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At least 649 records · Page 36Linked to original sources
PubMed2006

H2O2 induces abnormal tail flexure in Xenopus embryos: similarities with Paraquat teratogenic effects.

BACKGROUND: As previously shown, Paraquat (PQ) treatments of Xenopus developing embryos mainly induce a characteristic developmental alteration we named "abnormal tail flexure." PQ oxidative activity has been indicated as the cause of this malformation. Since PQ evokes reactive oxygen species (ROS), among which hydroxyl radicals (OH(*)), and H(2)O(2) can be converted to (OH(*)) via Fenton reaction, we compared here the lethal and teratogenic potentials of both oxidants by using the Frog Embryo Teratogenesis Assay-Xenopus (FETAX), in order to grasp eventual similarities in their teratogenic activity. METHODS: Xenopus embryos were exposed, from stage 8 to stage 47, at 368, 491, 612, and 735 microM H(2)O(2) and 0.388 microM PQ. The probit analysis of H(2)O(2) mortality and malformed larva percents gave a 598.82 microM Lethal Concentration 50% (LC(50)) and 536.04 microM Teratogenic Concentration 50% (TC(50)) from which a 1.11 Teratogenic Index (T.I.) has been calculated. This T.I. value should allow the classification of H(2)O(2) as a non-teratogenic compound. RESULTS: A comparison of H(2)O(2) mortality and malformed larva percents with those obtained from PQ exposure showed the higher embryotoxicity of PQ, but, markedly, both compounds mainly induced the "abnormal tail flexure." Histological analysis of both H(2)O(2) and PQ malformed embryo tails showed a similar distorted morphology of both somites and myocytes. Some of muscle cells were necrotic and affected by an apical enlargement as well as a detachment from the connective tissue of intersomitic boundaries. CONCLUSIONS: In our opinion, both of the tested chemicals likely weaken the mechanical bridge connecting the myocyte contractile apparatus to the extracellular matrix, therefore causing the detachment of some of tail myocytes from their connectival septum as well as their apical enlargement. This could lead to the unbalance of tail tensional forces and, in turn, to the appearance of the "abnormal tail flexure."

Abnormalities, Drug-Induced↗
PubMed2005

Neptune is involved in posterior axis and tail formation in Xenopus embryogenesis.

In order to elucidate the molecular mechanisms underlying the posterior axis and tail formation in embryogenesis, the function of Neptune, a zinc-finger transcription factor, in Xenopus laevis embryos was investigated. Injection of neptune mRNA into the animal pole area of embryos resulted in the formation of an additional tail structure that included a neural tube and muscle tissue. This activity required FGF signaling since coinjection of a dominant-negative FGF receptor RNA (XFD) completely blocked the formation of a tail structure. A loss-of-function experiment using a fusion construct of neptune and Drosophila engrailed (en-neptune) RNA showed that endogenous Neptune is necessary for formation of the posterior trunk and tail. Furthermore, activity of Neptune was necessary for the endogenous expression of brachyury and fgf-8 at the late gastrula stage. These findings demonstrate a novel function of Neptune in the process of anterior-posterior axis formation through the FGF and brachyury signaling cascades. An experiment using a combination explant with ventral and dorsal marginal tissues showed that cooperation of these two distinct tissues is important for the tail formation and that expression of Neptune in prospective ventral cells may be involved in the activation of the process of tail formation.

Animals↗
PubMed1995

Rat tail suspension reduces messenger RNA level for growth factors and osteopontin and decreases the osteoblastic differentiation of bone marrow stromal cells.

We previously reported that bone marrow stromal cells produce insulin-like growth factors (IGF-I and -II), and that medium conditioned by marrow stromal cells stimulates osteoblast proliferation in vitro. The present study employed the rat tail-suspension model to unload the hindlimbs. It was designed to test the hypothesis that the development of osteopenia or osteoporosis could be due to a deficit in the osteogenic function of marrow stromal cells. Although tail suspension suppressed body weight during the first 3 days of an 11-day pair-fed study, the overall weight gain recorded by these animals was normal. Nevertheless, bone growth was inhibited by suspension. Similarly, the total adherent marrow stromal cell population harvested from the femurs and tibias was decreased by tail suspension, and only half the normal number of fibroblastic stromal cell colonies grew when they were cultured. The proliferation of alkaline-phosphatase-positive cells in the stroma was also inhibited. Northern hybridization revealed that the messenger RNA level for transforming growth factor-beta 2 and IGF-II in stromal cell was reduced by tail suspension. The production of IGF-II by marrow stromal cells was also decreased. The steady-state level of five different transcript sizes of IGF-I mRNA was altered differentially by tail suspension. Osteopontin mRNA was also reduced in marrow stromal cells from tail-suspended rats compared with the normal rats. These data suggest that skeletal unloading not only alters the mRNA level for growth factors and peptide production, but also affects the proliferation and osteogenic differentiation of marrow stromal cells. These changes may be responsible for the reduced bone formation in osteopenia and osteoporosis.

Animals↗
PubMed2004

Seasonal variation in body mass and locomotor kinetics of the fat-tailed dwarf lemur (Cheirogaleus medius).

The fat-tailed dwarf lemur (Cheirogaleus medius) is unusual among primates in storing large amounts of fat subcutaneously prior to hibernating during the winter months. In doing so, it increases its body mass by more than 50%, with a substantial weight gain in the tail. This seasonal increase in mass provides a unique natural experiment to examine how changes in body mass affect substrate reaction forces during locomotion. As body mass increases, it is expected that the limbs of the fat-tailed dwarf lemur will be subjected to greater peak vertical substrate reaction forces during quadrupedal walking. However, whether or not these peak substrate reaction forces will increase proportionally across forelimbs and hindlimbs as body mass increases is unknown. Substrate reaction forces were collected on four adult C. medius walking quadrupedally on a 28-mm pole attached to a force platform. Peak vertical substrate reaction forces (Vpk) (N) were analyzed and compared for a cross-sectional sample of different body masses (180-300 g). Forelimb and hindlimb Vpk were positively correlated with body mass, with hindlimb Vpk always higher than forelimb Vpk. However, the rate at which Vpk increased relative to body mass was higher for the hindlimb than the forelimb. This disproportion in weight distribution between the forelimbs and hindlimbs as body mass increases appears to be linked to the accumulation of fat in the tail. It is likely that storing fat in the tail region may shift the center of mass more caudally, from a more cranial position when the tail is thinner. Such a caudal shift of the center of mass-either morphological or dynamic-is believed to have played an important role in the functional differentiation of the limbs and the evolution of locomotor modes of several tetrapod groups, including dinosaurs and primates.

Adipose Tissue↗
PubMed1975

An unusual two-tailed mouse.

A malformation that resulted in the formation of 2 complete tails is described in a mouse that was heterozygous for the sex-linked gene Bent-tail (Bn). One of the tails appeared normal and contained 29 vertebrae, whereas the other tail consisted of 27 vertebrae and had several bends or kinks in it and also had malformed vertebrae similar to those described for the Bn gene. A comparison of the malformation with previously described bifurcated tail conditions in the mouse is presented. It is possible that this 2-tailed mouse represents a special case of X-chromosome inactivation.

Animals↗
PubMed1989

Direct effects of retinoic acid on the development of the tail bud in chick embryos.

Retinoic acid (RA) has been reported to induce vascular lesions and haematoma formation in the vicinity of the tail bud during the critical period for inducing abnormalities of tail bud development in hamsters (Wiley, '83; Tibbles and Wiley, '88), mice (Tibbles and Wiley, '88) and chicken embryos (Jelinek and Kistler, '81). Experiments were conducted to determine whether or not these vascular lesions were the primary cause of the malformations which they accompanied. Chick embryos were exposed for varying lengths of time to several dosages of RA. Primitive streaks or tail buds from treated embryos were then excised prior to vascularization and transplanted to the coelomic walls of untreated host embryos. The grafts were harvested at 3 or 6 days after grafting and processed for histological examination. Observations of serial sections of controls showed that the primitive streak and early (stage 13-14) tail bud were able to form neural tubes and a variety of other structures including ganglia, nerve fibres, and kidney tubules. Treatment of donor embryos with RA prior to grafting, however, affected the frequency and characteristics of the neural tubes and other tissues developing in the grafts. The effects of RA on development were correlated with both the dosage and length of exposure to the teratogen prior to grafting. Since the grafts were made before the appearance of blood vessels in the tail buds, we have concluded that the effects of RA on the development of tail bud tissues, and especially the secondary neural tube, are direct and are not mediated solely through the disruptive effects of vascular lesions seen in intact embryos.

Animals↗
PubMed2002

Tail morphogenesis in the ascidian, Ciona intestinalis, requires cooperation between notochord and muscle.

We present evidence that notochord and muscle differentiation are crucial for morphogenesis of the ascidian tail. We developed a novel approach for embryological manipulation of the developing larval tissues using a simple method to introduce DNA into Ciona intestinalis and the several available tissue-specific promoters. With such promoters, we misexpressed the Xenopus homeobox gene bix in notochord or muscle of Ciona embryos as a means of interfering with development of these tissues. Ciona embryos expressing bix in the notochord from the 64-cell stage develop into larvae with very short tails, in which the notochord precursors fail to intercalate and differentiate. Larvae with mosaic expression of bix have intermediate phenotypes, in which a partial notochord is formed by the precursor cells that did not receive the transgene while the precursors that express the transgene cluster together and fail to undergo any of the cell-shape changes associated with notochord differentiation. Muscle cells adjacent to differentiated notochord cells are properly patterned, while those next to the notochord precursor cells transformed by bix exhibit various patterning defects. In these embryos, the neural tube extends in the tail to form a nerve cord, while the endodermal strand fails to enter the tail region. Similarly, expression of bix in muscle progenitors impairs differentiation of muscle cells, and as a result, notochord cells fail to undergo normal extension movements. Hence, these larvae have a shorter tail, due to a block in the elongation of the notochord. Taken together, these observations suggest that tail formation in ascidian larvae requires not only signaling from notochord to muscle cells, but also a "retrograde" signal from muscle cells to notochord.

Animals↗
PubMed1993

Binding of aldosterone by epidermal cytosol in the tail of bullfrog larvae.

Characteristics of aldosterone binding by epidermal cytosol in the tail of the larval bullfrog were investigated. Temperature-dependent binding experiments showed that the specific binding of [3H]aldosterone to the tail cytosol was thermolabile. A 3-hr incubation at 0 degrees was the optimum assay condition required for reaching equilibrium. Separation of bound and free hormone was performed using a hydroxylapatite method. Specific binding of aldosterone was observed in the tail epidermis but not in the tail mesenchyme. Saturation analysis revealed that specific binding of [3H]aldosterone to the epidermal cytosol reached maximum between 20 and 40 nM. Scatchard analysis for the cytosol of the tail epidermis yielded a straight line with a dissociation constant (Kd) of 7.0 nM and the maximum number of binding sites (Bmax) of 56.4 fmol/mg protein. Sucrose density gradient analysis of crude cytosol revealed a specific peak of radioactivity in the 8-9 S area. Steroid-binding specificity revealed a significant displacement of the [3H]aldosterone by radioinert aldosterone and, to a lesser extent, by cortisol, whereas 17 beta-estradiol and testosterone competed very poorly. However, corticosterone and dexamethasone, glucocorticoids in mammals, were better competitors of the aldosterone binding, whereas ZK91587, a selective synthetic antagonist for mineralocorticoid receptor in mammals, scarcely inhibited the aldosterone binding. These results suggest that the aldosterone-binding site may also be a corticosterone receptor and that there may be no other receptors specific for aldosterone at least in the tail epidermis.

Aldosterone↗
PubMed2001

Structural organisation of the head-to-tail interface of a bacterial virus.

In tailed icosahedral bacteriophages the connection between the 5-fold symmetric environment of the portal vertex in the capsid and the 6-fold symmetric phage tail is formed by a complex interface structure. The current study provides the detailed analysis of the assembly and structural organisation of such an interface within a phage having a long tail. The region of the interface assembled as part of the viral capsid (connector) was purified from DNA-filled capsids of the Bacillus subtilis bacteriophage SPP1. It is composed of oligomers of gp6, the SPP1 portal protein, of gp15, and of gp16. The SPP1 connector structure is formed by a mushroom-like portal protein whose cap faces the interior of the viral capsid in intact virions, an annular structure below the stem of the mushroom, and a second narrower annulus that is in direct contact with the helical tail extremity. The layered arrangement correlates to the stacking of gp6, gp15, and gp16 on top of the tail. The gp16 ring is exposed to the virion outside. During SPP1 morphogenesis, gp6 participates in the procapsid assembly reaction, an early step in the assembly pathway, while gp15 and gp16 bind to the capsid portal vertex after viral chromosome encapsidation. gp16 is processed during or after tail attachment to the connector region. The portal protein gp6 has 12-fold cyclical symmetry in the connector structure, whereas assembly-naïve gp6 exhibits 13-fold symmetry. We propose that it is the interaction of gp6 with other viral morphogenetic proteins that drives its assembly into the 12-mer state.

Bacillus subtilis↗
PubMed1994

Cold-induced perturbation of cutaneous blood flow in the rat tail: a model of nonfreezing cold injury.

Cold-induced alteration of cutaneous blood flow, measured with laser-Doppler flowmetry, was studied in a rat tail model of nonfreezing cold injury (NFCI). The NFCI-inducing condition consisted of prolonged tail immersion in 1 degree water. Before exposure to the injury condition, tail blood flow (laser Doppler flux) during brief 3 degrees immersion showed cold-induced cycles of vasoconstriction followed by cold-induced vasodilation (CIVD). Tail temperature exhibited cyclic patterns similar to blood flow in response to cold water immersion. Cold exposures to 1 degree for 1 or 3 hr induced no systematic change; however, cold exposures of 6 or 9 hr induced profound and long-lasting blood flow and temperature deviations. Following the cold injury condition, CIVD was completely absent and remained absent for several weeks, suggesting that CIVD loss is an important component in development of NFCI. Cold-induced disturbances of cutaneous blood flow in the rat tail consisted of a sequence of distinctive stages analogous to those described in human NFCI. These stages were evidenced initially by several days of reduced blood flow and thermal sensitivity, followed in a week by a hyperemia stage, and later by enhanced vascular and thermal sensitivity. The cutaneous blood flow alterations and sequence of variations following prolonged cold exposure suggest that the rat tail may be a valid model of human NFCI.

Animals↗
PubMed2025

Dynamic Evolution of Poly-A Tail Lengths Visualized by RNAse H Assay and Northern Blot Using Nonradioactive Probes in Yeast.

Poly-A tail length dynamics have been extensively studied from yeast to human, mostly using reporter transcripts. Recent studies have been carried out genome-wide to determine the status of poly-A tails at steady state. However, poly-A tail measurement at equilibrium gives an overall length that reflects a mixture of the different poly-A tail sizes for a single transcript. New genome-scale techniques are emerging to estimate dynamic of poly-A tails lengths, but they are not yet routine and individual validation experiments are useful. In this chapter we describe a protocol for visualizing poly-A tail lengths following transcription inhibition for a reporter mRNA using denaturing poly-acrylamide gel electrophoresis and northern blot assay. This protocol is quick to set up, requires the purchase of only a few specific reagents, does not rely on radioactivity for RNA monitoring, and can be easily implemented in any molecular biology laboratory.

Poly A↗
PubMed1991

N-CAM, polysialic acid and chick tail bud development.

We have previously shown that the binding of the lectin wheat germ agglutinin (WGA) to developing tail buds results in a range of caudal axial defects, which were most likely due to the affinity of the lectin for sialic acid residues. In the present study, we examined the distribution and role of a sialic acid-containing glycoprotein, N-CAM, in chick tail bud development. In the early tail bud, anti N-CAM, staining was found in the medullary cord. However, there was no uptake of an antibody specific to N-CAM containing moderate to long chains of polysialic acid (5A5 monoclonal antibody). At later stages, while N-CAM localized throughout the neural tube, staining with the 5A5 antibody was restricted to the floor plate. Sub-blastodermal injection of the anti N-CAM antibody beneath the tail bud region of HH stages 13-14 embryos produced caudal axial malformations. These malformations included the presence of accessory segments of neural tube and/or notochord, and fusion between the neural tube and underlying segment of notochord. Our results suggest that N-CAM is present during the development of the secondary neuraxis from the tail bud, although the highly sialylated form of this molecule could not be visualized until relatively late stages. N-CAM probably plays a role in the normal course of tail bud development, since perturbation of the molecule with an antibody resulted in malformations. Since these malformations were similar to those we have previously reported when we treated similarly staged chick embryos with WGA, there is a possibility that the sialic acid residues recognized and bound by the lectin are those associated with the N-CAM molecule.

Animals↗
PubMed1990

Evidence for the involvement of receptors for fibronectin in the promotion of chick tail segmentation.

In the chick embryo the paraxial mesoderm forms about 50-53 pairs of somites, the precise number depending on the extent to which segmentation proceeds along the tail. However, the terminal mesoderm of the tail fails to segment despite the fact that it appears to contain a reservoir of potential somites. Why does this mesoderm not segment? Some clues can be obtained by comparing this non-segmenting region with the segmental plate in the trunk. We and others have shown that in the trunk region of the chick, cell adhesion plays a major role in somitogenesis and that this increased cell adhesion is associated with compaction of segments of mesoderm immediately prior to segmentation. This compaction can be brought about prematurely by fibronectin and by the specific adhesion peptide GRGDS. The terminal mesoderm in the tail resembles the segmental plate mesoderm in the trunk in undergoing compaction in response to fibronectin and GRGDS. The tail mesoderm differs from the segmental plate mesoderm in that it can also respond to peptides closely related to GRGDS. The response suggests that, whereas the integrin receptors for fibronectin and GRGDS appear to be specific in the presomitic trunk mesoderm, responding only to the specific adhesion-peptide GRGDS, the tail mesoderm may contain more heterogeneous sets of receptors within the integrin/VLA family that respond to a wider variety of ligands. Coincident with these differences is the phenomenon of regional cell death in the tail bud mesoderm. All of these factors are thought to play a role in the extent of segmentation in the paraxial mesoderm of the embryonic chick.

Animals↗
PubMed1993

Mapping of the murine and rat Facc genes and assessment of flexed-tail as a candidate mouse homolog of Fanconi anemia group C.

Fanconi anemia is a rare, autosomal recessive disorder characterized at the cellular level by a combination of hypersensitivity to DNA-damaging agents and chromosomal instability. Clinical features include pancytopenia, often associated with specific congenital malformations, and a predisposition to leukemia. We previously cloned the gene defective in Fanconi anemia group C by complementation of the intrinsic sensitivity of Fanconi anemia cells to DNA cross-linking agents, and we recently cloned its mouse homolog (Facc). In this report, we localized Facc to mouse Chromosome (Chr) 13 and its rat homolog to rat Chr 17. A previously described anemic mouse mutant, flexed-tail, maps to the same chromosomal region. Differences were detected between DNA of the flexed-tail and congenic mice, indicating the proximity of the Facc probe to the disease mutation. Analysis of flexed-tail RNA did not reveal detectable difference in Facc message level or size between flexed-tail and congenic mice. On this basis, we conclude that, although flexed-tail remains a candidate for Fanconi anemia in the mouse, there is no evidence currently that Facc is mutated in flexed-tail mice.

Animals↗
PubMed1988

Studies of neural tube development in the chicken embryo tail.

The tail regions of chick embryos between stages 21 to 46 were studied by light microscopy using paraffin- and epoxyembedded serial sections. The embryonic tail attains its maximum length at about stage 22. The present study examined the morphogenesis of the caudal neural tube during the reduction and remodelling processes of the embryonic tail. Between stages 21 and 28, the embryonic tail became markedly shorter, and the neural tube, with a single central canal, merged caudally with the short medullary cord and tail bud. Between stages 29 and 31, the neural tube elongated and curved rostrally, while the caudal end of the notochord and the tail bud disappeared. Between stages 32 and 39, after showing various structural changes such as dilatation or rupture and abnormal elongation of its marginal zone the neural tube became shorter. By stage 40, development of the caudal neural tube was essentially complete and the neural tube was shorter than the notochord. The neural tube opened dorsally, as in the adult chicken. The caudal opening may be newly-formed as the open portion was found to contain numerous macrophages.

Animals↗
PubMed1985

Preferential antagonism by diltiazem of alpha 2-adrenoceptor mediated vasoconstrictor responses in perfused tail arteries of spontaneous hypertensive rats.

Vasoconstrictor responses mediated by the alpha 2-adrenoceptor agonist TL99, were particularly sensitive to blockade by the calcium antagonist drug diltiazem in isolated perfused tail arteries of spontaneously hypertensive rats (SHR). In contrast, the vasoconstrictor responses induced by the alpha 1-adrenoceptor agonist methoxamine were significantly more resistant to antagonism by diltiazem. At higher concentrations (greater than 300 nmol/l) diltiazem became an effective antagonist of all alpha-adrenoceptor mediated responses. In normotensive Wistar Kyoto (WKY) or Sprague-Dawley (SD) rats diltiazem was significantly less potent against vasoconstrictor responses to TL99 than in SHR. The blockade of alpha 1-adrenoceptor mediated vasoconstriction by diltiazem was not significantly different when normotensive rats and SHR were compared. The vasoconstrictor responses evoked by 5HT in the perfused tail arteries were particularly resistant to blockade by diltiazem in SHR arteries. The responses to endogenously released noradrenaline, evoked by electrical field stimulation, were significantly antagonised by diltiazem (30 nmol/1-3 mumol/l) in SHR-tail arteries, while they were not modified in WKY-tail arteries. At the concentrations of diltiazem which blocked end organ responses to field stimulation, there was no modification of total tritium overflow from SHR-tail arteries after labelling the tissue with 3H-noradrenaline, indicating that diltiazem does not inhibit transmitter release at these concentrations. The tail artery preparation of SHR contains a population of postsynaptic alpha 2-adrenoceptors which mediate contraction in this blood vessel and the calcium entry blocker diltiazem is a potent antagonist of vasoconstrictor responses mediated by vascular alpha 2-adrenoceptors in hypertensive rats. These findings may be relevant to the antihypertensive action of diltiazem.

Adrenergic alpha-Agonists↗
PubMed1986

An experimental and morphological analysis of the tail bud mesenchyme of the chick embryo.

In the chick embryo, the tail bud reaches its maximum length at about stage 22 of Hamburger and Hamilton, after which it starts to regress. By this stage the neural tube and notochord extend right to the tip of the tail, but the somites do not do so, the terminal tail bud mesoderm never becoming segmented. The investigation is concerned with analysing why this mesoderm fails to segment. When tail buds were explanted to the chorio-allantoic membrane, they continued to form somites only until the "correct" number had segmented, i.e., the tail bud formed no more somites when isolated from the embryo than it would have formed if undisturbed. Morphological studies suggest that in the normal embryo massive cell death overtakes the tail bud mesoderm before it can segment. It is suggested therefore that cell death may be a contributory factor in preventing segmentation.

Allantois↗
PubMed1992

N-methyl-D-aspartate lesions of the lateral hypothalamus do not reduce amphetamine or fenfluramine anorexia but enhance the acquisition of eating in response to tail pinch in the rat.

These experiments examine the acquisition of tail pinch-induced eating and responses to the anorectic agents d-amphetamine and d,l-fenfluramine by rats bearing N-methyl-D-aspartate (NMDA) lesions of the lateral hypothalamus. Lesioned rats lost weight following surgery but had no significant eating or drinking difficulties in the home cage (Clark et al. 1990). The acquisition of eating in response to tail pinch was enhanced in lateral hypothalamic-lesioned rats: they ate on earlier test sessions than controls and less pressure was required to elicit eating. Home cage food intake over the period when tail pinch was being examined was not affected by the lateral hypothalamic lesions. There were no significant differences between lateral hypothalamic-lesioned and control rats in terms of their anorectic responses to either d-amphetamine or d,l-fenfluramine, though the lesioned rats had a lower baseline intake. These data suggest that the lateral hypothalamus is not an important site for the mediation of amphetamine or fenfluramine anorexia but is involved in the acquisition of tail pinch-induced eating. The disinhibition of responding to tail pinch by lateral hypothalamic lesions is discussed in terms of the possible role the lateral hypothalamus plays in regulating cortical activity. The role of the medial hypothalamus and non-hypothalamic systems in the response to anorectic drugs and tail pinch is discussed.

Amphetamine↗