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PubMed2003

Human blood group antigen H is not the specific marker for type I cells in the taste buds.

We examined the localization of human blood antigen H (AbH) and its correlation with other cell type markers in the taste buds of circumvallate papillae of the adult rat. Immunoreactivity for AbH was localized in the membrane of two cell populations in the taste buds: in spindle-shaped cells extending from base to the apical portion of the taste buds as well as in round-shaped cells at the basal portion of the taste buds. Quantitative analysis revealed that approximately 47.8%, 24.4%, and 14.6% of cells within the taste buds displayed AbH-, alpha-gustducin- or protein gene product 9.5 (PGP 9.5)-immunoreactivity, respectively. Approximately 16.3% and 6.6% of AbH-immunoreactive taste bud cells displayed alpha-gustducin- or PGP 9.5-immunoreactivity, respectively. Although previous studies proposed that AbH immunoreactivity was specific for type I cells (dark cells or supporting cells), the present results indicate that AbH immunoreactivity is also present in some type II cells (alpha-gustducin immunoreactive cells) and type III cells (PGP 9.5-immunoreactive cells).

ABO Blood-Group System↗

PubMed1980

Ultrastructural and histochemical studies on the taste buds in some reptiles.

The taste buds in tortoises (Clemmys japonica and Geoclemys reevesii), lizards (Takydromus tachydromoides) and snakes (Elaphe quadrivirgata) were examined by both ultrastructural and histochemical methods. The taste buds consisted of at least three types of cells: the type I, II and III cells. The type I cells were characterized by the presence of secretory dense granules containing polysaccharides which were demonstrated by periodic acid-chromic acid-silver methenamine technique. The type II cells contained numerous tubular, vesicular and lamellated structures. The type III cells were characterized by dense cored vesicles and afferent synaptic contacts. Besides these cells, basally located cells which resembled the basal cells of other lower vertebrates were sometimes found in the tortoises. After administration of L-DOPA following nialamide, some taste bud cells of the tortoises, Clemmys japonica, showed weak yellowish green fluorescence by monoamine fluorescence histochemistry and the dense-cored vesicles in the type III cells increased in number. Acetylcholine esterase activity was not observed in tortoise taste buds. It is suggested that the three types of cells which compose the taste buds of the reptiles may correspond to the three types of cells in mammalian, and the type III cells represent the gustatory cells which are able to potentially produce biogenic monoamines. From these results, the taste buds of the reptiles may hold an intermediate position between those of mammals and amphibia or fishes.

5-Hydroxytryptophan↗

PubMed1998

Functional significance of the co-localization of taste buds and teeth in the pharyngeal jaws of the largemouth bass, Micropterus salmoides.

Studies of feeding behavior in the largemouth bass, Micropterus salmoides, revealed that live goldfish or artificial food balls are ingested in three discrete steps: inhalation of the food into the oral cavity, passage through the pharyngeal cavity, and swallowing. Food balls with or without a feeding stimulant were inhaled with equal frequency; thus, vision was clearly the major sense affecting inhalation. However, food balls with defined concentrations of a feeding stimulant were swallowed in a dose-dependent manner, whereas food balls without a feeding stimulant were promptly expelled. Thus, gustation played a major role in stimulating swallowing. Videotaped observations of feeding behavior suggested that both food processing and gustation occur in the pharynx and take place before the swallowing of either goldfish or food balls. The well-developed pharyngeal jaws of largemouth bass consist of six major pads of caniform teeth in the upper pharynx and two pads in the lower pharynx. Scanning electron microscopy showed that taste buds were abundant around most of these pharyngeal teeth. Histological sections prepared from all pharyngeal pads revealed that both elevated and flattened taste buds occur with the teeth. The morphology of these taste buds was typical of that described in other teleosts. Neuronal profiles, visualized with an HNK-1 monoclonal antibody, were observed entering each taste bud. The antibody also selectively stained a group of one to four putative sensory cells in each taste bud and the distal processes of these cells in the receptor area. The co-localization of teeth and taste buds on the pharyngeal jaws indicates that food processing and gustation both occur there, and that together these processes determine whether a potential food item is swallowed.

Animals↗

PubMed1979

The occurrence of taste buds in the palate of human adults as evidenced by light microscopy.

There is some uncertainty in the literature as to the existence of taste buds in the palate of the human adult. In those histologic studies in which the ages of the individuals have been reported, taste buds have not been found in the palates of adults, but have been found in fetuses or newborn. However, clinical studies have demonstrated taste perception in the palate of the human adult. Thus, the aim of the present study was to attempt to find taste buds in the human palate in subjects of different ages. In serial sections of selected areas of the palatal mucosa from autopsy material from individuals 0--80 years of age no taste buds could be demonstrated. However, in four of seven subjects aged 25--44 years, one or two taste buds were found in biopsies from areas of the soft palate where taste perception had been demonstrated clinically just prior to excision. Thus the present study indicates that scattered taste buds exist also in the soft palate of human adults.

Adolescent↗

PubMed1999

Behavior of cells in artificially made cell aggregates and tissue fragments after grafting to developing hind limb buds in Xenopus laevis.

During vertebrate limb development, the limb bud grows along the proximo-distal (P-D) direction, with the cells changing their adhesiveness. To know whether the position-related differences in cell adhesiveness are actually utilized by morphogenesis to constitute limb structures, we grafted cell aggregates made of dissociated cells derived from different positions and stages of developing hind limb buds into developing hind limb buds and observed the behavior of the cells. Cell aggregates made of dissociated mesenchymal cells from two different origins were implanted in different positions and stages of limb buds or grafted on limb stumps made by cutting. The two grafted cell populations in the aggregate always sorted out from each other, but their patterning of sorting-out was quite different according to the transplanted regions. In summary, cells in the aggregate that have closer positional identity to the transplanted site were always situated at the boundary between host and donor cells. The pattern of sorting-out seemed to be determined by the relative adhesiveness of surrounding cells to the constituent cells of the aggregates. We also transplanted fragments dissected out from different regions along the P-D axis into st. 50 limb buds. The descendants of grafted cells moved distally to the region corresponding to their positional identity and participated in the formation of more distal structures from that point. These results suggest that the difference in cell adhesiveness may probably play a role in arranging cells along the P-D axis of a developing limb bud.

Animals↗

PubMed1981

[Lingual taste buds following application of colchicine to the glossopharyngeal nerve in the rat].

Dissection of the glossopharyngeal nerve and application to it of colchicine that blocks axoplasmic drug transport were performed to study the effect of the nerves on the taste buds of foliate lingual papillae. It was observed that colchicine application to the nerve gave rise to destruction of the taste buds. The process of destruction proceeded more slowly as compared to that induced by nerve dissection. Colchicine application led to changes in the protein spectrum of the epithelium of foliate papillae. The absence of changes in the protein spectrum of the epithelium of foliate papillae and the presence of nerve fibers in the epithelium of the taste buds on exposure to colchicine provide evidence against its direct toxic effect on the taste buds, giving rise to their destruction. The changes seen in the taste buds result from the blocked transport of factors that participate in neurotropic control of the taste buds.

Animals↗

PubMed1998

The morphogenesis of mouse vallate gustatory epithelium and taste buds requires BDNF-dependent taste neurons.

The developmental absence of brain-derived neurotrophic factor (BDNF) in null mutant mice caused three interrelated defects in the vallate gustatory papilla: sparse innervation, a reduction in the area of the gustatory epithelium, and fewer taste buds. On postnatal day 7, the stunted vallate papilla of bdnf null mutant mice was 30% narrower, the trench walls 35% reduced in area, and the taste buds 75% less abundant compared with wild-type controls. Quantitative assessment of innervation density was carried out to determine if the small trench walls and shortage of taste buds could be secondary consequences of the depletion of gustatory neurons. The diminished gustatory innervation was linearly associated with a reduced trench wall area (r = +0.94) and fewer taste buds (r = +0.96). Residual taste buds were smaller than normal and were innervated by a few surviving taste neurons. We conclude that BDNF-dependent taste neurons contribute to the morphogenesis of lingual gustatory epithelia and are necessary for both prenatal and postnatal mammalian taste bud formation. The gustatory system provides a conspicuous example of impaired sense organ morphogenesis that is secondary to sensory neuron depletion by neurotrophin gene null mutation.

Animals↗

PubMed1998

Role of differential cell proliferation in the tail bud in aberrant mouse neurulation.

In the mouse mutant curly tail, the phenotypes spina bifida and curled tail result from a delay in closure of the posterior neuropore (PNP). At the developmental stage when this delay can first be recognized, the caudal region of the embryo demonstrates a transiently enhanced curvature of the body axis which likely inhibits elevation, convergence, and fusion of the neural folds. The enhanced curvature is thought to be the result of a decreased proliferation in the ventrally located gut endoderm and notochord, together with a normal proliferation of the overlying neuroepithelium of the PNP. However, the proliferation defect and the enhanced curvature were originally demonstrated at the same developmental stage, while it is expected that reduced proliferation should precede enhanced curvature and delayed PNP closure. The caudal region originates from the tail bud and we therefore propose that the enhanced curvature is induced by a disturbed dorso-ventral proliferation pattern in the tail bud. Using flow cytometry, proliferation patterns were determined separately for the dorsal and ventral halves of the tail bud of curly tail and of control embryos as well as of recombinant embryos having the curly tail phenotype with a genetic background which is matched to the BALB/c control strain. In general, it appeared that about half of the cell cycle duration in tail bud cells was occupied by S phase, about 40% by G0/G1 and the rest by G2/M. For the control embryos, no dorso-ventral differences in relative phase duration were demonstrated. However, curly tail and recombinant embryos at the 21-25 somite stage, prior to the onset of enhanced curvature, exhibited ventrally a higher proportion of G0/G1 phase cells than dorsally, and a complementary relationship for S phase cells. We interpret these observations as indicating a prolonged G1 phase at the ventral side of the tail bud, resulting in a prolongation of the cell cycle and thus a decreased proliferation. In 26-30 somite stage embryos, prior to the normalization of curvature in curly tail embryos, the dorso-ventral proliferation balance was re-established. We conclude that a reduced proliferation in the ventral part of the tail bud of the curly tail embryo precedes both the onset of enhanced curvature and the previously observed reduction in proliferation of the hindgut and notochord, and is a likely candidate for an early event in the pathogenetic sequence leading to the curly tail phenotype.

Animals↗

PubMed1999

Initial differentiation of the metanephric mesenchyme is independent of WT1 and the ureteric bud.

The early development of the metanephric kidney is characterized by the induced differentiation of mesenchymal cells into a stem cell population that undergoes a mesenchymal to epithelial transformation in response to stimuli from the ureteric bud. The Wilms' tumor suppressor gene, Wt1, is required for mesenchymal cells to complete this developmental program. In the absence of WT1, a prospective metanephric mesenchyme appears, but becomes apoptotic, and outgrowth of the ureteric bud from the Wolffian duct does not occur. Therefore, the examination of Wt1 -/- embryos allows the determination of those markers of early metanephric differentiation that do not require the ureteric bud or WT1 for their expression. Here, we demonstrate that several markers, including Pax-2, Six-2, and GDNF, were present as RNAs in the metanephric mesenchyme of Wt1 -/- embryos. These findings demonstrate that the metanephric mesenchyme in mutant embryos has begun to differentiate towards the nephrogenic lineage, and that this early differentiation does not require either WT1 or the presence of the ureteric bud. To determine whether WT1 functions other than to induce expression of factors that stimulate ureteric bud outgrowth, Wt1 -/- metanephric mesenchymes were recombined with wild-type ureteric buds in organ culture, but this failed to rescue tubulogenesis. However, the Wolffian duct from Wt1 -/- embryos was a competent inducer of wild-type metanephric mesenchyme.

Animals↗

PubMed2000

Tumor cell budding and laminin-5 expression in colorectal carcinoma can be modulated by the tissue micro-environment.

Expression of laminin-5 alpha3, beta3 and gamma2 protein subunits was investigated in colorectal adenocarcinomas using immunostaining and confocal microscopy. The laminin-5 heterotrimer was found in basement membranes and as extracellular deposits in tumor stroma. In contrast to the alpha3 subunit, which was under-expressed, the gamma2 and beta3 subunits were detected in the cytoplasm of carcinoma cells dissociating (budding) from neoplastic tubules, suggestive of focal alterations in laminin-5 assembly and secretion. Laminin-5 gamma2 or beta3 subunit-reactive budding carcinoma cells expressed cytokeratins but not vimentin; they did not proliferate and were not apoptotic. Furthermore, expression of laminin-5 gamma2 and beta3 subunits in budding cells was associated with focal under-expression of the E-cadherin-beta-catenin complex. Results from xenograft experiments showed that budding activity in colorectal adenocarcinomas could be suppressed when these tumors grew at ectopic s.c. sites in nude mice. In vitro, cultured colon carcinoma cells, but not adenoma-derived tumor cells, shared the laminin-5 phenotype expressed by carcinoma cells in vivo. Using colon carcinoma cell lines implanted orthotopically and invading the cecum of nude mice, the laminin-5-associated budding was restored, indicating that this phenotype is not only determined by tumor cell properties but also dependent on the tissue micro-environment. Our results indicate that both laminin-5 alpha3 subunit expression and cell-cell cohesiveness are altered in budding carcinoma cells, which we consider to be actively invading. We propose that the local tissue micro-environment contributes to these events.

Adenocarcinoma↗

PubMed2001

Induction of bud formation of embryonic mouse tracheal epithelium by fibroblast growth factor plus transferrin in mesenchyme-free culture.

Embryonic mouse tracheal epithelium, which branches in an epithelial-mesenchymal recombination culture with bronchial mesenchyme, was cultured under mesenchyme-free conditions. When embedded in a basement-membrane-like matrix and cultured in a serum-free medium supplemented with fibroblast growth factor 1 (FGF1), the tracheal epithelium did not branch, whereas the bronchial epithelium underwent branching morphogenesis. When the medium was enriched with transferrin (Tf), bud formation was induced in the tracheal epithelium and some buds branched secondarily. FGF7 and FGF10, in cooperation with Tf, induced tracheal bud formation to the same extent as FGF1, although the optimum concentrations differed. A bromodeoxyuridine-labeling study comparing cultures with and without Tf showed no Tf-specific amplification of cell proliferation. A whole-mount in situ hybridization study of the expression of Bmp4 and Shh genes in explants of mesenchyme-free culture revealed that both genes were ubiquitously expressed and that expression did not correlate with bud formation. This expression pattern was different from the distally localized expression pattern observed in normal lung rudiments and in extratracheal buds induced by the recombined bronchial mesenchyme. These results suggest that both bronchial and tracheal bud formations were initiated without localized exposure of the epithelium to FGFs and were not accompanied by localized expression of Bmp4 and Shh in the epithelium.

Age Factors↗

PubMed2005

Identification of a novel gene involved in asexual organogenesis in the budding ascidian Botryllus schlosseri.

Development via regeneration or budding shares some known genetic pathways with embryogenesis, but no concerted effort has been made to identify genes unique to asexual development. We have identified a novel gene that plays a role in cyclical bud formation and asexual organogenesis in the colonial ascidian Botryllus schlosseri. Athena mRNA is transcribed at high levels during the 24- to 36-hr interval of programmed cell death and new bud initiation at the conclusion of the budding cycle (takeover). Knockdown of Athena by RNAi and antisense morpholinos induced defects in the development of new buds ranging from retardation in growth and abnormal organogenesis to hollow buds lacking organs. As genetic intervention in this organism has not been possible, this study establishes the use of RNAi and morpholinos in Botryllus as well as describing the knockdown phenotype of a new gene.

Amino Acid Sequence↗

PubMed1991

Cellular morphogenesis in the Saccharomyces cerevisiae cell cycle: localization of the CDC11 gene product and the timing of events at the budding site.

The Saccharomyces cerevisiae CDC3, CDC10, CDC11, and CDC12 genes encode a family of homologous proteins that are not closely related to other known proteins [Haarer BK, Ketcham SR, Ford SK, Ashcroft DJ, and Pringle JR (submitted)]. Temperature-sensitive mutants defective in any of these four genes display essentially identical pleiotropic phenotypes that include abnormal cell-wall deposition and bud growth, an inability to complete cytokinesis, and a failure to form the ring of 10 nm filaments that normally lies directly subjacent to the plasma membrane in the neck region of budding cells. We showed previously that the CDC3 and CDC12 gene products localize to the region of the mother-bud neck and are probably constituents of the ring of 10 nm filaments. We now report the generation of polyclonal antibodies specific for the CDC11 product (Cdc11p) and the use of these antibodies in immunofluorescence experiments with wild-type and mutant cells. The results suggest that Cdc11p is also a constituent of the filament ring, and thus support the hypothesis that the S. cerevisiae 10 nm filaments represent a novel type of eukaryotic cytoskeletal element. Cdc11p and actin both localize to the budding site well in advance of bud emergence and at approximately the same time, and both proteins also remain localized at the old budding site for some time after cytokinesis. Cdc11p also localizes to regions of cell-wall reorganization in mating cells and in cells responding to purified mating pheromone. Surprisingly, most preparations of affinity purified Cdc11p-specific antibodies also stained the nuclear and cytoplasmic microtubules. Although this staining probably reflects the existence of an epitope shared by Cdc11p and some microtubule-associated protein, the possibility that a fraction of the Cdc11p is associated with the microtubules could not be eliminated.

Cell Cycle↗

PubMed1992

Retinoic acid respecifies limb bud cells in vitro.

Retinoic acid (RA) is known to have dramatic effects on limb pattern formation and has been shown to exert its effects on limbs by converting anterior limb bud cells into cells with posterior positional properties. In this study we find that dissociated posterior limb bud cells from chick and mouse embryos cultured at high density (micromass cultures) are able to stimulate the formation of supernumerary digits when grafted into developing wing buds and that the positional identity of both chick and mouse limb bud cells can be maintained for finite periods of time in vitro. Furthermore, using this assay system we have tested whether anterior cells from mouse and chick limb buds can be converted into cells with posterior identity by exposure to RA in vitro. We find that anterior limb bud cells acquire posterior properties after culture in the presence of RA.

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↗

PubMed1995

Slow and fast muscle fibers are preferentially derived from myoblasts migrating into the chick limb bud at different developmental times.

Avian limb myoblasts originate from somites and migrate into the periphery during limb bud formation. It is not known how these precursors become arranged into a stereotyped pattern of muscles and primary fiber types. We used in vivo surgical transplantation and anatomical analyses of thigh muscle patterns to ask whether myoblasts migrating into the limb bud at different developmental times adopt different fates. When myoblast migration was interrupted by transplanting limb bud tissue to the coelomic cavity of a host embryo early in the migratory period (stages 16-early 17), few thigh muscles were found at stages 30-33. Primordia that were present corresponded to muscles that normally contain a majority of slow myotubes. In limbs transplanted slightly later (stages late 17-18), the only missing muscles were those that normally contain the highest numbers of fast myotubes. Parallel results were obtained in chimeric limbs made by transplanting a quail limb bud to a chick host at different times during the migratory period, an experimental situation in which the limbs were not depleted of muscle precursors or nerves. These findings suggest that the earliest myoblast migrants give rise mainly to slow primary myotubes, the later migrants to fast myotubes. To determine whether the early limb bud environment defines the fate of migrating myoblasts, we assessed fiber type patterns in limbs that developed from young limb bud tissue (stages 15-early 16) transplanted to older hosts (stage 17). A significant depletion of slow myosin-positive profiles was found within slow muscles. Fast muscles were generally normal in size. These results provide in vivo evidence that limb myoblast diversity arises prior to the entry of myoblasts into the limb. We suggest that there is a gradual change in the proportions of myoblasts capable of forming slow and fast fiber types, a change which may begin in the somites or early in the migratory period.

Animals↗

PubMed1995

Insulin and insulin-like growth factor I prevent the mitogenic response of chick limb bud mesoderm cells to platelet-derived growth factor-AA.

Platelet-derived growth factor AA (PDGF-AA) increases DNA synthesis by chicken limb bud mesoderm in culture. Preincubation of either mesoderm from whole limb buds (stage 24-25) or mesoderm from the distal tip of the bud (stage 25) in insulin or insulin-like growth factor type I (IGF-I) resulted in increased DNA synthesis compared to control levels in two different types of medium. However, no further increase in DNA synthesis was then induced by PDGF-AA. This was found even when the level of DNA synthesis in IGF-I or insulin-containing medium was below that seen in cells treated only with PDGF. The response to PDGF was not dependent on the presence of serum in the medium. Insulin and IGF-I inhibited expression of the PDGF alpha receptor in mesoderm from whole limb buds. However, this was detected at times after the increase in DNA synthesis in response to PDGF was normally seen. IGF-I did not inhibit expression of the PDGF alpha receptor in mesoderm from distal limb bud tips. Thus, IGF-I and insulin modify the response of limb bud mesoderm to PDGF. The effects of IGF-I and insulin on receptor expression may be dependent on the cell populations present but do not appear to account for modulation of the PDGF-induced mitogenic response.

Animals↗

PubMed1996

Monooxygenase, Esterase, and Glutathione Transferase Activity Associated with Azinphosmethyl Resistance in the Tufted Apple Bud Moth, Platynota idaeusalis

Azinphosmethyl-selected tufted apple bud moths were compared to susceptible and reverted strains with respect to possible metabolic mechanisms of resistance within the third instar, fifth instar, and adults. Based upon bioassays conducted by topical application with azinphosmethyl, LD50s were as high as 867-fold in the selected strain as compared to that seen in susceptible bud moths. The LD50 of the reverted strain was intermediate to that of the susceptible and selected insects at all stages studied. Glutathione transferase activity measured with 1-chloro-2,4-dinitrobenzene was elevated in the selected strain 1.6- and 2.2-fold as compared to third and fifth stadium susceptible bud moths, respectively. No consistent strain differences were noted for 1,2-dichloro-4-nitrobenzene. Cytochrome P450 content and P450 mRNA was not significantly different in fifth instars of the susceptible and selected strain. However, there was a 2.7- and 1.9-fold increase in benzphetamine and p-nitroanisole metabolism, respectively, in the guts of azinphosmethyl-selected fifth instars. Benzo[a]pyrene metabolism was elevated 2.4-fold in the carcass of selected bud moths and no differences were noted for methoxyresorufrin in either gut or carcass. Susceptible fifth instars demonstrated a reduced rate of metabolism of azinphosmethyl to the oxon and methyl benzazamide. Piperonyl butoxide failed to synergize azinphosmethyl toxicity. Esterase activity measured with 1-naphthyl acetate and p-nitrophenyl acetate was elevated in selected larvae compared to that seen in susceptible tufted apple bud moths in both larvae and adults. This increased esterase activity was attributed to several isoforms as resolved by analytical isoelectric focusing. One of these forms was consistently overexpressed in all of the life stages examined. Pretreatment of selected fifth instars with S,S,S-tributylphosphorotrithioate increased the toxicity of azinphosmethyl 400-fold and had minimal effect on toxicity in susceptible insects. It appears that multiple hydrolases are the primary metabolic factor in azinphosmethyl resistance in the tufted apple bud moth.

Journal Article↗