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PubMed1991

Metabolic and cardiorespiratory responses to the performance of Wing Chun and T'ai Chi Chuan exercise.

The primary purpose of this study was to examine the metabolic and cardiorespiratory responses to the continuous performance of Wing Chun and T'ai Chi Chuan exercise. No significant differences in VO2max or HRmax obtained during treadmill exercise were found between the practitioners of the two styles. Average values for oxygen uptake (VO2) were 23.3 +/- 7.5 ml.kg-1.min-1 (6.6 METS) and 16.0 +/- 3.9 ml.kg-1.min-1 (4.6 METS) for Wing Chun and T'ai Chi Chuan exercise, respectively. Mean heart rates obtained during exercise were 137 +/- 25 beats.min-1 for Wing Chun and 116 +/- 22 beats.min-1 for T'ai Chi Chuan exercise. These exercise values corresponded to 52.4% of VO2max and 70.5% of HRmax for Wing Chun and only 36.4% of VO2max and 59.8% of HRmax for T'ai Chi Chuan exercise. Thus, only the continuous performance of Wing Chun exercise elicited VO2 and HR responses that would be expected to bring about a cardiorespiratory training effect in subjects with a relatively low initial VO2max. The ventilatory equivalent for oxygen (VE/VO2) obtained during T'ai Chi Chuan exercise (21.7) was significantly lower than for Wing Chun exercise (24.2), suggesting that T'ai Chi practitioners utilize efficient breathing patterns during exercise. Both Wing Chun and T'ai Chi Chuan styles may have a small static component that produces a slightly elevated heart rate relative to metabolic load when compared to traditional aerobic activities. However, the effect was not severe and these forms of exercise should not be considered dangerous for individuals at high risk for cardiovascular disease.

Adult↗
PubMed1993

Distance-independent inactivation of an enhancer by the suppressor of Hairy-wing DNA-binding protein of Drosophila.

When the gypsy retrotransposon of Drosophila inserts between an enhancer and promoter it prevents the enhancer from activating transcription. Enhancers are blocked because the protein (SUHW) encoded by the suppressor of Hairy-wing [su(Hw)] gene binds to gypsy. For example, gypsy insertions in an 85 kilobase region between a wing margin-specific enhancer and the promoter in the cut gene cause a cut wing phenotype that is suppressed by su(Hw) mutations. A temperature-sensitive combination of mutant su(Hw) alleles was used to investigate the mechanism by which SUHW blocks the cut wing margin enhancer. By shifting from the nonpermissive to the permissive temperature and vice versa at various stages in development it was found that active SUHW is only required around pupariation when the wing margin enhancer is active to cause a cut wing phenotype. This was true whether gypsy was in the embryonic control region near the promoter, or in the late larval control region near the wing margin enhancer. These results indicate that SUHW must be active only when an enhancer is active to block the enhancer. Furthermore, the observations also indicate that enhancer-blocking by SUHW is reversible and that it occurs soon after binding of active SUHW to gypsy DNA. These results are consistent with models in which SUHW structurally interferes with enhancer-promoter interactions.

Alleles↗
PubMed2004

The wing 2 region of the FOXC1 forkhead domain is necessary for normal DNA-binding and transactivation functions.

PURPOSE: To determine the biochemical defects that underlie Axenfeld-Rieger malformations, to determine a functional role for wing 2 in FOXC1, and to understand how mutations in this region disrupt FOXC1 function. METHODS: Sequencing DNA from patients with Axenfeld-Rieger malformation resulted in the identification of two novel missense mutations (G165R and R169P) in wing 2 of FOXC1. Site-directed mutagenesis was used to introduce these mutations, as well as previously reported mutation (M161K), into the FOXC1 cDNA. These FOXC1 mutants were evaluated to determine their ability to localize to the nucleus, bind DNA and activate gene expression. RESULTS: Two novel missense mutations were identified in unrelated patients, in wing 2 of the FOXC1 forkhead domain. Because there had been no previous biochemical analysis, the mutation M161K was also investigated. All three mutant proteins localized correctly to the nucleus. The G165R mutation maintained wild-type levels of DNA binding; however, both the M161K and R169P mutations displayed reduced DNA binding ability. Biochemical analysis showed that all three mutations disrupt FOXC1's transactivation ability. CONCLUSIONS: Biochemical analysis of mutations G165R and R169P and of a previously reported mutation, M161K, demonstrate the functional significance of wing 2. M161K and R169P disrupt DNA binding of FOXC1, consistent with the hypothesis that wing 2 is necessary for DNA binding. The results also suggest that wing 2 plays a role in gene activation. These results provide the first insights into how mutations in wing 2 disrupt FOXC1 function.

Amino Acid Sequence↗
PubMed1996

ERECT WING, the Drosophila member of a family of DNA binding proteins is required in imaginal myoblasts for flight muscle development.

The erect wing locus of the fruit fly Drosophila melanogaster encodes a protein, EWG, that shares extensive homology with the P3A2 DNA binding protein of sea urchin and a recently identified mammalian transcription factor. Loss-of-function erect wing alleles result in embryonic lethality. Viable alleles of erect wing cause severe abnormalities of the indirect flight muscles. We have analyzed the spatial pattern of erect wing expression in the developing indirect flight muscles during postembryonic development. EWG is detected, 10 hours after puparium formation, in myoblasts that will form the indirect flight muscles. The early events of muscle development are normal in ewg mutants. However, a few hours after the onset of erect wing expression in myoblasts, defects are seen in the developing indirect flight muscles which subsequently degenerate. We present results that show that the normal development of the indirect flight muscles requires erect wing expression in the progenitor myoblasts themselves. Finally, we examine the role of target muscles in the arborization of motor axons by studying the developing innervation to the flight muscle in erect wing mutants. Our study demonstrates, for the first time, a role for a regulatory gene expressed in imaginal myoblasts in Drosophila.

Animals↗
PubMed1984

The winged scapula.

Twenty-five patients with 23 different types of winging of the scapula are described. A simple clinical and etiologic classification of the winged scapula is proposed based on the study of these patients in conjunction with a review of the literature. Winging of the scapula is either static or dynamic. Static winging is due to fixed deformity in the shoulder girdle, spine, or ribs. Dynamic winging is due to a neuromuscular disorder. The great variety of lesions that produce winging of the scapula may be classified anatomically into four types: Type I, nerve; Type II, muscle; Type III, bone; and Type IV, joint. Winging of the scapula is a surprisingly common physical sign, but because it is often asymptomatic it receives little attention. However, symptoms of pain, weakness, or cosmetic deformity may demand attention, and it is hoped that this classification will help in the diagnosis and assessment of these patients.

Adolescent↗
PubMed2025

Analysis of Duplication and Potential Functional Divergence of Wing Gene Network Components in Pea Aphids.

A fundamental focus of evolutionary developmental biology is uncovering the genetic mechanisms responsible for the gain and loss of characters. One approach to this question is to investigate changes in the coordinated expression of a group of genes important for the development of a character of interest (a gene regulatory network). Here we consider the possibility that modifications to the wing gene regulatory network (wGRN), as defined by work primarily done in Drosophila melanogaster, were involved in the evolution of wing dimorphisms of the pea aphid (Acyrthosiphon pisum). We hypothesize that this may have occurred via changes in expression levels or by duplication followed by divergence of wGRN components. To test this, we annotated members of the wGRN in the pea aphid genome and assessed their expression levels in first and third nymphal instars of winged and wingless morphs of males and asexual females. We find that only 2 of the 32 assessed genes exhibit morph-biased expression. We also find that three wing genes (apterous (ap), warts (wts), and decapentaplegic (dpp)) have undergone gene duplication. In each case, the resulting paralogs show signs consistent with functional divergence, exhibiting either sex-, morph-, or stage-specific expression. Two gene duplicates, wts2 and dpp3, are of particular interest with respect to wing dimorphism, as they exhibit male morph-specific isoforms and wingless male-biased expression, respectively. These gene expression results provide an important first step toward identifying members of the pea aphid wGRN that may play a causative role in differentiating winged from wingless morphs. These findings supplement our understanding of trends in developmental gene network evolution, such as side-stepping pleiotropic constraint via duplication and sub-functionalization, underlying the emergence of novel phenotypes.

Animals↗
PubMed1999

Paraxial and lateral plate influences on reinitiation of wing development in chicken embryos.

Stephens et al. ([1993] Dev. Dynam. 197:157-168) hypothesized that the chick embryo wing territory is not an equipotential system. They proposed that following extirpation of the wing territory, limb formation is reinitiated, stimulated by more paraxial tissues. It was the purpose of this study to test this hypothesis. Four sets of procedures were undertaken in stage 11-12 chick embryos: 1) the wing territory lateral plate was removed (negative controls); 2) medial (between the central axis and somites), lateral (between the mesonephros and lateral plate), and intermediate (between the somites and mesonephros) foil barriers were placed adjacent to the wing territory (positive controls); 3) barriers were placed as above, with the removal of the lateral plate (experimental); and 4) barriers were placed lateral to the area of lateral plate extirpation (experimental). Normal limbs developed in 89% of the embryos without foil barriers with the lateral plate removed. In 93% of the embryos that contained medial barriers, normal wings developed whether or not the limb territory was extirpated, and in 100% of the embryos with intermediate or lateral barriers, with or without extirpation, deficient limbs occurred. When foil barriers were placed lateral to the wound, 87% of the chick wings were either reduced or absent. Closure of the wound following extirpation appeared to progress from lateral to medial. The data from this study appear to support the hypothesis that the limb territory is not equipotential but is reformed from cells closing the wound from lateral to medial, and is reinitiated from paraxial tissues (medial to lateral) following wound healing.

Animals↗
PubMed1996

The somatic white-ivory eye spot test does not detect the same spectrum of genotoxic events as the wing somatic mutation and recombination test in Drosophila melanogaster.

A groups of six chemical compounds was tested in parallel in two different somatic genotoxicity assays in Drosophila melanogaster, the wing somatic mutation and recombination test (SMART) and the white-ivory eye spot test. The wing spot test makes use of the wing cell markers multiple wing hairs (mwh) and flare (flr) and detects both mitotic recombination and various types of mutational events. The white-ivory eye spot test makes use of the white-ivory (wi) quadruplication and detects the somatic reversion of the recessive eye color mutation wi to the wild-type (w+). Three- or two-day-old larvae were fed chronically with the compounds ethylnitrosourea (ENU), N-nitrosopyrrolidine (NNP), caffeine (CAF), chromium (VI) oxide (CRO), potassium chromate (POC), and 2,4-dichlorophenoxyacetic acid (2,4-D). All six compounds are genotoxic to various degrees in the wing spot test. The percentage of the genotoxic activity that is due to mitotic recombination was between 84% and 91% for the hexavalent chromium compounds CRO and POC and about 68% for 2,4-D. In contrast, ENU and NNP showed only 46% and 25% recombinagenic activity, respectively. In the white-ivory eye spot test, the three compounds (CRO, POC, and 2,4-D) with high recombinagenic activity and CAF were clearly nongenotoxic, whereas only ENU and NNP gave a positive response. From these results, it is concluded that the spectrum of genotoxic events detected by the two assays is different. In particular, the white-ivory eye spot test appears not to detect mitotic recombination the way the wing spot test does.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1988

Preservation of the ability of dissociated quail wing bud mesoderm to elicit a position-related differentiative response.

Previous studies showed that grafting wedges of fresh or cultured anterior quail wing mesoderm into posterior slits in chick wing buds resulted in the formation of supernumerary cartilage in a high percentage of cases. When anterior quail mesoderm, which had been dissociated into single cells and pelleted by centrifugation, was grafted into posterior slits of host chick wing buds, supernumerary rods or nodules of cartilage formed in 74.3% of the cases. Few supernumerary skeletal structures formed following control operations in which pelleted dissociated anterior or posterior mesoderm was grafted into homologous locations in host chick wing buds. When pelleted, dissociated anterior mesoderm was cultured in vitro for 1 or 2 days prior to being implanted in posterior locations, the incidence of supernumerary cartilage formation increased to 95.5% and 93.8%, respectively. The incidence of supernumerary cartilage formation following control orthotopic grafts of cultured mesoderm was 11.8% for 1-day and 31% for 2-day cultured anterior mesoderm; for 1- and 2-day cultured posterior mesoderm, the incidence of supernumerary cartilage formation was 20% and 41.7%, respectively. Longer-term culture resulted in a substantial decrease in the percentage of supernumerary cartilage after anterior to posterior grafts and an increase in the incidence of supernumerary cartilage from control grafts. The results demonstrate that quail anterior wing bud mesodermal cells do not need to maintain constant contact with one another in order to retain the ability to form or stimulate the formation of supernumerary cartilage after being grafted into a posterior location in a host wing bud. This ability is retained when the pelleted dissociated mesoderm is cultured in vitro outside the limb field for at least 1 to 2 days.

Animals↗
PubMed1986

Development of the apical ectodermal ridge in the chick leg bud and a comparison with the wing bud.

Histologic examination of the leg bud of stage-18 to stage-23 chick embryos was carried out with special reference to the development of the apical ectodermal ridge. The leg bud apical ectoderm, initially an irregular columnar epithelium with an overlying simple squamous periderm, began to thicken during stage 18 and was a pseudostratified epithelium by stage 19. A notch in the base of the thickened ectoderm was seen as early as stage 19. The notch represented the cross-sectional view of a groove, which developed in the base of the ridge. As development proceeded, the ridge and its associated groove lengthened. In addition, the groove became more prominent, and irregularities were seen in its width and depth along the apex. Ectodermal cell death was not consistently seen until stage 21 at which time most of the length of the thickened ectoderm had evidence of necrosis. Development of the leg bud ridge and wing bud ridge were compared. The temporal sequence of ectodermal thickening and ridge development was very similar in both the leg and wing buds with one exception; namely, that leg bud ridge development preceded wing bud ridge development by several hours. In addition, ectodermal cell death was not evident until stage 20 in the leg bud ridge, but could be seen at late stage 18 in the wing bud apical ectoderm. However, by stage 21, cell death was associated with most of the ridge in both the wing and leg buds. Finally, with respect to the axial line, the ridge with its associated groove extended further preaxially in the leg bud than in the wing bud, making the leg bud ridge more symmetrical.

Animals↗
PubMed1991

Embryonic development and survival of brachial motoneurons projecting to muscleless chick wings.

The role of muscle cells in the survival of embryonic motoneurons projecting to the developing wing was directly examined. Embryos lacking muscle in one of their wings were produced by surgically removing the embryonic precursors of muscle cells, the somites. The resulting limb lacked only muscle cells, with the derivatives of the other limb contributor, the lateral plate mesoderm, left intact. Counts of apparently healthy lateral motor column (LMC) motoneurons supplying normal wings between stages 28 and 36 showed little decline in motoneuron number until stage 34; approximately 24% of the motoneurons died between stages 34 and 36. In contrast, the number of LMC motoneurons supplying muscleless wings declined progressively from stages 28 to 36. This decline resulted in the loss of about 77% of the motoneurons present at stage 28. In addition, the LMCs supplying muscleless wings had fewer motoneurons at all stages examined than similarly staged controls; this difference ranged from 27% in the youngest cases to 75% in the older embryos. Motoneurons were lost equivalently from all rostrocaudal levels of the brachial LMC. From these studies we conclude that motoneurons survival depends on the presence of muscle cells in the developing wing. In the absence of muscle cells, motoneuron death was increased compared to normal embryos at stages prior to the onset of naturally occurring cell death.

Animals↗
PubMed1993

Effect of temperature on frequencies of spots in Drosophila wing-spot assay.

The effect of temperature on spontaneous mutation frequencies was studied in the Drosophila somatic mutation and recombination test. Transdihybrid mwh +/+ flr3 larvae were grown at various temperatures (15, 18, 20, 22, 25, 27, and 29 degrees C) in the absence of any chemical mutagen. Wings of surviving adults were removed and scored for presence of small single spots, large single spots, and twin spots. No significant effect of temperature was found on mean frequency per wing of twin spots. Similarly, no significant effect of temperature was found for large singles within the temperature range of 18-29 degrees C; however, at 15 degrees C, the mean frequency per wing of large spots was significantly elevated. A significant quadratic relationship was found between mean frequency of small spots and temperature. Frequency of small spots per wing was minimized within the temperature range of 20-27 degrees C and increased at higher and lower temperatures. Maximum frequency of small spots per wing was observed at 15 degrees C. The qualitative nature of the small single spots induced at high and low temperatures is unclear; they may represent slow-growing segmentally aneuploid (deleted) cells or possibly even monosomic cells. Both heat and cold were found to be mutagenic in the Drosophila wing-spot assay. However, the mutagenic potency associated with temperature was much less than that of most chemical mutagens, and no significant effect of temperature was observed in the range of 20-27 degrees C.

Animals↗
PubMed2005

Birds have dinosaur wings: The molecular evidence.

Within developmental biology, the digits of the wing of birds are considered on embryological grounds to be digits 2, 3 and 4. In contrast, within paleontology, wing digits are named 1, 2, 3 as a result of phylogenetic analysis of fossil taxa indicating that birds descended from theropod dinosaurs that had lost digits 4 and 5. It has been argued that the development of the wing does not support the conclusion that birds are theropods, and that birds must have descended from ancestors that had lost digits 1 and 5. Here we use highly conserved gene expression patterns in the developing limbs of mouse and chicken, including the chicken talpid(2)mutant and polydactylous Silkie breed (Silkie mutant), to aid the assessment of digital identity in the wing. Digit 1 in developing limbs does not express Hoxd12, but expresses Hoxd13. All other digits express both Hoxd12and Hoxd13. We found this signature expression pattern identifies the anteriormost digit of the wing as digit 1, in accordance with the hypothesis these digits are 1, 2 and 3, as in theropod dinosaurs. Our evidence contradicts the long-standing argument that the development of the wing does not support the hypothesis that birds are living dinosaurs.

Animals↗
PubMed2003

Postembryonic development of the wing imaginal discs in the female wingless bagworm moth Eumeta variegata (Lepidoptera, Psychidae).

The process of wing disc development and degeneration in the bagworm moth Eumeta variegata was investigated histologically. Morphological differences between two sexes first appear in the penultimate (eighth) larval instar. In the male, wing discs proliferate rapidly in the penultimate larval instar and continue proliferating; a conspicuous peripodial epithelium forms in the last (ninth) larval instar. The hemopoietic organs break down in this stage and disappear completely by the prepupal stage. In the female, in contrast, the wing discs remain as in the previous (seventh) instar, without proliferation of cells inside. No peripodial epithelium forms in the penultimate instar or later. Hemopoietic organs are still attached to the wing discs in the last larval instar and the entire wing discs transform into a plain, thick epidermis in the prepupal period. It is suggested that the hemopoietic organs may prevent the wing discs from developing in E. variegata.

Animals↗
PubMed2004

New unusual miniature-like wing mutation in Drosophila virilis.

A new recessive, sex-linked, nonlethal in the homozygote, wing mutation in Drosophila virilis was studied using a hybridological assay, light microscopy, and transmission electron microscopy. The mutants have abnormally small wings; the phenotype is attributed to a cell-autonomous reduction in the size of the epidermal cells of the differentiating wing. The phenotype is also characterized by abnormally oriented wing hairs, wavy wing edge, temperature sensitivity, and some abnormalities in the wing veins.

Animals↗
PubMed1990

Topographical features of the substratum for growth of pioneering neurons in the Manduca wing disc.

The sensory neurons of the Manduca wing form a planar network nestled between the wing's upper and lower monolayers. The pioneering axons of this network grow in a distal-to-proximal direction over the basal surface of the upper epithelial monolayer. The basal surface of this monolayer has been examined ultrastructurally during the period of axonal outgrowth. The cellular terrain traversed by axons shows a graded distribution of epithelial processes, with the number of processes increasing in a proximal direction. Growth cones of axons, therefore, encounter increasing surface areas for contact with their substratum as they move toward the base of the wing. Because a basal lamina is laid down over these epithelial processes after axons have pioneered the neural pathways of the wing, axonal guidance cues apparently lie on surfaces of these basal processes. At branch points of the neural pathway examined in this study, axons avoid pathways in which the basal surfaces of cells in the upper wing monolayer interdigitate with basal surfaces of underlying tracheal cells. This interaction between wing epithelial cells and tracheal epithelial cells could act as a physical barrier to axonal outgrowth.

Animals↗
PubMed1995

Development of wing sensory axons in the central nervous system of Drosophila during metamorphosis.

The development of new, adult-specific axonal pathways in the central nervous system (CNS) of insects during metamorphosis is still largely uncharacterized. Here we used axonal labeling with DiI to describe the timing and pattern of growth of sensory axons originating in the wing of Drosophila as they establish their adult projection pattern in the CNS during pupal life. The wing of Drosophila carries a small number of readily identifiable sensory organs (sensilla) whose neurons are located in the periphery and whose axons travel along specific routes within the adult CNS. The neurons are born and undergo axonogenesis in a characteristic order. The order of axon arrival in the CNS appears to be the same as that of their development in the periphery. Within the CNS, the formation of four prominent axon bundles leading to distant termination sites is followed by the formation of a compact axon termination site near the point of wing nerve entry into the CNS. This sensillum-specific pattern persists into adulthood without discernible modification. We also find a small number of axons filled with DiI prior to the formation of the four permanent bundles. We have only been able to fill them for a few hours in early pupal life and therefore consider them to be transient. The bundles of wing sensory axons travel within tracts that contain other axons as well. Using immunocytochemistry, the tracts start to be histologically identifiable at around 12 h after pupariation (AP), and grow substantially as metamorphosis proceeds. Wing sensory neurons are found in the tracts by 18-20 h AP and the full adult pattern is established by 48 h AP. When sensory axons first enter the CNS, they fan out in the region where their appropriate tracts are located, but they do not wander extensively. They quickly form bundles that become increasingly compact over time. Calculations show that the rate of axon extension within the CNS varies from bundle to bundle and is equal to or greater than that of the same axons growing through wing tissue.

Animals↗
PubMed1987

Teratogenic effects of retinoic acid and dimethylsulfoxide on embryonic chick wing and somite.

In order to document the stage(s) at which the embryonic chick wing bud is sensitive to vitamin A teratogenesis and the kinds of defects produced by vitamin A insult to the embryonic chick wing, 1-microgram doses of retinoic acid (1 microliter RA in 90% DMSO at a concentration of 1 microgram/microliter) were locally applied to the right wing bud of chick embryos at stages 17-23 (Hamburger and Hamilton: J. Morphol., 88:49-92, '51), and the resulting limb skeleton anatomy was observed at 10 days of incubation. Local application of RA at stages 17-20 resulted in distal wing skeleton defects. There were significantly more wing skeleton defects among embryos treated at these stages with RA solution than among solvent (DMSO)-treated control embryos and than among untreated control embryos. Wings of embryos treated with RA at stages 21-23 were always normal. Scapular and vertebral defects were seen at 10 days of incubation among embryos which had been treated prior to stage 21 with both the RA solution and the solvent control. Statistical analysis and histological data suggest that scapular and vertebral defects were caused by DMSO-induced damage to somites.

Abnormalities, Drug-Induced↗