Wnt-1-dependent regulation of local E-cadherin and alpha N-catenin expression in the embryonic mouse brain

Development ◽  
1994 ◽  
Vol 120 (8) ◽  
pp. 2225-2234 ◽  
Author(s):  
K. Shimamura ◽  
S. Hirano ◽  
A.P. McMahon ◽  
M. Takeichi
Keyword(s):  
Mouse Brain ◽  
Embryonic Brain ◽  
Regulation Of Expression ◽  
Embryonic Mouse ◽  
Dorsal Midline ◽  
Roof Plate ◽  
Related Proteins ◽  
Mutant Genes ◽  
Spatiotemporal Relations ◽  
E Cadherin

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.

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
Keyword(s):  
Pattern Formation ◽  
Transient Expression ◽  
Neural Tube ◽  
Single Cells ◽  
Embryonic Brain ◽  
Antibody Treatment ◽  
Regional Pattern ◽  
Dorsal Midline ◽  
Cellular Events ◽  
E Cadherin

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.

Myf5 is a novel early axonal marker in the mouse brain and is subjected to post-transcriptional regulation in neurons

Development ◽  
2000 ◽  
Vol 127 (2) ◽  
pp. 319-331 ◽  
Author(s):  
P. Daubas ◽  
S. Tajbakhsh ◽  
J. Hadchouel ◽  
M. Primig ◽  
M. Buckingham
Keyword(s):  
Transcription Factor ◽  
Mouse Brain ◽  
Mrna Translation ◽  
Adult Brain ◽  
Protein Accumulation ◽  
Embryonic Mouse ◽  
Signalling Molecules ◽  
Basic Helix Loop Helix ◽  
Helix Loop Helix ◽  
The Brain

Myf5 is a key basic Helix-Loop-Helix transcription factor capable of converting many non-muscle cells into muscle. Together with MyoD it is essential for initiating the skeletal muscle programme in the embryo. We previously identified unexpected restricted domains of Myf5 transcription in the embryonic mouse brain, first revealed by Myf5-nlacZ(+/)(−) embryos (Tajbakhsh, S. and Buckingham, M. (1995) Development 121, 4077–4083). We have now further characterized these Myf5 expressing neurons. Retrograde labeling with diI, and the use of a transgenic mouse line expressing lacZ under the control of Myf5 regulatory sequences, show that Myf5 transcription provides a novel axonal marker of the medial longitudinal fasciculus (mlf) and the mammillotegmental tract (mtt), the earliest longitudinal tracts to be established in the embryonic mouse brain. Tracts projecting caudally from the developing olfactory system are also labelled. nlacZ and lacZ expression persist in the adult brain, in a few ventral domains such as the mammillary bodies of the hypothalamus and the interpeduncular nucleus, potentially derived from the embryonic structures where the Myf5 gene is transcribed. To investigate the role of Myf5 in the brain, we monitored Myf5 protein accumulation by immunofluorescence and immunoblotting in neurons transcribing the gene. Although Myf5 was detected in muscle myotomal cells, it was absent in neurons. This would account for the lack of myogenic conversion in brain structures and the absence of a neural phenotype in homozygous null mutants. RT-PCR experiments show that the splicing of Myf5 primary transcripts occurs correctly in neurons, suggesting that the lack of Myf5 protein accumulation is due to regulation at the level of mRNA translation or protein stability. In the embryonic neuroepithelium, Myf5 is transcribed in differentiated neurons after the expression of neural basic Helix-Loop-Helix transcription factors. The signalling molecules Wnt1 and Sonic hedgehog, implicated in the activation of Myf5 in myogenic progenitor cells in the somite, are also produced in the viscinity of the Myf5 expression domain in the mesencephalon. We show that cells expressing Wnt1 can activate neuronal Myf5-nlacZ gene expression in dissected head explants isolated from E9.5 embryos. Furthermore, the gene encoding the basic Helix-Loop-Helix transcription factor mSim1 is expressed in adjacent cells in both the somite and the brain, suggesting that signalling molecules necessary for the activation of mSim1 as well as Myf5 are present at these different sites in the embryo. This phenomenon may be widespread and it remains to be seen how many other potentially potent regulatory genes, in addition to Myf5, when activated do not accumulate protein at inappropriate sites in the embryo.

Inhibition of transient potassium current in cultured and acutely dissociated mouse hippocampal neurons by GABAA receptor activation

1996 ◽  
Vol 76 (2) ◽  
pp. 816-824
Author(s):  
R. L. Wu ◽  
M. E. Barish
Keyword(s):  
Mouse Brain ◽  
Hippocampal Neurons ◽  
Potassium Current ◽  
Receptor Activation ◽  
Gabab Receptors ◽  
Cell Swelling ◽  
Cultured Neurons ◽  
Embryonic Mouse ◽  
Voltage Gated ◽  
A Current

1. The regulation of A-current, one of several transient voltage-gated potassium currents, was studied using whole cell gigaohm seal voltage-clamp techniques on hippocampal pyramidal neurons that were either acutely dissociated from postnatal mouse brain or isolated from embryonic mouse brain and grown in dissociated culture. These neurons also express gamma-aminobutyric acid-A (GABAA) receptors, the activation of which can, under some circumstances, depolarize immature neurons and the dendrites of more mature neurons. 2. Application of GABA (50 microM) reduced the amplitude of A-current when potassium current amplitude was measured during a period of slow and incomplete desensitization of IGABA. A-current was reduced to 67 +/- 9% of control (mean +/- SD, n - 14) in acutely dissociated neurons, and to 64 +/- 11% of control (n = 15) in cultured neurons. Similar A-current reductions were seen in large outside-out membrane patches pulled from somata of cultured neurons, an observation suggesting that imperfect control of membrane voltage was not responsible for A-current inhibition. 3. A-current inhibition exhibited the sensitivity expected of a GABAA-sensitive process. It was mimicked by muscimol and blocked by bicuculline, picrotoxin, and reduction of [Cl-] in the external solution. Baclophen and phaclophen, effective as agonist and antagonist on GABAB receptors, did not affect A-currents or their inhibition. Reduction in extracellular osmolarity (to increase cell swelling as might occur with Cl- entry), or removal of external HCO3- (which might flow inward through GABAA channels and cause local external acidification), did not affect A-current or its inhibition. The mechanisms of inhibition is not clear at present. 4. We suggest that reduced A-current may favor GABA-induced depolarization and consequent activation of voltage-gated calcium channels.

scholarly journals Natural loss of function of ephrin-B3 shapes spinal flight circuitry in birds

2021 ◽  
Vol 7 (24) ◽  
pp. eabg5968
Author(s):  
Baruch Haimson ◽  
Oren Meir ◽  
Reut Sudakevitz-Merzbach ◽  
Gerard Elberg ◽  
Samantha Friedrich ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Mutant Mouse ◽  
Loss Of Function ◽  
Dorsal Midline ◽  
Roof Plate ◽  
Embryonic Spinal Cord ◽  
Guidance Molecule

Flight in birds evolved through patterning of the wings from forelimbs and transition from alternating gait to synchronous flapping. In mammals, the spinal midline guidance molecule ephrin-B3 instructs the wiring that enables limb alternation, and its deletion leads to synchronous hopping gait. Here, we show that the ephrin-B3 protein in birds lacks several motifs present in other vertebrates, diminishing its affinity for the EphA4 receptor. The avian ephrin-B3 gene lacks an enhancer that drives midline expression and is missing in galliforms. The morphology and wiring at brachial levels of the chicken embryonic spinal cord resemble those of ephrin-B3 null mice. Dorsal midline decussation, evident in the mutant mouse, is apparent at the chick brachial level and is prevented by expression of exogenous ephrin-B3 at the roof plate. Our findings support a role for loss of ephrin-B3 function in shaping the avian brachial spinal cord circuitry and facilitating synchronous wing flapping.

scholarly journals The specification of noradrenergic locus coeruleus (LC) neurones depends on bone morphogenetic proteins (BMPs)

Development ◽  
2002 ◽  
Vol 129 (4) ◽  
pp. 983-991 ◽  
Author(s):  
Astrid Vogel-Höpker ◽  
Hermann Rohrer
Keyword(s):  
Transcription Factors ◽  
Locus Coeruleus ◽  
Bone Morphogenetic Proteins ◽  
Chick Embryos ◽  
Dorsal Midline ◽  
Neural Crest Development ◽  
Roof Plate ◽  
Rhombic Lip ◽  
The Brain

The role of BMPs in the development of the major noradrenergic centre of the brain, the locus coeruleus (LC), was investigated. LC generation is reflected by initial expression of the transcription factors Phox2a and Phox2b in dorsal rhombomere1 (r1), followed by expression of dopamine-β-hydroxylase and tyrosine hydroxylase. Bmp5 is expressed in the dorsal neuroepithelium in proximity to Phox2-expressing cells. BMP inhibition in stage 10 chick embryos resulted in the lack of LC neurones or in their generation at the dorsal midline, and loss of roof plate and rhombic lip, but it did not affect neural crest development. These results reveal late essential BMP functions in the specification of dorsal neuronal phenotypes in r1, including LC neurones, and in the development of dorsal midline structures.

scholarly journals Aging-dependent expression of synapse-related proteins in the mouse brain

2017 ◽  
Vol 22 (5) ◽  
pp. 472-484 ◽  
Author(s):  
Hajime Shiotani ◽  
Tomohiko Maruo ◽  
Shotaro Sakakibara ◽  
Muneaki Miyata ◽  
Kenji Mandai ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Related Proteins
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