scholarly journals Pax3acts cell autonomously in the neural tube and somites by controlling cell surface properties

Development ◽  
2001 ◽  
Vol 128 (11) ◽  
pp. 1995-2005 ◽  
Author(s):  
Ahmed Mansouri ◽  
Patrick Pla ◽  
Lionel Larue ◽  
Peter Gruss
Keyword(s):  
Cell Surface ◽  
Neural Crest ◽  
Surface Properties ◽  
Neural Tube ◽  
Es Cells ◽  
Embryonic Stem ◽  
Neural Tube Closure ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Cell Surface Properties

Pax3 is a member of the paired-box-containing transcription factors. It is expressed in the developing somites, dorsal spinal cord, mesencephalon and neural crest derivatives. Several loss-of-function mutations are correlated with the Splotch phenotype in mice and Waardenburg syndrome in humans. Malformations include a lack of muscle in the limb, a failure of neural tube closure and dysgenesis of numerous neural crest derivatives. In this study we have used embryonic stem (ES) cells to generate a lacZ knock-in into the Pax3 locus. The Pax3 knock-in Splotch allele (Sp2G) was used to generate Pax3-deficient ES cells in order to investigate whether, in chimeric embryos, Pax3 is acting cell autonomously in the somites and the neural tube. We found that while Pax3 function is essential for the neuroepithelium and somites, a wild-type environment rescues mutant neural crest cells. In the two affected embryonic tissues, mutant and wild-type cells undergo segregation and do not intermingle.The contribution of mutant cells to the neural tube and the somites displayed temporal differences. All chimeric embryos showed a remarkable contribution of blue cells to the neural tube at all stages analyzed, indicating that the Pax3-deficient cells are not excluded from the neural epithelium while development proceeds. In contrast, this is not true for the paraxial mesoderm. The somite contribution of Pax3−/− ES cells becomes less frequent in older embryos as compared to controls with Pax3+/− ES cells. We propose that although Pax3 function is related to cell surface properties, its role may differ in various tissues. In fact, apoptosis was found in Pax3-deficient cells of the lateral dermomyotome but not in the neural tube.

Cell Surface Properties of Pseudomonas syringae pv. phaseolicola Wild-type and hrp Mutants

1992 ◽  
Vol 135 (2) ◽  
pp. 135-152 ◽  
Author(s):  
WilliamF. Fett ◽  
StanleyF. Osman ◽  
MichaelF. Dunn ◽  
NickolasJ. Panopoulos
Keyword(s):  
Cell Surface ◽  
Surface Properties ◽  
Pseudomonas Syringae ◽  
Wild Type ◽  
Cell Surface Properties

scholarly journals Chromatin remodeling factor CECR2 forms tissue-specific complexes with CCAR2 and LUZP1

2021 ◽  
Author(s):  
Farshad Niri ◽  
Alaina Terpstra ◽  
Kenji Rowel Quintana Lim ◽  
Heather McDermid
Keyword(s):  
Chromatin Remodeling ◽  
Neural Tube ◽  
Es Cells ◽  
Embryonic Stem ◽  
Neural Tube Closure ◽  
Loss Of Function ◽  
Cellular Processes ◽  
Novel Proteins ◽  
Chromatin Remodeling Complexes ◽  
And Function

Chromatin remodeling complexes alter chromatin structure to control access to DNA and therefore control cellular processes such as transcription, DNA replication, and DNA repair. CECR2 is a chromatin remodeling factor that plays an important role in neural tube closure and reproduction. Loss-of-function mutations in Cecr2 result primarily in the perinatal lethal neural tube defect exencephaly, with non-penetrant mice that survive to adulthood exhibiting subfertility. CECR2 forms a complex with ISWI proteins SMARCA5 and/or SMARCA1, but further information on the structure and function of the complex is not known. We therefore have identified candidate components of the CECR2-containing remodeling factor (CERF) complex in embryonic stem (ES) cells through mass spectroscopy. Both SMARCA5 and SMARCA1 were confirmed to be present in CERF complexes in ES cells and testis. However, novel proteins CCAR2 and LUZP1 are CERF components in ES cells but not testis. This tissue specificity in mice suggests these complexes may also have functional differences. Furthermore, LUZP1, loss of which is also associated with exencephaly, appears to play a role in stabilizing the CERF complex in ES cells. Keywords: CECR2, LUZP1, CCAR2, Chromatin remodeling factor, Neural tube defects

scholarly journals Recapitulating early development of mouse musculoskeletal precursors of the paraxial mesoderm in vitro

2017 ◽  
Author(s):  
Jérome Chal ◽  
Ziad Al Tanoury ◽  
Masayuki Oginuma ◽  
Philippe Moncuquet ◽  
Bénédicte Gobert ◽  
...  
Keyword(s):  
Neural Tube ◽  
Es Cells ◽  
Horse Serum ◽  
Muscle Fibers ◽  
Embryonic Stem ◽  
Paraxial Mesoderm ◽  
Mouse Muscle ◽  
Efficient System

AbstractIn vertebrates, body skeletal muscles and axial skeleton derive from the paraxial mesoderm which flanks the neural tube and notochord. The paraxial mesoderm forms in the posterior region of the embryo as presomitic mesoderm (PSM), which generates the embryonic segments called somites. Here, we characterized gene signatures identified using microarray series from the mouse PSM and compared the PSM transcriptome dynamics to that of the developing neural tube. In contrast to the PSM where an abrupt transcriptome reorganisation occurs at the level of the determination front, we show that transcriptome changes are progressive during parallel stages of neural tube differentiation. We show that these early differentiation stages of the paraxial mesoderm can be efficiently recapitulated in monolayer culture in vitro using murine Embryonic Stem (ES) cells. We describe a serum-containing protocol which parallels in vivo tissue maturation allowing differentiation of ES cells towards a paraxial mesoderm fate. We show that R-spondin treatment or Wnt activation alone can induce posterior PSM markers in both mouse and human ES/iPS cells but acquisition of a committed posterior PSM fate requires BMP inhibition to prevent induced cells to drift to a lateral plate mesoderm identity. We show that posterior PSM-like cells induced from mouse ES cells can be further differentiated in vitro to acquire an anterior PSM Pax3-positive identity. When grafted into injured adult muscle, these induced PSM-like precursors generated large numbers of immature muscle fibers. We further show that exposing ES-derived PSM-like cells to a brief FGF inhibition step followed by culture in horse serum-containing medium allows efficient recapitulation of the myogenic program. Differentiating ES cells first produce mononucleated embryonic myocytes and subsequently multinucleated myotubes, as well as Pax7-positive cells. The protocol described here results in improved differentiation and maturation of mouse muscle fibers differentiated in vitro over serum-free protocols. It provides an efficient system for the study of myogenic processes otherwise difficult to study in vivo such as fusion or satellite cell differentiation.

scholarly journals Alkyl hydroperoxide reductase has a role in oxidative stress resistance and in modulating changes in cell-surface properties in Azospirillum brasilense Sp245

Microbiology ◽  
2009 ◽  
Vol 155 (4) ◽  
pp. 1192-1202 ◽  
Author(s):  
Mariam Wasim ◽  
Amber N. Bible ◽  
Zhihong Xie ◽  
Gladys Alexandre
Keyword(s):  
Oxidative Stress ◽  
Cell Surface ◽  
Surface Properties ◽  
Azospirillum Brasilense ◽  
Type Strain ◽  
Wild Type Strain ◽  
Cell Aggregation ◽  
Wild Type ◽  
Cell Surface Properties ◽  
Alkyl Hydroperoxide

An ahpC mutant derivative of Azospirillum brasilense Sp245 (strain SK586) that encodes an alkyl hydroperoxide reductase was found to be more sensitive to oxidative stress caused by organic hydroperoxides compared with the wild-type. In addition, the ahpC mutant strain had multiple defects in a large array of cellular functions that were consistent with alteration of cell-surface properties, such as cell morphology in stationary phase, Calcofluor White-, Congo Red- and lectin-binding abilities, as well as cell-to-cell aggregation and flocculation. All phenotypes of the ahpC mutant were complemented by in trans expression of AhpC, and overexpression of AhpC in the wild-type strain was found to affect the same set of phenotypes, suggesting that the pleiotropic effects were caused by the ahpC mutation. SK586 was also found to be fully motile, but it lost motility at a higher rate than the wild-type during growth, such that most SK586 cells were non-motile in stationary phase. Despite these defects, the mutant did not differ from the wild-type in short-term colonization of sterile wheat roots when inoculated alone, and in competition with the wild-type strain; this implied that AhpC activity may not endow the cells with a competitive advantage in colonization under these conditions. Although the exact function of AhpC in affecting these phenotypes remains to be determined, changes in cell morphology, surface properties, cell-to-cell aggregation and flocculation are common adaptive responses to various stresses in bacteria, and the data obtained here suggest that AhpC contributes to modulating such stress responses in A. brasilense.

Alternating patterns of cell surface properties and neural crest cell migration during segmentation of the chick hindbrain

Development ◽  
1991 ◽  
Vol 113 (Supplement_2) ◽  
pp. 9-15 ◽  
Author(s):  
Andrew Lumsden ◽  
Sarah Guthrie
Keyword(s):  
Cell Surface ◽  
Neural Crest ◽  
Surface Properties ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Cell Surface Properties ◽  
Branchial Arches ◽  
Neural Crest Cell Migration ◽  
Migration Pathways ◽  
Crest Cell

The developing chick hindbrain is transiently divided into a series of repeating units or rhombomeres. Recent work has shown that an alternating periodicity exists both in the cell surface properties of rhombomeres and in the segmental origin of hindbrain neural crest cells. Experiments in which rhombomeres from different axial levels were confronted in the absence of an interrhombomere boundary showed that odd-numbered segments 3 and 5 combined without generating a boundary, as did even-numbered segments 2, 4 and 6. When rhombomeres originating from adjacent positions, or three rhombomeres distant from one another were combined, a new boundary was regenerated. Mapping of the migration pathways of neural crest cells showed that odd-numbered and even-numbered rhombomeres share properties with respect to the production of neural crest cells. In the hindbrain region the neural crest is segregated into streams. Neural crest cells migrating from rhombomeres 1 and 2, rhombomere 4 and rhombomere 6 respectively populate distinct cranial nerve ganglia and branchial arches. In contrast, rhombomeres 3 and 5 are free of neural crest cells.

Bifidobacterium longum and Bifidobacterium breve isolates from preterm and full term neonates: Comparison of cell surface properties

Anaerobe ◽  
2014 ◽  
Vol 28 ◽  
pp. 212-215 ◽  
Author(s):  
Valérie Andriantsoanirina ◽  
Anne-Claire Teolis ◽  
Liu Xin Xin ◽  
Marie Jose Butel ◽  
Julio Aires
Keyword(s):  
Cell Surface ◽  
Surface Properties ◽  
Bifidobacterium Longum ◽  
Full Term ◽  
Term Neonates ◽  
Bifidobacterium Breve ◽  
Cell Surface Properties

Brachyury - a gene affecting mouse gastrulation and early organogenesis

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 157-165 ◽  
Author(s):  
R. S. P. Beddington ◽  
P. Rashbass ◽  
V. Wilson
Keyword(s):  
Es Cells ◽  
Embryonic Stem ◽  
Primitive Streak ◽  
Coat Colour ◽  
Es Cell ◽  
Wild Type ◽  
Mesoderm Cell ◽  
Rostrocaudal Axis

Mouse embryos that are homozygous for the Brachyury (T) deletion die at mid-gestation. They have prominent defects in the notochord, the allantois and the primitive streak. Expression of the T gene commences at the onset of gastrulation and is restricted to the primitive streak, mesoderm emerging from the streak, the head process and the notochord. Genetic evidence has suggested that there may be an increasing demand for T gene function along the rostrocaudal axis. Experiments reported here indicate that this may not be the case. Instead, the gradient in severity of the T defect may be caused by defective mesoderm cell movements, which result in a progressive accumulation of mesoderm cells near the primitive streak. Embryonic stem (ES) cells which are homozygous for the T deletion have been isolated and their differentiation in vitro and in vivo compared with that of heterozygous and wild-type ES cell lines. In +/+ ↔ T/T ES cell chimeras the Brachyury phenotype is not rescued by the presence of wild-type cells and high level chimeras show most of the features characteristic of intact T/T mutants. A few offspring from blastocysts injected with T/T ES cells have been born, several of which had greatly reduced or abnormal tails. However, little or no ES cell contribution was detectable in these animals, either as coat colour pigmentation or by isozyme analysis. Inspection of potential +/+ ↔ T/T ES cell chimeras on the 11th or 12th day of gestation, stages later than that at which intact T/T mutants die, revealed the presence of chimeras with caudal defects. These chimeras displayed a gradient of ES cell colonisation along the rostrocaudal axis with increased colonisation of caudal regions. In addition, the extent of chimerism in ectodermal tissues (which do not invaginate during gastrulation) tended to be higher than that in mesodermal tissues (which are derived from cells invaginating through the primitive streak). These results suggest that nascent mesoderm cells lacking the T gene are compromised in their ability to move away from the primitive streak. This indicates that one function of the T genemay be to regulate cell adhesion or cell motility properties in mesoderm cells. Wild-type cells in +/+ ↔ T/T chimeras appear to move normally to populate trunk and head mesoderm, suggesting that the reduced motility in T/T cells is a cell autonomous defect

Choanal Atresia

1995 ◽  
Vol 16 (12) ◽  
pp. 475-476
Author(s):  
Lisa Menasse-Palmer ◽  
Anna Bogdanow ◽  
Robert W. Marion
Keyword(s):  
Soft Tissue ◽  
Neural Crest ◽  
Neural Tube ◽  
Choanal Atresia ◽  
Neural Tube Closure ◽  
Nasal Airway ◽  
Complete Obstruction ◽  
Live Births ◽  
Choanal Stenosis ◽  
Tube Closure

Choanal atresia is an abnormality of canalization during development of the nasal passages. It involves bone and/or soft tissue and may result in either partial (choanal stenosis) or complete obstruction of the posterior nasal airway. The most widely accepted mechanism for the development of choanal atresia is the persistence of the oronasal membrane beyond the sixth week of gestation, but abnormal migration of cephalic neural crest cells following neural tube closure also has been implicated. The incidence of choanal atresia is 1 in 7000 to 8000 live births. It is more common in females (2:1), more likely to be bony or cartilaginous than membranous (9:1), and more commonly unilateral and right-sided (2:1).

Cell-autonomous shift from axial to paraxial mesodermal development in zebrafish floating head mutants

Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4257-4264 ◽  
Author(s):  
M.E. Halpern ◽  
C. Thisse ◽  
R.K. Ho ◽  
B. Thisse ◽  
B. Riggleman ◽  
...  
Keyword(s):  
Neural Tube ◽  
Single Cells ◽  
Floor Plate ◽  
Paraxial Mesoderm ◽  
Wild Type ◽  
Genetic Mosaics ◽  
Essential Step ◽  
Ventral Neural Tube ◽  
Mesodermal Development

Zebrafish floating head mutant embryos lack notochord and develop somitic muscle in its place. This may result from incorrect specification of the notochord domain at gastrulation, or from respecification of notochord progenitors to form muscle. In genetic mosaics, floating head acts cell autonomously. Transplanted wild-type cells differentiate into notochord in mutant hosts; however, cells from floating head mutant donors produce muscle rather than notochord in wild-type hosts. Consistent with respecification, markers of axial mesoderm are initially expressed in floating head mutant gastrulas, but expression does not persist. Axial cells also inappropriately express markers of paraxial mesoderm. Thus, single cells in the mutant midline transiently co-express genes that are normally specific to either axial or paraxial mesoderm. Since floating head mutants produce some floor plate in the ventral neural tube, midline mesoderm may also retain early signaling capabilities. Our results suggest that wild-type floating head provides an essential step in maintaining, rather than initiating, development of notochord-forming axial mesoderm.

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