Severe defects in the formation of epaxial musculature in open brain (opb) mutant mouse embryos

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 79-86 ◽  
Author(s):  
R. Sporle ◽  
T. Gunther ◽  
M. Struwe ◽  
K. Schughart
Keyword(s):  
Neural Tube ◽  
Body Wall ◽  
Mutant Mouse ◽  
Expression Patterns ◽  
Mouse Embryos ◽  
Surface Ectoderm ◽  
Altered Expression ◽  
Dorsal Neural Tube ◽  
Mutant Mouse Embryos ◽  
Derivatives Of

The differentiation of somite derivatives is dependent on signals from neighboring axial structures. While ventral signals have been described extensively, little is known about dorsal influences, especially those from the dorsal half of the neural tube. Here, we describe severe phenotypic alterations in dorsal somite derivatives of homozygous open brain (opb) mutant mouse embryos which suggest crucial interactions between dorsal neural tube and dorsal somite regions. At Theiler stage 17 (day 10.5 post coitum) of development, strongly altered expression patterns of Pax3 and Myf5 were observed in dorsal somite regions indicating that the dorsal myotome and dermomyotome were not differentiating properly. These abnormalities were later followed by the absence of epaxial (dorsal) musculature; whereas, body wall and limb musculature formed normally. Analysis of Mox1 and Pax1 expression in opb embryos revealed additional defects in the differentiation of the dorsal sclerotome. The observed abnormalities coincided with defects in differentiation of dorsal neural tube regions. The implications of our findings for interactions between dorsal neural tube, surface ectoderm and dorsomedial somite regions in specifying epaxial musculature are discussed.

scholarly journals Morphology, topology and dimensions of the heart and arteries of genetically normal and mutant mouse embryos at stages S21-S23

2017 ◽  
Vol 231 (4) ◽  
pp. 600-614 ◽  
Author(s):  
Stefan H. Geyer ◽  
Lukas F. Reissig ◽  
Markus Hüsemann ◽  
Cordula Höfle ◽  
Robert Wilson ◽  
...  
Keyword(s):  
Mutant Mouse ◽  
Mouse Embryos ◽  
Mutant Mouse Embryos

scholarly journals Anterior neural plate regionalization in cripto null mutant mouse embryos in the absence of node and primitive streak

2003 ◽  
Vol 264 (2) ◽  
pp. 537-549 ◽  
Author(s):  
Giovanna L Liguori ◽  
Diego Echevarría ◽  
Raffaele Improta ◽  
Massimo Signore ◽  
Eileen Adamson ◽  
...  
Keyword(s):  
Mutant Mouse ◽  
Primitive Streak ◽  
Neural Plate ◽  
Mouse Embryos ◽  
Null Mutant ◽  
Mutant Mouse Embryos ◽  
Anterior Neural Plate ◽  
Null Mutant Mouse

The behaviour in vitro of epidermal cells from normal and pupoid foetus mutant mouse embryos

1985 ◽  
Vol 79 (1) ◽  
pp. 305-315
Author(s):  
S. Anderson ◽  
D.A. Ede
Keyword(s):  
Mutant Mouse ◽  
Cell Mass ◽  
Time Lapse ◽  
Epidermal Cells ◽  
Mouse Embryos ◽  
Sensory Nerves ◽  
Recessive Lethal Mutation ◽  
Mutant Mouse Embryos ◽  
Peripheral Sensory

Pupoid foetus (pf/pf) is a recessive lethal mutation of the mouse causing epidermal hypertrophy and disorganization of peripheral sensory nerves and mesoderm. The comparative behaviour of epidermal cells from normal and pupoid foetus mutant mouse embryos was studied in vitro. Epidermal explants from the snout region of 12.5- to 13-day embryos were grown in culture for periods of up to 2 weeks. Cultures from both phenotypes were filmed using time-lapse cinemicrography for up to 3 days following explantation. Paths of individual cells were traced as they migrated from the explant, and their rate of locomotion and directional persistence were calculated. Differences in these parameters between the two phenotypes were tested statistically. The overall morphology of the cultures, and the tendency of the cells to detach from the periphery of the cell mass were also compared. The results show that, between 25 and 60 h after explantation, epidermal cells from pupoid foetus embryos move consistently more slowly than normal cells, and follow a more erratic path. This situation is reversed, however, between 16 and 25 h. This suggests that the pf mutation causes an alteration in epidermal cells that affects their locomotion, and which is maintained for a minimum of 3 days in the absence of other influencing factors.

Control of somite number in normal and amputated mutant mouse embryos: an experimental and a theoretical analysis

Development ◽  
1978 ◽  
Vol 45 (1) ◽  
pp. 189-202
Author(s):  
O. P. Flint ◽  
D. A. Ede ◽  
O. K. Wilby ◽  
J. Proctor
Keyword(s):  
Quantitative Analysis ◽  
Theoretical Analysis ◽  
Mutant Mouse ◽  
Mouse Embryos ◽  
Mammalian Embryo ◽  
Size Number ◽  
Mutant Mouse Embryos ◽  
Recessive Mutant ◽  
Post Implantation ◽  
Somite Number

A regulation is shown for size and number of serially repeated axial structures, the somites, in a mammalian embryo. The mammalian embryo is normally inaccessible to operation at post-implantation stages. This problem is resolved by the quantitative analysis of somite size, number and development in a recessive mutant of the mouse, amputated, whose axial length is greatly reduced. The effect of the gene simulates an experiment ablating part of the embryonic tissue available for somitic segmentation. Regulation occurs at the time when the somite is first formed, by control of the quantity of cells included in each new somite. A model is devised for the control of somitic segmentation which explains most of the features observed and which can be simulated on a computer.

Developmental expression of syndecan, an integral membrane proteoglycan, correlates with cell differentiation

Development ◽  
1991 ◽  
Vol 111 (1) ◽  
pp. 213-220 ◽  
Author(s):  
M.S. Trautman ◽  
J. Kimelman ◽  
M. Bernfield
Keyword(s):  
Cell Differentiation ◽  
Epithelial Cell ◽  
Actin Cytoskeleton ◽  
Mouse Embryos ◽  
Developmental Expression ◽  
Spatiotemporal Pattern ◽  
Adhesion Receptors ◽  
Developmentally Regulated ◽  
Surface Ectoderm ◽  
Derivatives Of

Syndecan is an integral membrane proteoglycan that behaves as a matrix receptor by binding cells to interstitial matrix and associating intracellularly with the actin cytoskeleton. Using immunohistology, we have now localized this proteoglycan during the morphogenesis of various derivatives of the surface ectoderm in mouse embryos. Syndecan is expressed on ectodermal epithelia, but is selectively lost from the cells that differentiate into the localized placodes that initiate lens, nasal, otic and vibrissal development. The loss is transient on presumptive ear, nasal and vibrissal epithelia; the derivatives of the differentiating ectodermal cells that have lost syndecan subsequently re-express syndecan. In contrast, syndecan is initially absent from the mesenchyme underlying the surface ectoderm, and is transiently expressed when the surface ectoderm loses syndecan. These results demonstrate that expression of syndecan is developmentally regulated in a distinct spatiotemporal pattern. On epithelia, syndecan is lost at a time and, location that correlates with epithelial cell differentiation and, on mesenchyme, syndecan is acquired when the cells aggregate in proximity to the epithelium. This pattern of change with morphogenetic events is unique and not duplicated by other matrix molecules or adhesion receptors.

Relationship between Wnt-1 and En-2 expression domains during early development of normal and ectopic met-mesencephalon

Development ◽  
1992 ◽  
Vol 115 (4) ◽  
pp. 999-1009 ◽  
Author(s):  
L. Bally-Cuif ◽  
R.M. Alvarado-Mallart ◽  
D.K. Darnell ◽  
M. Wassef
Keyword(s):  
In Situ Hybridization ◽  
Neural Tube ◽  
Expression Patterns ◽  
Mouse Embryos ◽  
Chick Embryos ◽  
Expression Domain ◽  
General Role ◽  
Maximal Expression

Grafting a met-mesencephalic portion of neural tube from a 9.5-day mouse embryo into the prosencephalon of a 2-day chick embryo results in the induction of chick En-2 (ChickEn) expression in cells in contact with the graft (Martinez et al., 1991). In this paper we investigate the possibility of Wnt-1 being one of the factors involved in En-2 induction. Since Wnt-1 and En-2 expression patterns have been described as diverging during development of the met-mesencephalic region, we first compared Wnt-1 and En-2 expression in this domain by in situ hybridization in mouse embryos after embryonic day 8.5. A ring of Wnt-1-expressing cells is detected encircling the neural tube in the met-mesencephalic region at least until day 12.5. This ring consistently overlapped with the En-2 expression domain, and corresponds to the position of this latter gene's maximal expression. We subsequently studied ChickEn ectopic induction in chick embryos grafted with various portions of met-mesencephalon. When the graft originated from the level of the Wnt-1-positive ring, ChickEn induction was observed in 71% of embryos, and in these cases correlated with Wnt-1 expression in the grafted tissue. In contrast, this percentage dropped significantly when the graft was taken from more rostral or caudal parts of the mesencephalic vesicle. Taken together, these results are compatible with a prolonged role of Wnt-1 in the specification and/or development of the met-mesencephalic region, and show that Wnt-1 could be directly or indirectly involved in the regulation of En-2 expression around the Wnt-1-positive ring during this time. We also provide data on the position of the Wnt-1-positive ring relative to anatomical boundaries in the neural tube, which suggest a more general role for the Wnt-1 protein as a positional signal involved in organizing the met-mesencephalic domain.

Heightened activation of embryonic megakaryocytes causes aneurysms in the developing brain of mice lacking podoplanin

Blood ◽  
2021 ◽  
Author(s):  
Christopher Michael Hoover ◽  
Yuji Kondo ◽  
Bojing Shao ◽  
Michael McDaniel ◽  
Robert Lee ◽  
...  
Keyword(s):  
Embryonic Development ◽  
Platelet Activation ◽  
Mutant Mouse ◽  
Neural Tissue ◽  
Mouse Embryos ◽  
Wild Type ◽  
Primitive Hematopoiesis ◽  
Mutant Mouse Embryos ◽  
Granule Release ◽  
Angiopoietin 1

During early embryonic development in mammals, including humans and mice, megakaryocytes first originate from primitive hematopoiesis in the yolk sac. These embryonic megakaryocytes (eMk) circulate in the vasculature with unclear function. Here we report that podoplanin (PDPN), the ligand of C-type lectin-like receptor (CLEC-2) on megakaryocytes/platelets, is temporarily expressed in neural tissue during midgestation in mice. Loss of PDPN or CLEC-2 resulted in aneurysms and spontaneous hemorrhage specifically in the lower diencephalon during midgestation. Surprisingly, more eMks/platelets had enhanced granule release and localized to lower diencephalon in mutant mouse embryos than wild-type littermates prior to hemorrhage. We found that PDPN counteracted the collagen I-induced secretion of angiopoietin-1 from fetal megakaryocytes, which coincided with enhanced TIE2 activation in aneurysm-like sprouts of PDPN-deficient embryos. Blocking platelet activation prevented the PDPN-deficient embryo from developing vascular defects. Our data reveal a new role for PDPN in regulating eMk function during midgestation.

Wnt signaling from the dorsal neural tube is required for the formation of the medial dermomyotome

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 4969-4976 ◽  
Author(s):  
M. Ikeya ◽  
S. Takada
Keyword(s):  
Neural Tube ◽  
Marker Gene ◽  
Mouse Embryos ◽  
Medial Compartment ◽  
Dorsoventral Patterning ◽  
Dorsal Midline ◽  
Dorsal Neural Tube ◽  
Dorsal Portion ◽  
Lines Of Evidence

Signals originating from tissues surrounding somites are involved in mediolateral and dorsoventral patterning of somites and in the differentiation of the myotome. Wnt-1 and Wnt-3a, which encode members of the Wnt family of cystein-rich secreted signaling molecules, are coexpressed at the dorsal midline of the developing neural tube, an area adjacent to the dorsomedial portion of the somite. Several lines of evidence indicate that Wnt-1 and Wnt-3a have the ability to induce the development of the medial and dorsal portion of somites, as well as to induce myogenesis. To address whether these Wnt signalings are really essential for the development of somites during normal embryogenesis, we investigated the development of somites in mouse embryos lacking both Wnt-1 and Wnt-3a. Here we demonstrate that the medial compartment of the dermomyotome is not formed and the expression of a lateral dermomyotome marker gene, Sim-1, is expanded more medially in the absence of these Wnt signalings. In addition, the expression of a myogenic gene, Myf-5, is decreased at 9.5 days post coitum whereas the level of expression of a number of myogenic genes in the later stage appeared normal. These results indicate that Wnt-1 and Wnt-3a signalings actually regulate the formation of the medial compartment of the dermomyotome and the early part of myogenesis.

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