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At least 883 records · Page 49Linked to original sources
PubMed2004

Further characterization of the genetic defect of the Bent tail mouse, a mouse model for human neural tube defects.

BACKGROUND: Neural tube defects (NTDs) are congenital malformations arising mostly from incomplete neural tube closure during early embryogenesis. Most NTDs in humans have a complex etiology, with involvement of both genetic and environmental factors. More than 100 mouse models for human neural tube defects exist; Bent tail is one of them. The mouse mutant is caused by a submicroscopic deletion on Xq that completely encompasses the Zic3 gene. METHODS: We searched the ENSEMBL database for other genes/transcribed sequences in the Bent tail deletion in addition to Zic3, which we confirmed by PCR analysis. RESULTS: In our study, we show that the Bent tail deletion is at least 300 kb in size, encompassing a processed pseudogene and a number of expressed sequence tags in addition to Zic3. Although more research is needed to clarify the identity and function of the deleted transcripts, most of them are expressed during embryonic development and might therefore contribute to the phenotype of the Bent tail mouse. CONCLUSIONS: This study presents the first evidence for the fact that the Bent tail allele is not merely a Zic3 knockout allele, as has been previously suggested.

Animals↗
PubMed1990

Effect of negative air ions on morphine-induced changes in the latency of the tail-flick reflex.

Adult male Long-Evans rats were exposed to negatively charged air ions at high concentrations (7 x 10(5)/cm3) for six days. Sham-exposed rats were treated identically except that the source of ions was not activated. At the end of the exposure, the latency of the tail-flick reflex was measured in each rat before and 30 and 60 min after an injection of morphine sulphate. The tail-flick reflex was initiated by thermal stimulation. Two heat settings were employed, the lower considered to impart a submaximal and the higher a maximal thermal stimulus. Three morphine doses were tested: 0.5, 1.0, and 1.5 mg/kg. Statistically significant differences between ion-exposed and sham-exposed rats were observed in tail-flick latencies 30 min after the administration of the two lower doses, but not after the highest dose of morphine sulphate. These differences were found at both intensities of thermal stimulation. Tail-flick latencies measured in each group prior to morphine injection were not affected by negative-ion exposure. The data indicate that exposure of rats to negative air ions tends to inhibit the action of morphine on the latency of the tail-flick reflex at morphine doses below 1.0 mg/kg.

Air Ionization↗
PubMed2003

Dual mechanisms governing muscle cell death in tadpole tail during amphibian metamorphosis.

The tadpole tail, which is twice as long as the body, is induced to resorb completely by thyroid hormone within several days during the anuran metamorphosis. To investigate the underlying mechanism, we undertook two approaches. First, we examined the effect of dominant-negative thyroid hormone receptor (DNTR) on muscle cell death in vitro. The overexpression of DNTR suppressed the death of a tail-derived myoblastic cell line induced by thyroid hormone. Second, tadpole tails were injected with a reporter gene and the DNTR expression construct, and the reporter gene expression in muscle cells was followed during the spontaneous metamorphosis. DNTR overexpression inhibited a decrease of the reporter gene expression that began at stage 57 in the control tadpoles but only delayed massive muscle cell death at stage 63 when tails shrink very rapidly. Some remained even a few weeks after the metamorphosis, although most DNTR-overexpressing cells died by the end of the metamorphosis. These results led us to propose that thyroid hormone induces the suicide of muscle cells (the cell-autonomous death) in the tail between stage 57 and 62 and that both the murder and suicide mechanisms execute muscle cell death in stage 62-64 to remove muscle promptly and completely.

Animals↗
PubMed1975

Regeneration of the tail bud in Xenopus embryos.

In an attempt to solve some aspect of the long-standing controversy about the regenerative ability of appendages in vertebrate embryos, the tail bud of Xenopus laevis embryos has beenamputated at stage sranging from St. 26 to St. 32 and its ability to regenerate duringa culture period of 2-3 days has been studied. At amputation stages 26-28,the tail bud consisted only undifferentialted mesoderm and ectoderm, but at stage 32 it had afully differentiated neural tube, a vaculotaed notochord and segmented somites. A total of 137amputations at differnt stages gace consistent results: a tail formed in all the operated larvacand it had normal, well-developed axial tissues in most cases. The relatively few cases with abnormal tail struture were stunted, oedematour larvae with defects in the trunk region as well. It is concluded from these experiments that cells near the original tail budare able to differentiate into tialbud tissues and to replace the amputated regoin, even at these late embryoic stages. The implications of these findings for comparative studies on regeneration in vertebrates are discussed.

Amputation, Surgical↗
PubMed2005

Wound keratins in the regenerating epidermis of lizard suggest that the wound reaction is similar in the tail and limb.

The keratin cytoskeleton of the wound epidermis of lizard limb (which does not regenerate) and tail (which regenerates) hase been studied by qualitative ultrastructural, immunocytochemical, and immunoblotting methods. The process of re-epithelialization is much shorter in the tail than in the limb. In the latter, a massive tissue destruction of bones, and the shrinkage of the old skin over the stump surface, delay wound closure, maintain inflammation, reduce blastemal cell population, resulting in inhibition of regeneration. The expression of special wound keratins found in the newt epidermis (W6) or mammalian epidermis (K6, K16, and K17) is present in the epidermis of both tail and limb of the lizard. These keratins are not immunolocalized in the migrating epithelium or normal (resting) epidermis but only after it has formed the thick wound epithelium, made of lacunar cells. The latter are proliferating keratinocytes produced during the cyclical renewal or regeneration of lizard epidermis. W6-immunolabeled proteic bands mainly at 45-47 kDa are detected by immunoblotting in normal, regenerating, and scarring epidermis of the tail and limb. Immunolabeled proteic bands at 52, 62-67 kDa (with K6), at 44-47, 60, 65 kDa (with K16), and at 44-47 kDa (with K17) were detected in normal and regenerating epidermis. It is suggested that: (1) these keratins constitute normal epidermis, especially where the lacunar layer is still differentiating; (2) the wound epidermis is similar in the limb and tail in terms of morphology and keratin content; (3) the W6 antigen is similar to that of the newt, and is associated with tonofilaments; (4) lizard K6 and K17 have molecular weights similar to mammalian keratins; (5) K16 shows some isoforms or degradative products with different molecular weight from those of mammals; (6) K17 increases in wound keratinocytes and localizes over sparse filaments or small bundles of short filaments, not over tonofilaments joined to desmosomes; and (7) failure of limb regeneration in lizards may not depend on the wound reaction of keratinocytes.

Amputation Stumps↗
PubMed1995

Identification of heterotrimeric G proteins in human sperm tail membranes.

Heterotrimeric G proteins play important roles as signal transducing components in various mammalian sperm functions. We were interested in the distribution of G proteins in human sperm tails. Prior to membrane preparation, spermatozoa were separated from contaminating cells which are frequently present in human ejaculates. Enriched human sperm tail membranes were generated by using hypoosmotic swelling and homogenization procedures. Antisera against synthetic peptides were used to identify G proteins in immunoblots. AS 8, an antiserum directed against an amino acid sequence that is found in most G protein alpha-subunits, and A 86, which detects all known pertussis toxin-sensitive alpha-subunits, reacted specifically with a 40-kDa protein. Antisera against individual G protein alpha-subunits failed to detect any specific antigens in enriched tail membranes. AS 36, recognizing the beta 2-subunit of G proteins, identified a 35-kDa protein in sperm tail membranes. Antisera against the 36-kDa beta 1-subunit did not detect any relevant proteins in the membrane fraction. Neither G protein alpha-subunits nor G protein beta-subunits were found in the cytosol. ADP ribosylation of spermatozoal membrane or cytosolic proteins revealed no pertussis toxin-sensitive alpha-subunits. However, membrane preparations of nonpurified human spermatozoa contained alpha i2 subunits, as shown immunologically and by ADP ribosylation; they most probably derived from somatic cells which are frequently present in human ejaculates. Our results stress the fact that spermatozoa need to be purified before sperm membrane preparation to avoid misinterpretations caused by contaminating cells. Furthermore, we suggest that G proteins in membranes of human sperm tails belong to a novel subtype of G protein alpha-subunits; the putative beta-subunit was identified as a beta 2-subunit.

Cell Membrane↗
PubMed1993

Tail short variable: characterization of a new mouse mutant, and its possible analogy to certain human vascular disruption defects.

A new mouse mutant, tail short variable (Tsv) produces a reduction deformity of the tail, growth retardation, and, in adults, a mild anemia. Genetic and embryological studies show that on all genetic backgrounds there is variable viability of Tsv/Tsv and Tsv/+ and phenotypic overlap within these and with +/+. A modifier is located to a short segment of chromosome 7, which alters the tail length of Tsv/+ mice up to 15%. The modifier, Tsv, and a coat texture mutant come from the same wild Peru mouse. The tail deformity is associated with, and may be caused by, a vascular disruption of the caudal aorta starting on day 11 of gestation. Thus Tsv appears to be different from each of the thirty known mouse mutants involving the tail. It is suggested that Tsv could be a mouse model for human conditions involving transverse terminal limb defects such as Moebius and de Lange syndromes.

Anemia↗
PubMed1993

Schistosoma mansoni: fatty acid-induced cercarial tail loss does not involve eicosanoid production and chemoreceptors.

Inhibitors of eicosanoid production had no effect on linoleic acid-induced Schistosoma mansoni cercarial tail loss. In addition, linoleic acid-induced cercarial tail loss was not inhibited by silver nitrate, which binds to putative chemoreceptors for fatty acids in cercariae. There was no correlation between molecular structures of fatty acids and their potencies to induce tail loss. Furthermore, transcompounds of fatty acids which cannot be precursors of eicosanoids elicited tail loss as potently as cis-compounds did. The present results suggest that fatty acid-induced cercarial tail loss is not mediated by eicosanoid production and chemoreceptors, which are involved in cercarial penetration behavior stimulated by fatty acids.

Animals↗
PubMed1994

The use of ubiquitin as a marker of thyroxine-induced apoptosis in cultured Rana catesbeiana tail tips.

Cultured Rana catesbeiana tadpole tail tips were used in combination with a fluoroimmunoassay to determine the levels of ubiquitin--a protein marker of programmed cell death in other systems--during the tissue regression induced by thyroxine (T4). After a 3-day pretreatment with the hormone, tail tips cultured in T4 showed significant increases in ubiquitin levels by 48 hr. Tail tips taken from tadpoles that had been immersed in T4 for 6 days showed a parallel increase in ubiquitin levels, demonstrating the same change in vivo. Treatment of cultured tail tips with the protein kinase C inhibitor, H-7, blocks both regression and the rise in ubiquitin seen in tips treated with T4 alone. Treatment of cultured tips with T4 and either cycloheximide or actinomycin D inhibits regression compared to T4 alone; however, the rise in ubiquitin is only blocked by cycloheximide, suggesting that ubiquitin is being made from RNA that was synthesized during the pretreatment period or earlier. These results suggest that ubiquitin will serve as a good molecular marker of tissue regression in the T4-treated tadpole tail and that it will be productive to consider tissue regression during amphibian metamorphosis as a specific case of programmed cell death or apoptosis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Mutational analysis of two structural genes of the temperate lactococcal bacteriophage TP901-1 involved in tail length determination and baseplate assembly.

Two putative structural genes, orf tmp (tape measure protein) and orf bpp (baseplate protein), of the temperate lactococcal phage TP901-1 were examined by introduction of specific mutations in the prophage strain Lactococcus lactic ssp. cremoris 901-1. The adsorption efficiencies of the mutated phages to the indicator strain L. lactic ssp. cremoris 3107 were determined and electron micrographs were obtained. Specific mutations in orf tmp resulted in the production of mostly phage head structures without tails and a few wild-type looking phages. Furthermore, construction of an inframe deletion or duplication of 29% in orf tmp was shown to shorten or lengthen the phage tail by approximately 30%, respectively. The orf tmp is proposed to function as a tape measure protein, TMP, important for assembly of the TP901-1 phage tail and involved in tail length determination. Specific mutations in orf bpp produced phages which were unable to adsorb to the indicator strain and electron microscopy revealed particles lacking the baseplate structure. The orf bpp is proposed to encode a highly immunogenic structural baseplate protein, BPP, important for assembly of the baseplate. Finally, an assembly pathway of the TP901-1 tail and baseplate structure is presented.

Adsorption↗
PubMed1992

The vertebrate tail bud: three germ layers from one tissue.

The tail bud of amniote embryos comprises a mass of apparently undifferentiated mesenchymal cells located at the caudal limit of the embryo, representing the remains of Hensen's node and the primitive streak. These cells have the potential to give rise to a variety of different tissues including the posterior or 'secondary' neural tube, the tail gut, and somites and their derivatives. This seemingly homogeneous accumulation of cells therefore has the capacity to differentiate into tissues which in more cranial regions of the embryo are derived from cells of different germ layers. In this review, the tissue contributions of the tail bud in various vertebrate classes are discussed, with particular attention to the mesenchymal-to-epithelial transformation that characterizes the process of secondary neurulation, and which distinguishes it from the epithelial folding that occurs during primary neurulation in more cranial regions. Recent studies suggest that the transformation is accompanied by extensive changes in the cell surface oligosaccharide complement of the differentiating cells, and that the sialyted form of N-CAM is expressed both temporally and spatially in a manner that suggests a role for it in the process. The pluripotential nature of the tail bud mesenchyme may be revealed experimentally by grafting the tissue ectopically, or by culturing it on different substrata. In the latter case, the mesenchyme can be demonstrated to give rise to myocytes, chondrocytes, neuroepithelium and neural crest derivatives such as melanocytes, depending on the nature of the culture substratum. It is concluded that the tail bud mesenchyme represents a developing system which is readily amenable to experimentation and should provide insights into the general mechanisms of cell differentiation and transformation.

Amphibians↗
PubMed1994

Adult precursor cells in the tail epidermis of Xenopus tadpoles.

Polyclonal antibodies were raised against Xenopus larva-specific 58 kDa keratin (PAK58) and adult-specific 63 kDa keratin (PAK63), in order to examine the origin of 63 kDa-keratin-producing cells in the tail skin. By immunofluorescent staining of the tail skin, the 58 kDa keratin was recognized in almost all of the larval epidermal cells, although a small number of PAK58-negative cells were detected at stage 64. In contrast, 63 kDa keratin was immunohistochemically recognized at stage 58, but the signal was very weak. The number of epidermal layers in the tail epidermis increased during a period from stage 58 to stage 64. At stage 64, a small number of PAK63-positive cells was clearly identified in the multilayered tail epidermis. Comparative analysis of successive sections showed that PAK63-positive cells are derived from a cell group differing from PAK58-positive cells. Immunohistochemical studies using cultured epidermal cells demonstrated that 58 kDa keratin is localized in the cytoskeletal bundles of skein cells, whereas 63 kDa keratin is produced not by skein cells but by basal cells and their descendants. These results suggest that basal cells are the adult precursor cells within the larval epidermis even in the tail area.

Animals↗
PubMed1989

Origin of the notochord in the rat embryo tail.

The origin of the notochord in the rat tail was investigated on transverse serial semi-thin and ultra-thin sections of 12- and 13-day embryo tails. It was found that the notochord develops from a mass of condensed mesenchymal cells which is located ventrally to the secondary neural tube, and which subsequently splits into a) a thin cord which becomes notochord and b) a thick portion which gives rise to the tail gut. By analogy with the secondary neurulation and the secondary gut formation, one might therefore speak of a secondary notochord formation in the tail. It occurs in close relationship with the formation of the tail gut.

Animals↗
PubMed1984

Activation of central warm-sensitive neurons and the tail vasomotor response in rats during brain and scrotal thermal stimulation.

The effects of preoptic and hypothalamic thermal stimulation on tail skin temperature were observed at different scrotal temperatures. The threshold hypothalamic temperature for tail vasodilation at a scrotal temperature of 40 degrees C was significantly lower than that at a scrotal temperature of either 25 degrees C or 33 degrees C. The effects of scrotal thermal stimulation on tail skin vasodilated by higher hypothalamic temperatures were observed. Cooling the scrotum from 42 to 30 degrees C invariably caused a rapid fall in tail temperature, whereas scrotal cooling from 30 to 25 degrees C did not cause any significant change. Cooling of either the left or right half of the scrotum caused a similar fall in tail temperature. The temperature characteristics of the preoptic hypothalamic thermo-sensitive neurons were determined at scrotal temperatures of 32, 36 and 26 degrees C. The firing rate of warm-sensitive neurons at a given hypothalamic temperature was highest at a scrotal temperature of 36 degrees C, while that of cold-sensitive neurons was lowest at that temperature. The scrotal temperature range over which the number of neurons activated by scrotal warming increased rapidly was between 36 and 39 degrees C when hypothalamic temperature was held at 36-37 degrees C.

Animals↗
PubMed1980

Tail skin vasodilatation and bath test in capsaicin-desensitized rats.

Vasodilatation in response to heat, the role of tail vasodilatation in thermolysis and the ability of the animals to use free water for evaporative cooling were studied in control and capsaicin-desensitized rats. 1) While vasodilatation in the tail began in the controls as soon as their temperatures reached 38.5-39 degrees C, in most of the desensitized rats the onset of this reaction was above a body temperature of 40 degrees C. 2) When exposed to 32 degrees C, desalivated capsaicin-treated rats showed a significant hyperthermia as compared to the controls. If the tails were amputated too, the temperatures of the controls rose to near those of the desensitized animals. 3) In the case of prolonged heat exposure or at a higher ambient temperature (38 degrees C), the desalivated tail-amputated controls still remained more tolerant to heat than the desensitized rats. 4) Even at an ambient temperature of 38 degrees C, desalivated controls without tails exhibited excellent thermoregulation when a water bath was present; they used the free water for evaporation. Capsaicin-treated rats neglected the water bath, and their temperatures rose continuously. 5) The results suggests that capsaicin treatment impaired reflex vasodilatation to heat and the behaviour of using free water for heat dissipation.

Animals↗
PubMed2002

The relationship between tail use and positional behavior in Alouatta palliata.

The relationship between tail use and positional behavior is explored in Alouatta palliata. During bridging, climbing, suspension, standing, and sprawling, the tail is attached to a substrate for the majority of sample points. Tail attachment was more likely to occur when the animal is traveling on vertical or terminal substrates. Quadrupedalism showed few instances of attachment and sitting reflected nearly equal amounts of prehension and non-prehension. Tail prehension is used in all behavioral contexts but shows higher frequencies of attachment during feeding than during resting, or foraging. Tail prehension appears to aid in the stability, support, and balance of the animal across numerous positional behaviors.

Alouatta↗
PubMed2002

Genetics analysis of mouse mutations Abnormal feet and tail and rough coat, which cause developmental abnormalities and alopecia.

Mutations in the mouse Brachyury (T) gene are characterized by a dominant reduction of tail length and recessive lethality. Two quantitative trait loci, Brachyury-modifier 1 and 2 (Brm1 and Brm2) are defined by alleles that enhance the short-tail Brachyury phenotype. Here we report on a genetic analysis of a visible dominant mutation Abnormal feet and tail (Aft) located in the vicinity of Brm1. Affected animals display kinky tails and syndactyly in the hindlimbs, both likely resulting from a defect in apoptosis. We observed an unusual genetic incompatibility between Aft and certain genetic backgrounds. We show that Aft and T are likely to interact genetically, since some double heterozygotes are tailless. In addition to the tail and hindlimb phenotypes, Aft-bearing mutants display characteristic late-onset skin lesions. We therefore tested for allelism between Aft and a closely linked recessive mutation rough coat (rc) and found that these two mutations are likely nonallelic. Our results provide a valuable resource for the study of mammalian skin development and contribute to the genetic analysis of Brachyury function.

Abnormalities, Multiple↗
PubMed2006

Centrally acting imidazolines stimulate vascular alpha 1A-adrenergic receptors in Rat-Tail Artery.

: 1. Centrally acting imidazoline antihypertensive agents clonidine and moxonidine also act peripherally to contract blood vessels. While these agents act at both I(1)-imidazoline and alpha 2 adrenergic receptors centrally, the receptor types by which they mediate contraction require further definition. We therefore characterized the receptor subtype by which these agents mediate contraction of proximal rat-tail artery. 2. Dose-response curves were determined for phenylephrine and for several imidazoline ligands, using endothelium denuded, isolated ring segments, of tail arteries from adult male Sprague-Dawley rats. Ring segments were mounted on a force transducer with platinum wires and immersed in a tissue bath containing Krebs solution, to which drugs could be added. Signals were digitized and recorded by a computer. 3. Tail artery contractions expressed as a percent of contraction to 106 mM potassium were phenylephrine (96%), moxonidine (88%), clonidine (52%), and UK14304 (30%). Neither rilmenidine nor harmane caused contraction. Contraction of tail artery to moxonidine or clonidine could be blocked by alpha 1 antagonist urapidil or prazosin, and also by alpha 1A subtype selective antagonist WB4101. Schild plots were generated and a calculated pA2 value of 9.2 for prazosin in the presence of clonidine confirms clonidine as an agonist at alpha 1A receptors in proximal segments of rat-tail artery. 4. Our work suggests that clonidine and moxonidine are promiscuous compounds at micromolar concentrations and that harmane and rilmenidine are more selective compounds for in vivo imidazoline research.

Animals↗