels of VEGF, angiopoietin-1, NG2 and TGF-β, cytokines produced by pericytes during angiogenesis and linked to their differentiation and activation, were also significantly reduced. Overall, the data suggest a functional role of EBF1 in the cell fate commitment toward the pericyte phenotype.

The Role of Nuclear Stiffness and Resilience in Mechanotransduction

2010 ◽  
Author(s):  
Kris Noel Dahl ◽  
Elizabeth A. Booth-Gauthier ◽  
Alexandre J. S. Ribeiro ◽  
Zhixia Zhong
Keyword(s):  
Gene Expression ◽  
Cell Fate ◽  
Live Cell Imaging ◽  
Volume Fraction ◽  
Direct Role ◽  
Intact Cells ◽  
Large Volume Fraction ◽  
Nuclear Mechanics ◽  
Model Cell

Mechanical force is found to be increasingly important during development and for proper homeostatic maintenance of cells and tissues. The nucleus occupies a large volume fraction of the cell and is interconnected with the cytoskeleton. Here, to determine the direct role of the nucleus itself in converting forces to changes in gene expression, also known as, mechanotransduction, we examine changes in nuclear mechanics and gene reorganization associated with cell fate and with extracellular force. We measure mechanics of nuclei in many model cell systems using micropipette aspiration to show changes in nuclear mechanics. In intact cells we characterize the rheological changes induced in the genome organization with live cell imaging and particle tracking, and we suggest how these changes relate to gene expression.

The segment polarity gene armadillo interacts with the wingless signaling pathway in both embryonic and adult pattern formation

Development ◽  
1991 ◽  
Vol 111 (4) ◽  
pp. 1029-1043 ◽  
Author(s):  
M. Peifer ◽  
C. Rauskolb ◽  
M. Williams ◽  
B. Riggleman ◽  
E. Wieschaus
Keyword(s):  
Pattern Formation ◽  
Imaginal Discs ◽  
Protein Accumulation ◽  
Segment Polarity Genes ◽  
Adult Pattern ◽  
Segment Polarity ◽  
Lethal Allele ◽  
Segment Polarity Gene ◽  
Polarity Gene

The segment polarity genes of Drosophila were initially defined as genes required for pattern formation within each embryonic segment. Some of these genes also function to establish the pattern of the adult cuticle. We have examined the role of the armadillo (arm) gene in this latter process. We confirmed and extended earlier findings that arm and the segment polarity gene wingless are very similar in their effects on embryonic development. We next discuss the role of arm in pattern formation in the imaginal discs, as determined by using a pupal lethal allele, by analyzing clones of arm mutant tissue in imaginal discs, and by using a transposon carrying arm to produce adults with a reduced level of arm. Together, these experiments established that arm is required for the development of all imaginal discs. The requirement for arm varies along the dorsal-ventral and proximal-distal axes. Cells that require the highest levels of arm are those that express the wingless gene. Further, animals with reduced arm levels have phenotypes that resemble those of weak alleles of wingless. We present a description of the patterns of arm protein accumulation in imaginal discs. Finally, we discuss the implications of these results for the role of arm and wingless in pattern formation.

Differential effects of EGF receptor signalling on neuroblast lineages along the dorsoventral axis of the Drosophila CNS

Development ◽  
1998 ◽  
Vol 125 (17) ◽  
pp. 3291-3299 ◽  
Author(s):  
G. Udolph ◽  
J. Urban ◽  
G. Rusing ◽  
K. Luer ◽  
G.M. Technau
Keyword(s):  
Cell Fate ◽  
Egf Receptor ◽  
Cell Lineage ◽  
Dorsoventral Patterning ◽  
Cell Fates ◽  
Regulatory Pathways ◽  
Differential Effects ◽  
Receptor Signalling ◽  
Cns Midline ◽  
Lineage Analysis

The Drosophila ventral nerve cord derives from a stereotype population of about 30 neural stem cells, the neuroblasts, per hemineuromere. Previous experiments provided indications for inductive signals at ventral sites of the neuroectoderm that confer neuroblast identities. Using cell lineage analysis, molecular markers and cell transplantation, we show here that EGF receptor signalling plays an instructive role in CNS patterning and exerts differential effects on dorsoventral subpopulations of neuroblasts. The Drosophila EGF receptor (DER) is capable of cell autonomously specifiying medial and intermediate neuroblast cell fates. DER signalling appears to be most critical for proper development of intermediate neuroblasts and less important for medial neuroblasts. It is not required for lateral neuroblast lineages or for cells to adopt CNS midline cell fate. Thus, dorsoventral patterning of the CNS involves both DER-dependent and -independent regulatory pathways. Furthermore, we discuss the possibility that different phases of DER activation exist during neuroectodermal patterning with an early phase independent of midline-derived signals.

Eto2/MTG16 Regulates E-Protein Activity and Subset Specification in Dendritic Cell Development

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1229-1229
Author(s):  
Hiyaa Singhee Ghosh ◽  
Kang Liu ◽  
Scott Hiebert ◽  
Boris Reizis
Keyword(s):  
Dendritic Cells ◽  
Transcription Factors ◽  
T Cell ◽  
Dendritic Cell ◽  
Cell Fate ◽  
Cell Lineage ◽  
Transcriptional Regulators ◽  
E Proteins ◽  
E Protein

Abstract Abstract 1229 Eto-family proteins were first discovered as translocation fusion in AML1 (Runx1), a gene most frequently disrupted in human leukemia. Of the translocations that disrupt the AML1 gene in leukemia, Eto1(MTG8)/AML1 translocation accounts for ∼15% of Acute Myeloid Leukemia (AML). The Eto-family proteins function as transcriptional co-repressors that bind to DNA-binding transcription factors to regulate their target genes. Eto2 (MTG16) is an Eto-family member implicated in secondary or therapy-related AML, although recent reports provide evidence for Eto2/MTG16 translocations in de novo AML as well. Furthermore, recent studies have highlighted a role for MTG16 in HSC self renewal and T cell lineage specification, indicating its emerging role overall in hematopoiesis. The co-repressor function of Eto for E-proteins has been described previously in the context of Eto/AML1 fusion proteins. E-proteins are a class of basic-helix-loop-helix (bHLH) transcription factors that play an important role in hematopoiesis. Among the E-protein family, the role of E2A has been extensively studied in B and T cell development. Recently, our lab discovered the specific requirement of the E-protein E2-2 in the development of Plasmacytoid Dendritic Cells (pDC). pDC are the professional interferon producing (IPC) cells of our immune system important in anti-viral, anti-tumor and auto-immunity. pDC are a subtype of the antigen-presenting classical Dendritic Cells (cDC) with distinct structural and functional properties. Recently, we demonstrated that the putative cell fate plasticity of pDC was a direct manifestation of continuous E2-2 function. Using pDC-reporter mice in which E2-2 could be inducibly deleted from mature pDC we showed that the continuous expression of E2-2 was required to prevent the conversion of pDC to cDC. Here we report our current studies that investigate the molecular players underlying the E2-2 orchestrated genetic program for pDC cell fate decision and maintenance. Analyzing the transcriptome of the transitioning pDC, we have identified MTG16 as an important player in the fine regulation of DC lineage decisions. Using knock-out and chimeric mice, progenitor studies, promoter and biochemical analyses, we demonstrate MTG16 as an important E2-2 corepressor, promoting E2-2 mediated genetic program. We report that in order to facilitate the pDC cell fate, MTG16 enables E2-2 to suppress the cDC gene expression program, by negatively regulating the E-protein inhibitor Id2. The cell-fate conversion through deletion or overexpression of lineage-deciding transcriptional regulators has been described previously for B- and T cells. Theseh studies highlight the susceptibility of blood cells to aberrant functions of crucial transcriptional regulators, potentially leading to pathologic conditions. Therefore, understanding the interrelationship between the various genetic regulators that control lineage decisions and cell-fate plasticity is cardinal to accurate diagnosis and therapy for hematopoietic pathologies. Our study provides the first evidence for a physiological role of E-protein/Eto-protein interaction in dendritic cell lineage decision. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The Laminar Organization of Piriform Cortex Follows a Selective Developmental and Migratory Program Established by Cell Lineage

2017 ◽  
Vol 29 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Eduardo Martin-Lopez ◽  
Kimiko Ishiguro ◽  
Charles A Greer
Keyword(s):  
Cell Fate ◽  
Functional Organization ◽  
Piriform Cortex ◽  
Cell Lineage ◽  
Afferent Input ◽  
Laminar Organization ◽  
The Past ◽  
Laminar Specificity ◽  
Inside Out

Abstract Piriform cortex (PC) is a 3-layer paleocortex receiving primary afferent input from the olfactory bulb. The past decade has seen significant progress in understanding the synaptic, cellular and functional organization of PC, but PC embryogenesis continues to be enigmatic. Here, using birthdating strategies and clonal analyses, we probed the early development and laminar specificity of neurogenesis/gliogenesis as it relates to the organization of the PC. Our data demonstrate a temporal sequence of laminar-specific neurogenesis following the canonical “inside-out” pattern, with the notable exception of PC Layer II which exhibited an inverse “outside-in” temporal neurogenic pattern. Of interest, we found no evidence of a neurogenic gradient along the anterior to posterior axis, although the timing of neuronal migration and laminar development was delayed rostrally by approximately 24 h. To begin probing if lineage affected cell fate in the PC, we labeled PC neuroblasts using a multicolor technique and analyzed their laminar organization. Our results suggested that PC progenitors were phenotypically committed to reach specific layers early in the development. Collectively, these studies shed new light on the determinants of the laminar specificity of neuronal/glial organization in PC and the likely role of subpopulations of committed progenitors in regulating PC embryogenesis.

scholarly journals Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control

2019 ◽  
Author(s):  
Aaron D. Viny ◽  
Robert L. Bowman ◽  
Yu Liu ◽  
Vincent-Philippe Lavallée ◽  
Shira E. Eisman ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Lineage ◽  
Chromatin Accessibility ◽  
Lineage Specification ◽  
Hematopoietic Stem ◽  
Chip Sequencing ◽  
Cell Fate Decisions ◽  
Transcriptional Dysregulation ◽  
Topologically Associated Domains

AbstractTranscriptional regulators, including the cohesin complex member STAG2, are recurrently mutated in cancer. The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved. We show Stag2 deletion in hematopoietic stem/progenitor cells (HSPC) results in altered hematopoietic function, increased self-renewal, and impaired differentiation. ChIP-sequencing revealed that while Stag2 and Stag1 can bind the same loci, a component of Stag2 binding sites are unoccupied by Stag1 even in Stag2-deficient HSPCs. While concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin accessibility and transcription of lineage-specification genes, including Ebf1 and Pax5, leading to blunted HSPC commitment to the B-cell lineage. Our data illustrate a role for Stag2 in transformation and transcriptional dysregulation distinct from its shared role with Stag1 in chromosomal segregation.One Sentence SummaryStag1 rescues topologically associated domains in the absence of Stag2, but cannot restore chromatin architecture required for hematopoietic lineage commitment

scholarly journals The role of atoh1 genes in the development of the lower rhombic lip during zebrafish hindbrain morphogenesis

2019 ◽  
Author(s):  
Ivan Belzunce ◽  
Cristina Pujades
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Cell Lineage ◽  
Positional Information ◽  
Neuronal Population ◽  
Dependent Manner ◽  
Rhombic Lip ◽  
Differentiation Gene

ABSTRACTBACKGROUNDThe Lower Rhombic Lip (LRL) is a transient neuroepithelial structure of the dorsal hindbrain, which expands from r2 to r7, and gives rise to deep nuclei of the brainstem, such as the vestibular and auditory nuclei and most posteriorly the precerebellar nuclei. Although there is information about the contribution of specific proneural-progenitor populations to specific deep nuclei, and the distinct rhombomeric contribution, little is known about how progenitor cells from the LRL behave during neurogenesis and how their transition into differentiation is regulated.RESULTSIn this work, we investigated the atoh1 gene regulatory network operating in the specification of LRL cells, and the kinetics of cell proliferation and behavior of atoh1a-derivatives by using complementary strategies in the zebrafish embryo. We unveiled that atoh1a is necessary and sufficient for specification of LRL cells by activating atoh1b, which worked as a differentiation gene to transition progenitor cells towards neuron differentiation in a Notch-dependent manner. This cell state transition involved the release of atoh1a-derivatives from the LRL: atoh1a progenitors contributed first to atoh1b cells, which are committed non-proliferative precursors, and to the lhx2b-neuronal lineage as demonstrated by cell fate studies and functional analyses. Using in vivo cell lineage approaches we showed that the proliferative cell capacity, as well as their mode of division, relied on the position of the atoh1a progenitors within the dorsoventral axis.CONCLUSIONSOur data demonstrates that the zebrafish provides an excellent model to study the in vivo behavior of distinct progenitor populations to the final neuronal differentiated pools, and to reveal the subfunctionalization of ortholog genes. Here, we unveil that atoh1a behaves as the cell fate selector gene, whereas atoh1b functions as a neuronal differentiation gene, contributing to the lhx2b neuronal population. atoh1a-progenitor cell dynamics (cell proliferation, cell differentiation, and neuronal migration) relies on their position, demonstrating the challenges that progenitor cells face in computing positional information from a dynamic two-dimensional grid in order to generate the stereotyped neuronal structures in the embryonic hindbrain.

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