Local and transient expression of E-cadherin involved in mouse embryonic brain morphogenesis

Development ◽  
1992 ◽  
Vol 116 (4) ◽  
pp. 1011-1019 ◽  
Author(s):  
K. Shimamura ◽  
M. Takeichi

We found that E-cadherin (uvomorulin) is transiently expressed in restricted regions of the metencephalon, mesencephalon and diencephalon of mouse embryonic brain. This expression first occurred in parts of the mesencephalon and diencephalon at around E9.5, and subsequently extended to the primordia of cerebellum, the dorsal midline of mesencephalon and some other regions of the embryonic brain. These E-cadherin expressions ceased by E15 except at the dorsal midline. Immunohistological analyses showed that E-cadherin-positive cells are radially arranged in the neural tube and the E-cadherin-positive regions are sharply demarcated from E-cadherin-negative regions. Axons extending from some of the E-cadherin-positive regions also expressed this molecule. When embryonic brains were dissociated into single cells and cultured as monolayers, E-cadherin-positive cells formed clusters that were segregated from E-cadherin-negative cells. E9.5 brain fragments containing metencephalon and mesencephalon were isolated, explanted on Nucleopore filters and cultured in the absence or presence of antibodies to E-cadherin. This antibody treatment removed most of the E-cadherin molecules from the explants and consequently affected their growth pattern. To analyze cellular events induced by the antibody treatment, we stained these explants with an antiserum to En whose distribution was found to overlap in part with that of E-cadherin and found that the pattern of En staining was altered by the anti-E-cadherin antibody treatment. These results suggest that the local and transient expression of E-cadherin in embryonic brain is involved in regional pattern formation in this organ.

Development ◽  
1994 ◽  
Vol 120 (8) ◽  
pp. 2225-2234 ◽  
Author(s):  
K. Shimamura ◽  
S. Hirano ◽  
A.P. McMahon ◽  
M. Takeichi

E-cadherin is transiently expressed in local regions of the embryonic mouse brain, which include several patchy areas on the mesencephalon and diencephalon and their roof plate and part of cerebellar rudiments. In the present study, we compared this E-cadherin expression with that of Wnt-1, which occurs in specific zones in the embryonic brain, and found certain spatiotemporal relations between them: Wnt-1 expression tended to run parallel or overlap with peripheries of the E-cadherin-positive areas. For example, in the dorsal midline, Wnt-1 was expressed at the middle of the roof plate, while E-cadherin was absent in the middle zone but detected in two arrays of marginal roof plate cells. Furthermore, alpha N-catenin, a cadherin-associated protein, was found to occur at the roof plate of the mesencephalon and diencephalon, coinciding with Wnt-1 expression. The expression of these molecules was then studied in two alleles of the Wnt-1 mutation, Wnt-1sw and Wnt-1neo. In mice homozygous for these mutant genes, E-cadherin expression in the roof plate was up-regulated; the middle E-cadherin-negative zone disappeared. Moreover, E-cadherin expression in the roof plate began earlier in the mutant mice than in wild-type mice. On the contrary, alpha N-catenin expression in the dorsal midline was suppressed in these mutants. These changes in cadherin and catenin expression occurred at the level of mRNA expression. These results suggest that the Wnt-1 signal is, either directly or indirectly, involved in the regulation of expression of E-cadherin and alpha N-catenin in restricted regions of the embryonic brain. This mechanism may contribute to the patterning of the expression of these adhesion-related proteins in the embryonic brain.


Development ◽  
1995 ◽  
Vol 121 (12) ◽  
pp. 4257-4264 ◽  
Author(s):  
M.E. Halpern ◽  
C. Thisse ◽  
R.K. Ho ◽  
B. Thisse ◽  
B. Riggleman ◽  
...  

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.


1999 ◽  
Vol 24 (12) ◽  
pp. M60-M64 ◽  
Author(s):  
Joshua M Shulman ◽  
Daniel St Johnston

2005 ◽  
Vol 16 (2) ◽  
pp. 550-561 ◽  
Author(s):  
Hanane Khoury ◽  
Monica A. Naujokas ◽  
Dongmei Zuo ◽  
Veena Sangwan ◽  
Melanie M. Frigault ◽  
...  

Activation of the hepatocyte growth factor receptor Met induces a morphogenic response and stimulates the formation of branching tubules by Madin-Darby canine kidney (MDCK) epithelial cells in three-dimensional cultures. A constitutively activated ErbB2/Neu receptor, NeuNT, promotes a similar invasive morphogenic program in MDCK cells. Because both receptors are expressed in breast epithelia, are associated with poor prognosis, and hepatocyte growth factor (HGF) is expressed in stroma, we examined the consequence of cooperation between these signals. We show that HGF disrupts NeuNT-induced epithelial morphogenesis, stimulating the breakdown of cell-cell junctions, dispersal, and invasion of single cells. This correlates with a decrease in junctional proteins claudin-1 and E-cadherin, in addition to the internalization of the tight junction protein ZO-1. HGF-induced invasion of NT-expressing cells is abrogated by pretreatment with a pharmacological inhibitor of the mitogen-activated protein kinase kinase (MEK) pathway, which restores E-cadherin and ZO-1 at cell-cell junctions, establishing the involvement of MEK-dependent pathways in this process. These results demonstrate that physiological signals downstream from the HGF/Met receptor synergize with ErbB2/Neu to enhance the malignant phenotype, promoting the breakdown of cell-cell junctions and enhanced cell invasion. This is particularly important for cancers where ErbB2/Neu is overexpressed and HGF is a physiological growth factor found in the stroma.


2017 ◽  
Author(s):  
Gioele La Manno ◽  
Ruslan Soldatov ◽  
Hannah Hochgerner ◽  
Amit Zeisel ◽  
Viktor Petukhov ◽  
...  

AbstractRNA abundance is a powerful indicator of the state of individual cells, but does not directly reveal dynamic processes such as cellular differentiation. Here we show that RNA velocity—the time derivative of RNA abundance—can be estimated by distinguishing unspliced and spliced mRNAs in standard single-cell RNA sequencing protocols. We show that RNA velocity is a vector that predicts the future state of individual cells on a timescale of hours. We validate the accuracy of RNA velocity in the neural crest lineage, demonstrate its use on multiple technical platforms, reconstruct the branching lineage tree of the mouse hippocampus, and measure RNA kinetics in human embryonic brain. We expect RNA velocity to greatly aid the analysis of developmental lineages and cellular dynamics, particularly in humans.


2011 ◽  
Vol 193 (3) ◽  
pp. 455-464 ◽  
Author(s):  
Maria Teresa Abreu-Blanco ◽  
Jeffrey M. Verboon ◽  
Susan M. Parkhurst

When single cells or tissues are injured, the wound must be repaired quickly in order to prevent cell death, loss of tissue integrity, and invasion by microorganisms. We describe Drosophila as a genetically tractable model to dissect the mechanisms of single-cell wound repair. By analyzing the expression and the effects of perturbations of actin, myosin, microtubules, E-cadherin, and the plasma membrane, we define three distinct phases in the repair process—expansion, contraction, and closure—and identify specific components required during each phase. Specifically, plasma membrane mobilization and assembly of a contractile actomyosin ring are required for this process. In addition, E-cadherin accumulates at the wound edge, and wound expansion is excessive in E-cadherin mutants, suggesting a role for E-cadherin in anchoring the actomyosin ring to the plasma membrane. Our results show that single-cell wound repair requires specific spatial and temporal cytoskeleton responses with distinct components and mechanisms required at different stages of the process.


Development ◽  
1985 ◽  
Vol 89 (Supplement) ◽  
pp. 333-347
Author(s):  
P. D. Nieuwkoop

After a short discussion on cell interactions in general and inductive interactions in particular, the almost completely epigenetic nature of amphibian development is emphasized. In the symmetrized egg undergoing cleavage a large-scale inductive interaction occurs which leads to the formation of the meso—endoderm. Meso—endoderm formation gives rise to the morphogenic process of gastrulation. In the ensuing triple-layered embryo inductive interactions are strongly enhanced. The following large-scale inductive interaction leads to the formation of the neural anlage. This is again followed by the morphogenetic process of neurulation or neural tube formation. Subsequent interactions between the germ layers of the triple-layered embryo give rise to the formation of the regional pattern of organ anlagen. Finally, the most promising approaches to the nature of inductive interactions for mesoderm and endoderm formation are discussed.


2019 ◽  
Vol 31 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Giulia Cagnotti ◽  
Federica Sammartano ◽  
Iride Bertone ◽  
Maria Teresa Capucchio ◽  
Isabella Nicola ◽  
...  

A 15-d-old female crossbreed calf was referred because of paraplegia since birth. Clinical examination revealed a skin defect covered by hair on the dorsal midline in the thoracic area of the spine. Thoracolumbar spinal cord neuroanatomic localization was determined based on neurologic examination. Computed tomography of the thoracolumbar spine revealed incomplete fusion of the vertebral arches from T6 to T10 and duplication of the vertebral arch of T7. At the level of T6-T7, duplication of the spinal cord with 2 segments completely separated by a septum of hyperattenuating, probably cartilaginous, tissue was noted. Histologically, the spinal segments had different degrees of duplication. Three central canals were detected in one region. Genetic investigation for the presence of methylenetetrahydrofolate reductase (MTHFR) polymorphism, which has been investigated in both human and veterinary medicine as a possible cause of neural tube defects and abortion, was carried out and was negative in both the calf and her dam.


1999 ◽  
Vol 15 (12) ◽  
pp. M60-M64
Author(s):  
Joshua M Shulman ◽  
Daniel St Johnston

2007 ◽  
Vol 2007 (389) ◽  
pp. tw193-tw193
Author(s):  
J. F. Foley
Keyword(s):  

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