scholarly journals Goosecoid is not an essential component of the mouse gastrula organizer but is required for craniofacial and rib development

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 3005-3012 ◽  
Author(s):  
J.A. Rivera-Perez ◽  
M. Mallo ◽  
M. Gendron-Maguire ◽  
T. Gridley ◽  
R.R. Behringer
Keyword(s):  
Organizer Region ◽  
Embryonic Stem ◽  
Homeobox Gene ◽  
Primary Body ◽  
Evolutionarily Conserved ◽  
Vertebrate Embryos ◽  
Organizer Activity ◽  
Craniofacial Defects ◽  
Transplantation Experiments

Goosecoid (gsc) is an evolutionarily conserved homeobox gene expressed in the gastrula organizer region of a variety of vertebrate embryos, including zebrafish, Xenopus, chicken and mouse. To understand the role of gsc during mouse embryogenesis, we generated gsc-null mice by gene targeting in embryonic stem cells. Surprisingly, gsc-null embryos gastrulated and formed the primary body axes; gsc-null mice were born alive but died soon after birth with numerous craniofacial defects. In addition, rib fusions and sternum abnormalities were detected that varied depending upon the genetic background. Transplantation experiments suggest that the ovary does not provide gsc function to rescue gastrulation defects. These results demonstrate that gsc is not essential for organizer activity in the mouse but is required later during embryogenesis for craniofacial and rib cage development.

scholarly journals Neural induction by the node and placode induction by head mesoderm share an initial state resembling neural plate border and ES cells

2017 ◽  
Vol 115 (2) ◽  
pp. 355-360 ◽  
Author(s):  
Katherine E. Trevers ◽  
Ravindra S. Prajapati ◽  
Mark Hintze ◽  
Matthew J. Stower ◽  
Anna C. Strobl ◽  
...  
Keyword(s):  
Time Course ◽  
Es Cells ◽  
Embryonic Stem ◽  
Neural Induction ◽  
Neural Plate ◽  
Initial State ◽  
Head Mesoderm ◽  
Neural Plate Border ◽  
Vertebrate Embryos ◽  
Transplantation Experiments

Around the time of gastrulation in higher vertebrate embryos, inductive interactions direct cells to form central nervous system (neural plate) or sensory placodes. Grafts of different tissues into the periphery of a chicken embryo elicit different responses: Hensen’s node induces a neural plate whereas the head mesoderm induces placodes. How different are these processes? Transcriptome analysis in time course reveals that both processes start by induction of a common set of genes, which later diverge. These genes are remarkably similar to those induced by an extraembryonic tissue, the hypoblast, and are normally expressed in the pregastrulation stage epiblast. Explants of this epiblast grown in the absence of further signals develop as neural plate border derivatives and eventually express lens markers. We designate this state as “preborder”; its transcriptome resembles embryonic stem cells. Finally, using sequential transplantation experiments, we show that the node, head mesoderm, and hypoblast are interchangeable to begin any of these inductions while the final outcome depends on the tissue emitting the later signals.

scholarly journals The homeobox gene Hhex regulates the earliest stages of definitive hematopoiesis

Blood ◽  
2010 ◽  
Vol 116 (8) ◽  
pp. 1254-1262 ◽  
Author(s):  
Helicia Paz ◽  
Maureen R. Lynch ◽  
Clifford W. Bogue ◽  
Judith C. Gasson
Keyword(s):  
Es Cells ◽  
Embryonic Stem ◽  
Homeobox Gene ◽  
Hematopoietic Progenitors ◽  
Hematopoietic Stem ◽  
Molecular Events ◽  
G2 Phase ◽  
Definitive Hematopoiesis

Abstract The development and emergence of the hematopoietic stem cell involves a series of tightly regulated molecular events that are not well characterized. The hematopoietically expressed homeobox (Hhex) gene, a member of the homeobox gene family, is an essential regulator of embryogenesis and hematopoietic progenitor development. To investigate the role of Hhex in hematopoiesis we adapted a murine embryonic stem (ES) cell coculture system, in which ES cells can differentiate into CD41+ and CD45+ hematopoietic progenitors in vitro. Our results show that in addition to delayed hemangioblast development, Hhex−/− ES-derived progeny accumulate as CD41+ and CD41+c-kit+ cells, or the earliest definitive hematopoietic progenitors. In addition, Hhex−/− ES-derived progeny display a significantly reduced ability to develop into mature CD45+ hematopoietic cells. The observed reduction in hematopoietic maturation was accompanied by reduced proliferation, because Hhex−/− CD41+CD45−c-kit+ hematopoietic progenitors accumulated in the G2 phase of the cell cycle. Thus, Hhex is a critical regulator of hematopoietic development and is necessary for the maturation and proliferation of the earliest definitive hematopoietic progenitors.

scholarly journals Ciona embryonic tail bending is driven by asymmetrical notochord contractility and coordinated by epithelial proliferation

Development ◽  
2020 ◽  
Vol 147 (24) ◽  
pp. dev185868 ◽  
Author(s):  
Qiongxuan Lu ◽  
Yuan Gao ◽  
Yuanyuan Fu ◽  
Hongzhe Peng ◽  
Wenjie Shi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Ventral Side ◽  
Epithelial Proliferation ◽  
The People ◽  
Passive Response ◽  
Evolutionarily Conserved ◽  
Morphogenetic Event ◽  
Vertebrate Embryos ◽  
Epidermis Cell

ABSTRACTVentral bending of the embryonic tail within the chorion is an evolutionarily conserved morphogenetic event in both invertebrates and vertebrates. However, the complexity of the anatomical structure of vertebrate embryos makes it difficult to experimentally identify the mechanisms underlying embryonic folding. This study investigated the mechanisms underlying embryonic tail bending in chordates. To further understand the mechanical role of each tissue, we also developed a physical model with experimentally measured parameters to simulate embryonic tail bending. Actomyosin asymmetrically accumulated at the ventral side of the notochord, and cell proliferation of the dorsal tail epidermis was faster than that in the ventral counterpart during embryonic tail bending. Genetic disruption of actomyosin activity and inhibition of cell proliferation dorsally caused abnormal tail bending, indicating that both asymmetrical actomyosin contractility in the notochord and the discrepancy of epidermis cell proliferation are required for tail bending. In addition, asymmetrical notochord contractility was sufficient to drive embryonic tail bending, whereas differential epidermis proliferation was a passive response to mechanical forces. These findings showed that asymmetrical notochord contractility coordinates with differential epidermis proliferation mechanisms to drive embryonic tail bending.This article has an associated ‘The people behind the papers’ interview.

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.

scholarly journals Switching on pluripotency: a perspective on the biological requirement of Nanog

2011 ◽  
Vol 366 (1575) ◽  
pp. 2222-2229 ◽  
Author(s):  
Thorold W. Theunissen ◽  
José C. R. Silva
Keyword(s):  
Transcription Factor ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Primordial Germ Cells ◽  
Embryonic Stem ◽  
Induced Pluripotency ◽  
Somatic Cell Reprogramming ◽  
Evolutionarily Conserved

Pluripotency is a transient cellular state during early development which can be recreated in vitro by direct reprogramming. The molecular mechanisms driving entry into and exit from the pluripotent state are the subject of intense research interest. Here, we review the role of the homeodomain-containing transcription factor Nanog in mammalian embryology and induced pluripotency. Nanog was originally thought to be confined to the maintenance of pluripotency, but recent insights from genetic studies uncovered a new biological function. Embryonic stem cells deficient in Nanog alleles are more prone to differentiate but do not lose pluripotency per se . Instead, Nanog is transiently required for the specification of the naive pluripotent epiblast and development of primordial germ cells. Nanog is also essential to finalize somatic cell reprogramming during induction of pluripotency. We propose that this unique transcription factor acts as a molecular switch to turn on the naive pluripotent programme in mammalian cells. In this context, the capacity of Nanog to resist differentiation can be regarded as recapitulation of effects normally associated with the specification of pluripotency. Pertinent questions are how Nanog specifies naive pluripotency and whether this mechanism is evolutionarily conserved.

scholarly journals The role of nucleotide excision repair in protecting embryonic stem cells from genotoxic effects of UV-induced DNA damage

1999 ◽  
Vol 27 (16) ◽  
pp. 3276-3282 ◽  
Author(s):  
P. P. H. Van Sloun ◽  
J. G. Jansen ◽  
G. Weeda ◽  
L. H. F. Mullenders ◽  
A. A. van Zeeland ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Damage ◽  
Embryonic Stem Cells ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Embryonic Stem ◽  
Genotoxic Effects ◽  
Nucleotide Excision

scholarly journals The chromosomal protein SMCHD1 regulates DNA methylation and the 2c-like state of embryonic stem cells by antagonizing TET proteins

2021 ◽  
Vol 7 (4) ◽  
pp. eabb9149
Author(s):  
Zhijun Huang ◽  
Jiyoung Yu ◽  
Wei Cui ◽  
Benjamin K. Johnson ◽  
Kyunggon Kim ◽  
...  
Keyword(s):  
Es Cells ◽  
Embryonic Stem ◽  
Homeobox Gene ◽  
Dna Demethylation ◽  
Chromosomal Protein ◽  
Dna Hypomethylation ◽  
Tet Proteins ◽  
Target Sites ◽  
Structural Maintenance Of Chromosomes ◽  
Hinge Domain

5-Methylcytosine (5mC) oxidases, the ten-eleven translocation (TET) proteins, initiate DNA demethylation, but it is unclear how 5mC oxidation is regulated. We show that the protein SMCHD1 (structural maintenance of chromosomes flexible hinge domain containing 1) is found in complexes with TET proteins and negatively regulates TET activities. Removal of SMCHD1 from mouse embryonic stem (ES) cells induces DNA hypomethylation, preferentially at SMCHD1 target sites and accumulation of 5-hydroxymethylcytosine (5hmC), along with promoter demethylation and activation of the Dux double-homeobox gene. In the absence of SMCHD1, ES cells acquire a two-cell (2c) embryo–like state characterized by activation of an early embryonic transcriptome that is substantially imposed by Dux. Using Smchd1/Tet1/Tet2/Tet3 quadruple-knockout cells, we show that DNA demethylation, activation of Dux, and other genes upon SMCHD1 loss depend on TET proteins. These data identify SMCHD1 as an antagonist of the 2c-like state of ES cells and of TET-mediated DNA demethylation.

scholarly journals Nuclear m6A reader YTHDC1 regulates the scaffold function of LINE1 RNA in mouse ESCs and early embryos

2021 ◽  
Author(s):  
Chuan Chen ◽  
Wenqiang Liu ◽  
Jiayin Guo ◽  
Yuanyuan Liu ◽  
Xuelian Liu ◽  
...  
Keyword(s):  
Inner Cell Mass ◽  
Cell Mass ◽  
Embryonic Stem ◽  
Rrna Synthesis ◽  
Binding Ability ◽  
Transcriptome Regulation ◽  
Early Embryos ◽  
Intrinsic Mechanism ◽  
Regulatory Rnas

AbstractN6-methyladenosine (m6A) on chromosome-associated regulatory RNAs (carRNAs), including repeat RNAs, plays important roles in tuning the chromatin state and transcription, but the intrinsic mechanism remains unclear. Here, we report that YTHDC1 plays indispensable roles in the self-renewal and differentiation potency of mouse embryonic stem cells (ESCs), which highly depends on the m6A-binding ability. Ythdc1 is required for sufficient rRNA synthesis and repression of the 2-cell (2C) transcriptional program in ESCs, which recapitulates the transcriptome regulation by the LINE1 scaffold. Detailed analyses revealed that YTHDC1 recognizes m6A on LINE1 RNAs in the nucleus and regulates the formation of the LINE1-NCL partnership and the chromatin recruitment of KAP1. Moreover, the establishment of H3K9me3 on 2C-related retrotransposons is interrupted in Ythdc1-depleted ESCs and inner cell mass (ICM) cells, which consequently increases the transcriptional activities. Our study reveals a role of m6A in regulating the RNA scaffold, providing a new model for the RNA-chromatin cross-talk.

scholarly journals Modulation of Differentiation of Embryonic Stem Cells by Polypyrrole: The Impact on Neurogenesis

2021 ◽  
Vol 22 (2) ◽  
pp. 501
Author(s):  
Kateřina Skopalová ◽  
Katarzyna Anna Radaszkiewicz ◽  
Věra Kašpárková ◽  
Jaroslav Stejskal ◽  
Patrycja Bober ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Stem Cell Differentiation ◽  
Active Role ◽  
Low Molecular Weight ◽  
Conducting Materials ◽  
The Impact ◽  
Erk Kinase

The active role of biomaterials in the regeneration of tissues and their ability to modulate the behavior of stem cells in terms of their differentiation is highly advantageous. Here, polypyrrole, as a representantive of electro-conducting materials, is found to modulate the behavior of embryonic stem cells. Concretely, the aqueous extracts of polypyrrole induce neurogenesis within embryonic bodies formed from embryonic stem cells. This finding ledto an effort to determine the physiological cascade which is responsible for this effect. The polypyrrole modulates signaling pathways of Akt and ERK kinase through their phosphorylation. These effects are related to the presence of low-molecular-weight compounds present in aqueous polypyrrole extracts, determined by mass spectroscopy. The results show that consequences related to the modulation of stem cell differentiation must also be taken into account when polypyrrole is considered as a biomaterial.

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