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PubMed2003

Region-specific inhibition of prostatic epithelial bud formation in the urogenital sinus of C57BL/6 mice exposed in utero to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

In utero 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure causes abnormal ventral, dorsolateral, and anterior prostate development in wild-type but not aryl hydrocarbon receptor (AhR) null mutant C57BL/6 mice. Experiments have now been conducted to test the hypothesis that TCDD causes an AhR-dependent inhibition of the earliest visible stage of prostate development, the formation of prostatic buds by urogenital sinus (UGS) epithelium. A novel method for viewing budding was developed that uses scanning electron microscopy of isolated UGS epithelium instead of three-dimensional reconstruction of serial histological sections of intact UGS. In the initial experiment, the time course for prostatic epithelial bud formation in vehicle- and TCDD-exposed wild-type C57BL/6J mice was determined. A single maternal dose of TCDD (5 mug/kg) on gestation day 13 delayed the appearance of dorsal, lateral, and anterior buds by about one day, reduced dorsolateral bud number, and prevented ventral buds from forming. No such effects were seen in TCDD-exposed AhR null mutant fetuses, while AhR null mutation, alone, had no detectable effect on budding. Treatment of wild-type dams with sufficient 5alpha-dihydrotestosterone (DHT) to masculinize female fetuses failed to protect against the inhibition of budding caused by TCDD. These results demonstrate that in utero TCDD exposure causes an AhR-dependent inhibition of prostatic epithelial bud formation commensurate with its inhibitory effects on ventral and dorsolateral prostate development, and that the inhibition of budding is not due to insufficient DHT. Inhibited bud formation appears to be the primary cause of abnormal prostate development in TCDD-exposed mice.

Animals↗

PubMed2006

Transient etiolation: protochlorophyll(ide) and chlorophyll forms in differentiating plastids of closed and breaking leaf buds of horse chestnut (Aesculus hippocastanum).

An accompanying paper reports the accumulation of photoactive protochlorophyllide (Pchlide) in the innermost leaf primordia of buds of many tree species. In this paper, we describe plastid differentiation, changes in pigment concentrations and spectral properties of bud scales and leaf primordia of horse chestnut (Aesculus hippocastanum L.) from January until the end of bud break in April. The bud scales contained plastids with grana, stroma thylakoids characteristic of chloroplasts and large dense bodies within the stroma. In January, proplastids and young chloroplasts were present in the leaf primordia, and the fluorescence spectra of the primordia were similar to those of green leaves except for a minor band at 630 nm, indicative of a protochlorophyll(ide). During bud break, the pigment concentrations of the green bud scales and the outermost leaf primordia increased, and Pchlide forms with emission maxima at 633, 644 and 655 nm accumulated in the middle and innermost leaf primordia. Depending on the position of the leaf primordia within the bud, their plastids and their pigment concentrations varied. Etio-chloroplasts with prolamellar bodies (PLBs) and prothylakoids with developing grana were observed in the innermost leaves. Besides the above-mentioned Pchlide forms, the middle and innnermost leaf primordia contained only a Chl band with an emission maximum at 686 nm. The outermost leaf primordia contained etio-chloroplasts with well-developed grana and small, narrow-type PLBs. These outermost leaves contained only chlorophyll forms like the mature green leaves. No Pchlide accumulation was observed after bud break, indicating that etiolation of the innermost and middle leaves is transient. The Pchlide forms and the plastid types of the primordia in buds grown in nature were similar to those of leaves of dark-germinated seedlings and to those of the leaf primordia of dark-forced buds. We conclude that transient etiolation occurs under natural conditions. The formation of PLBs and etio-chloroplasts and the accumulation of the light-dependent NADPH:protochlorophyllide oxidoreductase are involved in the natural greening process and ontogenesis of young leaf primordia of horse chestnut buds.

Aesculus↗

PubMed1979

Effect of Fruits on Dormancy and Abscisic Acid Concentration in the Axillary Buds of Phaseolus vulgaris L.

The mechanism regulating the growth of adult plants in two determinate bean (Phaseolus vulgaris L.) cultivars was investigated. "Redkloud" plants flowered, formed fruits, and ceased shoot growth earlier than "Redkote" plants. Redkloud attained a smaller plant size, compared to Redkote, by imposing dormancy on axillary buds at an earlier age. In both cultivars, cessation of bud growth coincided with maximum combined fruit length per plant. Removal of fruits caused resumption of axillary bud growth within 4 to 5 days. The amount of new growth induced by fruit removal depended on the cultivar and plant age. In fully developed Redkloud plants, where shoot growth had already ceased, total leaf and shoot number per plant nearly doubled within 2 weeks following fruit removal. A much smaller response was observed in the still growing Redkote plants. Fruits, therefore, are assumed to play a major role in the regulation of shoot growth and total plant size through the control of axillary bud dormancy. It seems that smaller plant size, earlier maturity, and earlier senescence of Redkloud, compared to Redkote, were the result of earlier flowering, and accomplished in part through the growth-inhibiting action of fruits.The endogenous abscisic acid (ABA) concentration of axillary buds was higher in Redkloud than in Redkote. It increased with plant age in both cultivars. Five days after fruit removal the ABA level in bud tissue dropped to approximately 10 to 30% of the control level. When buds were treated with a solution of ABA containing 5 nanomoles of ABA per bud, growth was substantially inhibited. Fifteen days after ABA application the mean length of growing buds on intact and defruited plants was reduced by 40 and 62%, respectively, compared to the untreated controls. A role for ABA in axillary bud growth regulation was not firmly established, but these data suggest correlation between the growth potential of axillary buds and their ABA concentration.

Journal Article↗

PubMed1991

Changes in Cytokinins before and during Early Flower Bud Differentiation in Lychee (Litchi chinensis Sonn.).

Lychee (Litchi chinensis) has been analyzed for cytokinins in buds before and after flower bud differentiation, using reversephase high performance liquid chromatography in combination with Amaranthus bioassay and gas chromatography-mass spectrometry-selected ion monitoring. Four cytokinins, zeatin, zeatin riboside, N(6)-(delta(2)-isopentenyl)adenine, and N(6)-(delta(6)-isopentenyl) adenine riboside, were detected in buds. There was an increase of cytokinin activity in the buds during flower bud differentiation. In dormant buds, the endogenous cytokinin content was low, and the buds did not respond to exogenous cytokinin application. Application of kinetin promotes flower bud differentiation significantly after bud dormancy. These results are interpreted as an indication that the increase in endogenous cytokinin levels during flower bud differentiation may be correlative rather than the cause of flower bud initiation.

Journal Article↗

PubMed2004

Lysines close to the Rous sarcoma virus late domain critical for budding.

The release of retroviruses from the plasma membrane requires host factors that are believed to be recruited to the site of budding by the late (L) domain of the virus-encoded Gag protein. The L domain of Rous sarcoma virus (RSV) has been shown to interact with a ubiquitin (Ub) ligase, and budding of this virus is dependent on Ub. RSV is similar to other retroviruses in that it contains approximately 100 molecules of Ub, but it is unique in that none of these molecules has been found to be conjugated to Gag. If transient ubiquitination of RSV Gag is required for budding, then replacement of the target lysine(s) with arginine should prevent the addition of Ub and reduce budding. Based on known sites of ubiquitination in other viruses, the important lysines would likely reside near the L domain. In RSV, there are five lysines located just upstream of the L domain in a region of the matrix (MA) protein that is dispensable for membrane binding, and replacement of these with arginine (mutant 1-5KR) reduced budding 80 to 90%. The block to budding was found to be on the plasma membrane; however, the few virions that were released had normal size, morphology, and infectivity. Budding was restored when any one of the residues was changed back to lysine or when lysines were inserted in novel positions, either within this region of MA or within the downstream p10 sequence. Moreover, the 1-5KR mutant could be rescued into particles by coexpression of budding-competent Gag molecules. These data argue that the phenotype of mutant 1-5KR is not due to a conformational defect. Consistent with the idea that efficient budding requires a specific role for lysines, human T-cell leukemia virus type 1, which does not bud well compared to RSV and lacks lysines close to its L domain, was found to be released at a higher level upon introduction of lysines near its L domain. This report strongly supports the hypothesis that ubiquitination of the RSV Gag protein (and perhaps those of other retroviruses) is needed for efficient budding.

Amino Acid Substitution↗

PubMed2000

Polarized growth controls cell shape and bipolar bud site selection in Saccharomyces cerevisiae.

We examined the relationship between polarized growth and division site selection, two fundamental processes important for proper development of eukaryotes. Diploid Saccharomyces cerevisiae cells exhibit an ellipsoidal shape and a specific division pattern (a bipolar budding pattern). We found that the polarity genes SPA2, PEA2, BUD6, and BNI1 participate in a crucial step of bud morphogenesis, apical growth. Deleting these genes results in round cells and diminishes bud elongation in mutants that exhibit pronounced apical growth. Examination of distribution of the polarized secretion marker Sec4 demonstrates that spa2Delta, pea2Delta, bud6Delta, and bni1Delta mutants fail to concentrate Sec4 at the bud tip during apical growth and at the division site during repolarization just prior to cytokinesis. Moreover, cell surface expansion is not confined to the distal tip of the bud in these mutants. In addition, we found that the p21-activated kinase homologue Ste20 is also important for both apical growth and bipolar bud site selection. We further examined how the duration of polarized growth affects bipolar bud site selection by using mutations in cell cycle regulators that control the timing of growth phases. The grr1Delta mutation enhances apical growth by stabilizing G(1) cyclins and increases the distal-pole budding in diploids. Prolonging polarized growth phases by disrupting the G(2)/M cyclin gene CLB2 enhances the accuracy of bud site selection in wild-type, spa2Delta, and ste20Delta cells, whereas shortening the polarized growth phases by deleting SWE1 decreases the fidelity of bipolar budding. This study reports the identification of components required for apical growth and demonstrates the critical role of polarized growth in bipolar bud site selection. We propose that apical growth and repolarization at the site of cytokinesis are crucial for establishing spatial cues used by diploid yeast cells to position division planes.

Cell Cycle↗

PubMed1991

Altered expression of the chicken homeobox-containing genes GHox-7 and GHox-8 in the limb buds of limbless mutant chick embryos.

It has been suggested that the reciprocal expression of the chicken homeobox-containing genes GHox-8 and GHox-7 by the apical ectodermal ridge and subjacent limb mesoderm might be involved in regulating the proximodistal outgrowth of the developing chick limb bud. In the present study the expression of GHox-7 and GHox-8 has been examined by in situ and dot blot hybridization in the developing limb buds of limbless mutant chick embryos. The limb buds of homozygous mutant limbless embryos form at the proper time in development (stage 17/18), but never develop an apical ectodermal ridge, fail to undergo normal elongation, and eventually degenerate. At stage 18, which is shortly following the formation of the limb bud, the expression of GHox-7 is considerably reduced (about 3-fold lower) in the mesoderm of limbless mutant limb buds compared to normal limb bud mesoderm. By stages 20 and 21, as the limb buds of limbless embryos cease outgrowth, GHox-7 expression in limbless mesoderm declines to very low levels, whereas GHox-7 expression increases in the mesoderm of normal limb buds which are undergoing outgrowth. In contrast to GHox-7, expression of GHox-8 in limbless mesoderm at stage 18 is quantitatively similar to its expression in normal limb bud mesoderm, and in limbless and normal mesoderm GHox-8 expression is highly localized in the anterior mesoderm of the limb bud. In normal limb buds, GHox-8 is also expressed in high amounts by the apical ectodermal ridge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1999

Dominant effects of RET receptor misexpression and ligand-independent RET signaling on ureteric bud development.

During kidney development, factors from the metanephric mesenchyme induce the growth and repeated branching of the ureteric bud, which gives rise to the collecting duct system and also induces nephrogenesis. One signaling pathway known to be required for this process includes the receptor tyrosine kinase RET and co-receptor GFR(&agr;)-1, which are expressed in the ureteric bud, and the secreted ligand GDNF produced in the mesenchyme. To examine the role of RET signaling in ureteric bud morphogenesis, we produced transgenic mice in which the pattern of RET expression was altered, or in which a ligand-independent form of RET kinase was expressed. The Hoxb7 promoter was used to express RET throughout the ureteric bud branches, in contrast to its normal expression only at the bud tips. This caused a variable inhibition of ureteric bud growth and branching reminiscent of, but less severe than, the RET knockout phenotype. Manipulation of the level of GDNF, in vitro or in vivo, suggested that this defect was due to insufficient rather than excessive RET signaling. We propose that RET receptors expressed ectopically on ureteric bud trunk cells sequester GDNF, reducing its availability to the normal target cells at the bud tips. When crossed to RET knockout mice, the Hoxb7/RET transgene, which encoded the RET9 isoform, supported normal kidney development in some RET-/- animals, indicating that the other major isoform, RET51, is not required in this organ. Expression of a Hoxb7/RET-PTC2 transgene, encoding a ligand-independent form of RET kinase, caused the development of abnormal nodules, outside the kidney or at its periphery, containing branched epithelial tubules apparently formed by deregulated growth of the ureteric bud. This suggests that RET signaling is not only necessary but is sufficient to induce ureteric bud growth, and that the orderly, centripetal growth of the bud tips is controlled by the spatially and temporally regulated expression of GDNF and RET.

Animals↗

PubMed1990

An analysis of chick limb bud intercellular adhesion underlying the establishment of cartilage aggregates in suspension culture.

To examine the mechanism of intercellular adhesion in the establishment of limb skeletal elements we have investigated the process of limb bud cell aggregation in vitro. Limb bud cells are aggregation-competent immediately after their trypsin:collagenase dissociation in the absence of calcium. This aggregation is largely Ca2(+)-independent (CI) and is completely and reversibly inhibited by cycloheximide. In contrast, when limb bud cells are first allowed to recover from Ca2(+)-free trypsin:collagenase dissociation, aggregation of the surviving population is exclusively Ca2(+)-dependent (CD) and completely and reversibly inhibited by cycloheximide. The presence of exogenous calcium during initial cell dissociation retains a functional CD aggregation mechanism. However, incubation of such cells with EGTA releases the CD component and converts the cells to a predominantly CI aggregation. Rabbits were immunized with limb bud cells exhibiting the recovered CD aggregation mechanism and the resulting immune sera were screened for their effect on cell aggregation. Relative to pre-immune sera, intact immune IgG agglutinated dissociated limb bud cells whilst immune Fab fragments inhibited their aggregation. The aggregation-inhibiting antiserum recognizes five major limb bud cell surface components with apparent molecular weights of 72K, 50K, 23K, 14.5K and 8.5K (K = 10(3) Mr), respectively. Limb bud cell surface plasma membranes were isolated by sucrose gradient density centrifugation and detergent-solubilized proteins coupled to Sepharose 4B with cyanogen bromide. Equivalent cell surface plasma membrane proteins were 125I-iodinated and applied to the affinity column. Limb bud cell surface protein affinity chromatography in the presence of exogenous calcium yields a single protein with an apparent molecular weight of approximately 8.5 K. This protein molecule elutes at 0.6 M NaCl, indicating a high affinity, is recognized by the aggregation-inhibiting antiserum, and is itself capable of inhibiting CD limb bud cell aggregation. Fab fragments prepared from rabbit antisera specifically directed against the affinity-purified material also inhibit CD limb bud cell aggregation and this inhibition is neutralized by the 8.5 K protein. Our data thus demonstrate that CD limb bud cell aggregation is not mediated by fibronectin and/or collagen type I and indicate that this process is governed by a novel 8.5 K cell adhesion molecule.

Animals↗

PubMed1995

Development and physiological degradation of tooth buds and development of rudiment of baleen plate in southern minke whale, Balaenoptera acutorostrata.

The development and degradation of temporary tooth buds and the development of rudiment of baleen plate were observed by gross-anatomical and histological examinations in twenty-four fetuses of the southern minke whale, Balaenoptera acutorostrata. The primary patterns of development of tooth buds were similar to those of deciduous tooth buds in the terrestrial species. Degradation of tooth buds was observed in the fetuses more than 615 mm body length (BL) and might proceed throughout the dental surface of the tooth buds. That degradation pattern was a little different from that of deciduous tooth buds in terrestrial species, which has a limited degradation area at the root of the tooth buds. In the fetuses with 135 and 153 mm BL, the upper jaw had a larger number of tooth buds than the lower jaw, although the number of buds varied in different individuals. Formation of rudiment of baleen plate was observed with degraded tooth buds in the fetus of 903 mm BL and it may be induced by the degradation of tooth buds.

Animals↗

PubMed1999

Phenylurea cytokinins assayed for induction of shoot buds in the moss Funaria hygrometrica.

The induction of shoot buds from the filamentous protonema of moss is a classic bioassay for cytokinin. While a large literature documents this response in many species of moss and for a wide range of natural and synthetic cytokinins, to date only substituted adenine cytokinins have been examined in detail. This paper shows that at least some of the novel phenylurea cytokinins will induce bud formation in mosses. Funaria responds to thidiazuron much as it responds to benzyladenine. Exposure to either substance results in log-linear dose-dependent increases in bud number that reach similar maximal numbers of buds at the optimal concentration of compound. The related compound chloro-pyridyl-phenylurea (CPPU) is slightly less active, but induces buds over a wider range of concentration. Carbanilide (diphenylurea or DPU), an active cytokinin in other systems, induces very few buds in Funaria, but does so over a wide range of concentration. Bioassay of mixtures of benzyladenine and DPU finds no evidence of competition for cytokinin receptors. That result could support suggestions that the phenylurea cytokinins act indirectly, by altering endogenous cytokinin metabolism, but we favor another interpretation. Unlike other cytokinin-responsive systems, the induction of buds from moss protonema involves two cytokinin-mediated events. The number of buds is controlled by the second cytokinin-mediated event. If DPU has little or no affinity for the receptor triggering this second event, DPU treatments will produce few to no buds, and kinetic analysis using bud number would find no evidence for competition with benzyladenine. Our results would support the hypothesis that bud induction in Funaria involves two chemically distinct cytokinin receptors.

Journal Article↗

PubMed1980

Commitment of stem cells to nerve cells and migration of nerve cells precursors in preparatory bud development in Hydra.

Budding in Hydra starts as an evagination of the double-layered tissue in the parent animal's gastric region. Five hours later the density of nerve cells in the bud's tissue doubles, representing the first detectable difference from the cellular composition of the surrounding tissue. These new nerve cells derive from multipotent stem cells which are in S-phase one day before evagination starts. Some of the bud's new nerve cells derive from stem cells which have migrated into the future bud's tissue after their commitment, apparently attracted by the bud anlage. The bud anlage recruits precursors of nerve cells even during starvation, during which nerve cell production ceases in other parts of the body. Furthermore, the bud anlage controls the duration of the development from commitment to final differentiation of the resulting nerve cells. Experiments with an inhibitor purified from hydra tissue indicate a tight correlation between stages of preparatory bud development and stages of recruitment of nerve cells for the bud. Whether or not precursors of nerve cells are involved in the control of bud formation in normal hydra, as compared to epithelial hydra which still bud though consisting of epithelial cells only, will be discussed.

Animals↗

PubMed1986

Chorda tympani innervation of anterior mandibular taste buds in the chicken (Gallus gallus domesticus).

While the mammalian chorda tympani innervates taste buds on the anterior two-thirds of the tongue, the chorda tympani of chickens does not enter the tongue, but rather is reported to supply the oral epithelium of the lower beak subjacent to the tongue. This study in the chicken investigated whether the integrity of taste buds in the lower beak is normally dependent upon innervation by the chorda tympani. Following unilateral ligation and removal of a large section of the chorda tympani, animals were sacrificed at 11, 14, and 21 days postoperatively. Oral tissue between the lingual frenulum and beak tip was serially examined, and the presence of each bud was recorded, noting the point at which the bud opened into the oral cavity. No buds were observed on the operated side in any of the cases, while the average bud count on the unoperated side was 33 +/- 10 (SD). On the unoperated side, taste buds were generally associated with anterior mandibular salivary gland ducts that reached surface epithelium and opened into the oral cavity. On the operated side, the cellular organization adjacent to gland ducts and in duct-free epithelium appeared as in control (i.e., bud-free) epithelium. The number of salivary gland duct openings into the oral cavity was equivalent on the operated and control sides. It is concluded that the chorda tympani of chickens innervates taste buds in the anterior lower beak epithelium and that it functions to maintain the structural integrity of these buds.

Animals↗

PubMed1994

Fine structure of taste buds located on the lamb epiglottis.

BACKGROUND: Taste buds located on the aryepiglottal folds and laryngeal surface of the epiglottis are the principal receptors responsible for the initiation of the laryngeal chemoreflex. In contrast to the wealth of information available concerning the ultrastructure of oral taste buds, little comparable data exists for taste buds located at the entrance to the larynx. Therefore, the present study was designed to investigate the fine structure of taste buds located on the lamb epiglottis. MATERIALS: Stained thick and semi-serial thin sections from taste buds located on the lamb epiglottis were examined with light and electron microscopy. RESULTS: Based on morphological criteria, three types of cells could be identified in the taste bud: Type I, Type II, and basal cells. Both Type I and Type II cells extended into the apical taste pore, but there were differences between these two cell types with regard to nuclear profiles, electron density, and the relative density of ribosomes, apical mitochondria, and rough and smooth endoplasmic reticulum. Basal cells did not extend a process into the taste pore. Nerve processes were observed throughout the taste bud. Synapses were observed between both Type I and Type II cells and nerve fibers. These synapses exhibited membrane thickenings and accumulations of clear and dense-cored vesicles of varying proportions in the taste cell cytoplasm adjacent to membrane specializations. CONCLUSIONS: The taste buds located on the lamb epiglottis share several structural similarities to taste buds located in the oral cavity and other regions of the pharynx and larynx of many mammalian species. The presence of synapses on both Type I and Type II cells of the lamb epiglottal taste bud suggests that both cell types are involved in laryngeal chemoreception.

Animals↗

PubMed2001

Development and maturation of taste buds of the palatal epithelium of the rat: histological and immunohistochemical study.

Palatal taste buds are intriguing partners in the mediation of taste behavior and their spatial distribution is functionally important for suckling behavior, especially in the neonatal life. Their prenatal development has not been previously elucidated in the rat, and the onset of their maturation remains rather controversial. We delineated the development and frequency distribution of the taste buds as well as the immunohistochemical expression of alpha-gustducin, a G protein closely related to the transduction of taste stimuli, in the nasoincisor papilla (NIP) and soft palate (SP) from the embryonic day 17 (E17) till the postnatal day 70 (PN70). The main findings in the present study were the development of a substantial number of taste pores in the SP of fetal rats (60.3 +/- 1.7 out of 122.8 +/- 5.5; mean +/- SD/animal at E19) and NIP of neonatal rats (9.8 +/- 1.0 out of 44.8 +/- 2.2 at PN4). alpha-gustducin-like immunoreactivity (-LI) was not expressed in the pored taste buds of either prenatal or newborn rats. The earliest expression of alpha-gustducin-LI was demonstrated at PN1 in the SP (1.5 +/- 0.5 cells/taste bud; mean +/- SD) and at PN4 in the NIP (1.4 +/- 0.5). By age the total counts of pored taste buds continuously increased and their morphological features became quite discernible. They became pear in shape, characterized by distinct pores, long subporal space, and longitudinally oriented cells. Around the second week, a remarkable transient decrease in the total number of taste buds was recorded in the oral epithelium of NIP and SP, which might be correlated with the changes of ingestive behaviors. The total counts of cells showing alpha-gustducin-LI per taste bud gradually increased till the end of our investigation (14.1 +/- 2.7 in NIP and 12.4 +/- 2.5 in SP at PN70). We conclude that substantial development of taste buds began prenatally in the SP, whereas most developed entirely postnatal in the NIP. The present study provides evidence that the existence of a taste pore which is considered an important criterion for the morphological maturation of taste buds is not enough for the onset of the taste transduction, which necessitates also mature taste cells. Moreover, the earlier maturation of palatal taste buds compared with the contiguous populations in the oral cavity evokes an evidence of their significant role in the transmission of gustatory information, especially in the early life of rat.

Animals↗

PubMed2003

Brain-derived neurotrophic factor-, neurotrophin-3-, and tyrosine kinase receptor-like immunoreactivity in lingual taste bud fields of mature hamster.

The neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), as well as their respective tyrosine kinase (Trk) receptors, TrkB and TrkC, influence peripheral target cell innervation, survival, and proliferation. In the mature taste system the role of neurotrophins and their receptors is not known. The mature hamster is an intriguing model because anterior lingual fungiform, unlike posterior lingual foliate and circumvallate, taste buds survive denervation. In light of this difference, we examined whether the degree of neurotrophin- or neurotrophin receptor-like immunoreactivity (IR) normally differs among lingual gemmal fields. In single- and double-labeled immunofluorescent experiments, 3,209 taste bud sections (profiles) from 13 hamsters were examined for immunopositive gemmal cells or nerve fibers using antibodies to BDNF and NT-3, their respective receptors TrkB and TrkC, and the neural marker ubiquitin c-terminal hydrolase L-1 [protein gene product (PGP) 9.5]. In each gemmal field, more than 75% of taste bud profiles showed immunopositivity to BDNF, NT-3, and TrkB. Across bud fields, BDNF-, TrkB-, and BDNF/TrkB-like IR, as well as PGP 9.5 and PGP 9.5/BDNF-like IR in centrally located, fungiform bud cells was greater (P < 0.0001 to P < 0.002) than in circumvallate or foliate buds. Within bud fields, the number of BDNF-like, labeled bud cells/bud profile was greater than that for NT-3-like IR in fungiform (P < 0.0002) and foliate (P < 0.0001) buds. TrkC was immunonegative in gemmal cells. The average density of TrkB- and TrkC-like fiber IR was more pronounced in fungiform than posterior gemmal-bearing papillae. Thus, fungiform papillae, whose taste buds are least affected by denervation, exhibit specific neurotrophin and receptor enrichment.

Animals↗

PubMed2002

Taste bud development in the zebrafish, Danio rerio.

Taste buds are chemosensory endorgans consisting of modified epithelial cells. Fish and other vertebrates use their taste bud cells to sample potential food, either selecting or rejecting substances according to their edibility. The adult gustatory system in fish has been studied thoroughly, including regeneration experiments. Taste buds occur in the epithelia of the lips, the mouth cavity, the oropharyngeal cavity, and also in the skin of the barbels, the head, and sometimes even all over the body surface. Despite its importance for feeding, little is known about the ontogeny of the fish taste system. We examined the development of taste buds in the zebrafish on the light microscopical and the scanning and transmission electron microscopical levels. Taste buds develop later than the olfactory organ and the solitary chemosensory cells, two other chemosensory systems in aquatic vertebrates. The first few taste bud primordia are visible within the epithelia of lips and gill arches 3 to 4 days after fertilization, and the first few taste buds with open receptor areas appear on the lips and simultaneously on the gill arches 4-5 days after fertilization, which coincides with the onset of feeding. Taste buds in the mouth cavity, on the head, and on the barbels are formed later in development. As seen in other fish, zebrafish taste buds contain elongate dark and light cells, termed according to their electron density. Dark cells with a cell apex of many short microvilli appear first, followed by the light cells with one large microvillus. In addition, the zebrafish has a third fusiform cell type, which appears last. This cell type is low in electron density and has a brush-like apical ending with several small microvilli. This cell type has not been described previously. Furthermore, in zebrafish, the ontogenetic processes of taste bud formation differ from regenerative processes described in the literature.

Animals↗

PubMed2006

Espin cytoskeletal proteins in the sensory cells of rodent taste buds.

Espins are multifunctional actin-bundling proteins that are highly enriched in the microvilli of certain chemosensory and mechanosensory cells, where they are believed to regulate the integrity and/or dimensions of the parallel-actin-bundle cytoskeletal scaffold. We have determined that, in rats and mice, affinity purified espin antibody intensely labels the lingual and palatal taste buds of the oral cavity and taste buds in the pharyngo-laryngeal region. Intense immunolabeling was observed in the apical, microvillar region of taste buds, while the level of cytoplasmic labeling in taste bud cells was considerably lower. Taste buds contain tightly packed collections of sensory cells (light, or type II plus type III) and supporting cells (dark, or type I), which can be distinguished by microscopic features and cell type-specific markers. On the basis of results obtained using an antigen-retrieval method in conjunction with double immunofluorescence for espin and sensory taste cell-specific markers, we propose that espins are expressed predominantly in the sensory cells of taste buds. In confocal images of rat circumvallate taste buds, we counted 21.5 +/- 0.3 espin-positive cells/taste bud, in agreement with a previous report showing 20.7 +/- 1.3 light cells/taste bud when counted at the ultrastructural level. The espin antibody labeled spindle-shaped cells with round nuclei and showed 100% colocalization with cell-specific markers recognizing all type II [inositol 1,4,5-trisphosphate receptor type III (IP(3)R(3))(,) alpha-gustducin, protein-specific gene product 9.5 (PGP9.5)] and a subpopulation of type III (IP(3)R(3), PGP9.5) taste cells. On average, 72%, 50%, and 32% of the espin-positive taste cells were labeled with antibodies to IP(3)R(3), alpha-gustducin, and PGP9.5, respectively. Upon sectional analysis, the taste buds of rat circumvallate papillae commonly revealed a multi-tiered, espin-positive apical cytoskeletal apparatus. One espin-positive zone, a collection of approximately 3 mum-long microvilli occupying the taste pore, was separated by an espin-depleted zone from a second espin-positive zone situated lower within the taste pit. This latter zone included espin-positive rod-like structures that occasionally extended basally to a depth of 10-12 mum into the cytoplasm of taste cells. We propose that the espin-positive zone in the taste pit coincides with actin bundles in association with the microvilli of type II taste cells, whereas the espin-positive microvilli in the taste pore are the single microvilli of type III taste cells.

Adaptor Proteins, Vesicular Transport↗