Comparative remarks on the development of the tail cord among higher vertebrates

Development ◽  
1974 ◽  
Vol 32 (2) ◽  
pp. 355-363
Author(s):  
A. F. Hughes ◽  
R. B. Freeman
Keyword(s):  
Neural Tube ◽  
Tail Bud ◽  
Caudal Region ◽  
Posterior Neuropore ◽  
Irregular Growth

The development of the caudal region of the neural tube is compared in tailed mammals with that of the chick and human. In rat, mouse, opossum and pig, the lumen of the cord extends caudally in an even manner, whereas in the chick and in man the addition of small cavities to the lumen results in a phase of irregular growth. In mammals with unreduced tails, the site of closure of the posterior neuropore is at the tip of the tail, whereas in pig, man and in the chick closure occurs before the formation of the tail-bud. The teratological implications of these findings are discussed.

Intrinsic and extrinsic factors in the mechanism of neurulation: effect of curvature of the body axis on closure of the posterior neuropore

Development ◽  
1993 ◽  
Vol 117 (3) ◽  
pp. 1163-1172 ◽  
Author(s):  
H.W. van Straaten ◽  
J.W. Hekking ◽  
C. Consten ◽  
A.J. Copp
Keyword(s):  
Neural Tube ◽  
The Body ◽  
Body Axis ◽  
Normal Closure ◽  
General Mechanism ◽  
Extrinsic Factors ◽  
Caudal Region ◽  
Posterior Neuropore ◽  
Axial Curvature

Neurulation has been suggested to involve both factors intrinsic and extrinsic to the neuroepithelium. In the curly tail (ct) mutant mouse embryo, final closure of the posterior neuropore is delayed to varying extents resulting in neural tube defects. Evidence was presented recently (Brook et al., 1991 Development 113, 671–678) to suggest that enhanced ventral curvature of the caudal region is responsible for the neurulation defect, which probably originates from an abnormally reduced rate of cell proliferation affecting the hindgut endoderm and notochord, but not the neuroepithelium (Copp et al., 1988, Development 104, 285–295). This axial curvature probably generates a mechanical stress on the posterior neuropore, opposing normal closure. We predicted, therefore, that the ct/ct posterior neuropore should be capable of normal closure if the neuropore should be capable of normal closure if the neuroepithelium is isolated from its adjacent tissues. This prediction was tested by in vitro culture of ct/ct posterior neuropore regions, isolated by a cut caudal to the 5th from last somite. In experimental explants, the neuroepithelium of the posterior neuropore, together with the contiguous portion of the neural tube, were separated mechanically from all adjacent non-neural tissues. The posterior neuropore closed in these explants at a similar rate to isolated posterior neuropore regions of non-mutant embryos. By contrast, control ct/ct explants, in which the caudal region was isolated but the neuroepithelium was left attached to adjacent tissues, showed delayed neurulation. To examine further the idea that axial curvature may be a general mechanism regulating neurulation, we cultured chick embryos on curved substrata in vitro. Slight curvature of the body axis (maximally 1 degree per mm axial length), of either concave or convex nature, resulted in delay of posterior neuropore closure in the chick embryo. Both incidence and extent of closure delay correlated with the degree of curvature that was imposed. We propose that during normal embryogenesis the rate of neurulation is related to the angle of axial curvature, such that experimental alterations in curvature will have differing effects (either enhancement or delay of closure) depending on the angle of curvature at which neurulation normally occurs in a given species, or at a given level of the body axis.

Genesis and prevention of spinal neural tube defects in the curly tail mutant mouse: involvement of retinoic acid and its nuclear receptors RAR-beta and RAR-gamma

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 681-691
Author(s):  
W.H. Chen ◽  
G.M. Morriss-Kay ◽  
A.J. Copp
Keyword(s):  
Retinoic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
In Situ Hybridisation ◽  
Tail Bud ◽  
Retinoic Acid Signalling ◽  
All Trans Retinoic Acid ◽  
Posterior Neuropore ◽  
Computerised Image Analysis ◽  
Curly Tail

A role for all-trans-retinoic acid in spinal neurulation is suggested by: (1) the reciprocal domains of expression of the retinoic acid receptors RAR-beta and RAR-gamma in the region of the closed neural tube and open posterior neuropore, respectively, and (2) the preventive effect of maternally administered retinoic acid (5 mg/kg) on spinal neural tube defects in curly tail (ct/ct) mice. Using in situ hybridisation and computerised image analysis we show here that in ct/ct embryos, RAR-beta transcripts are deficient in the hindgut endoderm, a tissue whose proliferation rate is abnormal in the ct mutant, and RAR-gamma transcripts are deficient in the tail bud and posterior neuropore region. The degree of deficiency of RAR-gamma transcripts is correlated with the severity of delay of posterior neuropore closure. As early as 2 hours following RA treatment at 10 days 8 hours post coitum, i.e. well before any morphogenetic effects are detectable, RAR-beta expression is specifically upregulated in the hindgut endoderm, and the abnormal expression pattern of RAR-gamma is also altered. These results suggest that the spinal neural tube defects which characterise the curly tail phenotype may be due to interaction between the ct gene product and one or more aspects of the retinoic acid signalling pathway.

The T gene is necessary for normal mesodermal morphogenetic cell movements during gastrulation

Development ◽  
1995 ◽  
Vol 121 (3) ◽  
pp. 877-886 ◽  
Author(s):  
V. Wilson ◽  
L. Manson ◽  
W.C. Skarnes ◽  
R.S. Beddington
Keyword(s):  
T Cells ◽  
Neural Tube ◽  
Es Cells ◽  
Embryonic Stem ◽  
Primitive Streak ◽  
Distal Portion ◽  
Adhesion Properties ◽  
Cell Clones ◽  
Posterior Neuropore ◽  
Pass Through

The T (Brachyury) deletion in mouse is responsible for defective primitive streak and notochord morphogenesis, leading to a failure of the axis to elongate properly posterior to the forelimb bud. T/T embryonic stem (ES) cells colonise wild-type embryos, but in chimeras at 10.5 days post coitum (dpc) onwards they are found predominantly in the distal tail, while trunk paraxial and lateral mesoderm are deficient in T/T cells (Wilson, V., Rashbass, P. and Beddington, R. S. P. (1992) Development 117, 1321–1331). To determine the origin of this abnormal tissue distribution, we have isolated T/T and control T/+ ES cell clones which express lacZ constitutively using a gene trap strategy. Visualisation of T/T cell distribution in chimeric embryos throughout gastrulation up to 10.5 dpc shows that a progressive buildup of T/T cells in the primitive streak during gastrulation leads to their incorporation into the tailbud. These observations make it likely that one role of the T gene product is to act during gastrulation to alter cell surface (probably adhesion) properties as cells pass through the primitive streak. As the chimeric tail elongates at 10.5 dpc, abnormal morphology in the most distal portion becomes apparent. Comparison of T expression in the developing tailbud with the sites of accumulation of T/T cells in chimeras shows that T/T cells collect in sites where T would normally be expressed. T expression becomes internalised in the tailbud following posterior neuropore closure while, in abnormal chimeric tails, T/T cells remain on the surface of the distal tail. We conclude that prevention of posterior neuropore closure by the wedge of T/T cells remaining in the primitive streak after gastrulation is one source of the abnormal tail phenotypes observed. Accumulation of T/T cells in the node and anterior streak during gastrulation results in the preferential incorporation of T/T cells into the ventral portion of the neural tube and axial mesoderm. The latter forms compact blocks which are often fused with the ventral neural tube, reminiscent of the notochordal defects seen in intact mutants. Such fusions may be attributed to cell-autonomous changes in cell adhesion, possibly related to those observed at earlier stages in the primitive streak.

The histogenetic capacity of tissues in the caudal end of the embryonic axis of the mouse

Development ◽  
1984 ◽  
Vol 82 (1) ◽  
pp. 253-266
Author(s):  
P. P. L. Tam
Keyword(s):  
Developmental Stages ◽  
Primitive Streak ◽  
Mouse Embryos ◽  
Embryonic Axis ◽  
Tail Bud ◽  
Germ Layers ◽  
Kidney Capsule ◽  
Caudal Region ◽  
Caudal Portion ◽  
Adult Body

The caudal end of the embryonic axis consists of the primitive streak and the tail bud. Small fragments of this caudal tissue were transplanted from mouse embryos of various developmental stages to the kidney capsule in order to test their histogenetic capacity. The variety of mature tissues obtained from these small fragments was similar to that obtained by grafting a larger caudal portion of the embryo. Initially, the grafted tissue broke up into loose masses of embryonic mesenchyme and this was later re-organized into more compact tissues and into cysts that were lined with various types of epithelia. After 14 days in the ectopic site, grafted tissues coming from embryos of the primitive-streak, the early-somite and the forelimb-bud stages differentiated into structures that has presumably originated from the three embryonic germ layers. Many of these structures were related to the caudal region of the adult body, such as the mid- and hindgut segments and urogenital derivatives. The histogenetic capacity for endodermal tissues and urogenital organs was lost when the grafted tissue consisted entirely of the tail bud of the hindlimb-bud-stage embryos. The behaviour of the caudal tissues suggested that (1) the primordia for the various parts of embryonic body were derived from a small progenitor population in the primitive streak and the tail bud, and (2) the histogenetic capacity of this population changed during development.

Neural tube development in mutant (curly tail) and normal mouse embryos: the timing of posterior neuropore closure in vivo and in vitro

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 151-167
Author(s):  
A. J. Copp ◽  
M. J. Seller ◽  
P. E. Polani
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Mouse Embryos ◽  
Injection Technique ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Mechanisms Of Development ◽  
Delayed Closure

A dye-injection technique has been used to determine the developmental stage at which posterior neuropore (PNP) closure occurs in normal and mutant curly tail mouse embryos. In vivo, the majority of non-mutant embryos undergo PNP closure between 30 and 34 somites whereas approximately 50% of all mutant embryos show delayed closure, and around 20% maintain an open PNP even at advanced stages of development. A similar result has been found for embryos developing in vitro from the headfold stage. Later in development, 50–60% of mutant embryos in vivo develop tail flexion defects, and 15–20% lumbosacral myeloschisis. This supports the view that delayed PNP closure is the main developmental lesion leading to the appearance of caudal neural tube defects in curly tail mice. The neural tube is closed in the region of tail flexion defects, but it is locally overexpanded and abnormal in position. The significance of these observations is discussed in relation to possible mechanisms of development of lumbosacral and caudal neural tube defects. This paper constitutes the first demonstration of the development of a genetically induced malformation in vitro.

A cell-type-specific abnormality of cell proliferation in mutant (curly tail) mouse embryos developing spinal neural tube defects

Development ◽  
1988 ◽  
Vol 104 (2) ◽  
pp. 285-295 ◽  
Author(s):  
A.J. Copp ◽  
F.A. Brook ◽  
H.J. Roberts
Keyword(s):  
Cell Proliferation ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
A Cell ◽  
Notochord Cells ◽  
Cell Type Specific ◽  
Reduced Rate ◽  
Gut Endoderm

The mouse mutant curly tail (ct) provides a model system for studies of neurulation mechanisms. 60% of ct/ct embryos develop spinal neural tube defects (NTD) as a result of delayed neurulation at the posterior neuropore whereas the remaining 40% of embryos develop normally. In order to investigate the role of cell proliferation during mouse neurulation, cell cycle parameters were studied in curly tail embryos developing spinal NTD and in their normally developing litter-mates. Measurements were made of mitotic index, median length of S-phase and percent reduction of labelling index during a [3H]thymidine pulse-chase experiment. These independent measures of cell proliferation rate indicate a reduced rate of proliferation of gut endoderm and notochord cells in the neuropore region of embryos developing spinal NTD compared with normally developing controls. The incidence of cell death and the relative frequency of mitotic spindle orientations does not differ consistently between normal and abnormal embryos. These results suggest a mechanism of spinal NTD pathogenesis in curly tail embryos based on failure of normal cell proliferation in gut endoderm and notochord.

Relationship between timing of posterior neuropore closure and development of spinal neural tube defects in mutant (curly tail) and normal mouse embryos in culture

Development ◽  
1985 ◽  
Vol 88 (1) ◽  
pp. 39-54
Author(s):  
Andrew J. Copp
Keyword(s):  
Causal Relationship ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Genetic Predisposition ◽  
Normal Mouse ◽  
Mouse Embryos ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Genetically Determined ◽  
The Relationship

The relationship between timing of closure of the posterior neuropore (PNP) and development of spinal neural tube defects (NTD) has been studied in individual mutant curly tail mouse embryos maintained in culture. Moderate delay in PNP closure results in development of tail flexion defects whereas extreme delay of PNP closure is associated with development of open NTD. Experimental enlargement of the PNP at the stage of 25 to 29 somites leads to delayed PNP closure and development of tail flexion defects in 36 % and 38 % respectively of non-mutant A/Strong embryos. In curly tail embryos, the effect of experimental enlargement of the PNP summates with the genetic predisposition to produce an increased incidence of spinal NTD among which open defects are proportionately more common. These results indicate that a causal relationship exists between delay in PNP closure and development of spinal NTD in mouse embryos. The method described for distinguishing between prospective normal and abnormal curly tail embryos at a stage prior to the appearance of malformations provides an opportunity to study the morphogenetic processes that precede the development of genetically determined spinal NTD.

Curvature of the caudal region is responsible for failure of neural tube closure in the curly tail (ct) mouse embryo

Development ◽  
1991 ◽  
Vol 113 (2) ◽  
pp. 671-678 ◽  
Author(s):  
F.A. Brook ◽  
A.S. Shum ◽  
H.W. Van Straaten ◽  
A.J. Copp
Keyword(s):  
Neural Tube ◽  
Mouse Embryo ◽  
Mouse Embryos ◽  
The Body ◽  
Neural Tube Closure ◽  
Posterior Neuropore ◽  
Curly Tail ◽  
Delayed Closure ◽  
Tube Closure

Delayed closure of the posterior neuropore (PNP) occurs to a variable extent in homozygous mutant curly tail (ct) mouse embryos, and results in the development of spinal neural tube defects (NTD) in 60% of embryos. Previous studies have suggested that curvature of the body axis may delay neural tube closure in the cranial region of the mouse embryo. In order to investigate the relationship between curvature and delayed PNP closure, we measured the extent of ventral curvature of the neuropore region in ct/ct embryos with normal or delayed PNP closure. The results show significantly greater curvature in ct/ct embryos with delayed PNP closure in vivo than in their normal littermates. Reopening of the posterior neuropore in non-mutant mouse embryos, to delay neuropore closure experimentally, did not increase ventral curvature, suggesting that increased curvature in ct/ct embryos is not likely to be a secondary effect of delayed PNP closure. Experimental prevention of ventral curvature in ct/ct embryos, brought about by implantation of an eyelash tip longitudinally into the hindgut lumen, ameliorated the delay in PNP closure. We propose, therefore, that increased ventral curvature of the neuropore region of ct/ct embryos imposes a mechanical stress, which opposes neurulation and thus delays closure of the PNP. Increased ventral curvature may arise as a result of a cell proliferation imbalance, which we demonstrated previously in affected ct/ct embryos.

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