A role for Pax-1 as a mediator of notochordal signals during the dorsoventral specification of vertebrae

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 649-660 ◽  
Author(s):  
H. Koseki ◽  
J. Wallin ◽  
J. Wilting ◽  
Y. Mizutani ◽  
A. Kispert ◽  
...  
Keyword(s):  
Structural Changes ◽  
Genetic Interaction ◽  
Paraxial Mesoderm ◽  
Lumbar Region ◽  
Subsequent Formation ◽  
Developmental Abnormalities ◽  
Short Tail ◽  
Antibody Staining ◽  
Skeletal Phenotype ◽  
Subsequent Loss

The notochord plays an important role in the differentiation of the paraxial mesoderm and the neural tube. We have analyzed the role of the notochord in somite differentiation and subsequent formation of the vertebral column using a mouse mutant, Danforth's short-tail (Sd). In this mutant, the skeletal phenotype is most probably a result of degeneration and subsequent loss of the notochord. The Sd gene is known to interact with undulated (un), a sclerotome mutant. Double mutants between Sd and un alleles show an increase in the severity of the defects, mainly in the ventral parts of the vertebrae. We also show that part of the Sd phenotype is strikingly similar to that of the un alleles. As un is known to be caused by a mutation in the Pax-1 gene, we analyzed Pax-1 expression in Sd embryos. In Sd embryos, Pax-1 expression is reduced, providing a potential molecular basis for the genetic interaction observed. A complete loss of Pax-1 expression in morphologically intact mesenchyme was found in the lower thoracic-lumbar region, which is phenotypically very similar to the corresponding region in a Pax-1 null mutant, Undulated short-tail. The sclerotome developmental abnormalities in Sd coincide closely, both in time and space, with notochordal changes, as determined by whole-mount T antibody staining. These findings indicate that an intact notochord is necessary for normal Pax-1 expression in sclerotome cells, which is in turn required for the formation of the ventral parts of the vertebrae. The observed correlation among structural changes of the notochord, Pax-1 expression levels and skeletal phenotypes, suggests that Pax-1 might be an intrinsic mediator of notochordal signals during the dorsoventral specification of vertebrae.

scholarly journals Immunocytochemical Labeling of Rhabdomeric Proteins inDrosophilaPhotoreceptor Cells Is Compromised by a Light-dependent Technical Artifact

2019 ◽  
Vol 67 (10) ◽  
pp. 745-757 ◽  
Author(s):  
Krystina Schopf ◽  
Thomas K. Smylla ◽  
Armin Huber
Keyword(s):  
Structural Changes ◽  
Protein Transport ◽  
Light Exposure ◽  
Protein Localization ◽  
Photoreceptor Cells ◽  
Antibody Staining ◽  
Technical Artifact ◽  
Stage Process ◽  
Stage 1 ◽  
Antibody Labeling

Drosophila photoreceptor cells are employed as a model system for studying membrane protein transport. Phototransduction proteins like rhodopsin and the light-activated TRPL ion channel are transported within the photoreceptor cell, and they change their subcellular distribution in a light-dependent way. Investigating the transport mechanisms for rhodopsin and ion channels requires accurate histochemical methods for protein localization. By using immunocytochemistry the light-triggered translocation of TRPL has been described as a two-stage process. In stage 1, TRPL accumulates at the rhabdomere base and the adjacent stalk membrane a few minutes after onset of illumination and is internalized in stage 2 by endocytosis after prolonged light exposure. Here, we show that a commonly observed crescent shaped antibody labeling pattern suggesting a fast translocation of rhodopsin, TRP, and TRPL to the rhabdomere base is a light-dependent antibody staining artifact. This artifact is most probably caused by the profound structural changes in the microvillar membranes of rhabdomeres that result from activation of the signaling cascade. By using alternative labeling methods, either eGFP-tags or the self-labeling SNAP-tag, we show that light activation of TRPL transport indeed results in fast changes of the TRPL distribution in the rhabdomere but not in the way described previously.

Role of the GABAA receptors in the long-term cognitive impairments caused by neonatal sevoflurane exposure

2019 ◽  
Vol 30 (8) ◽  
pp. 869-879 ◽  
Author(s):  
Tao Li ◽  
Zeyi Huang ◽  
Xianwen Wang ◽  
Ju Zou ◽  
Sijie Tan
Keyword(s):  
Structural Changes ◽  
Cognitive Impairments ◽  
Elevated Serum ◽  
Developmental Abnormalities ◽  
Inhalational Anesthetic ◽  
Excitatory Gaba ◽  
Hpa Axis Activity ◽  
The Brain

Abstract Sevoflurane is a widely used inhalational anesthetic in pediatric surgeries, which is considered reasonably safe and reversible upon withdrawal. However, recent preclinical studies suggested that peri-neonatal sevoflurane exposure may cause developmental abnormalities in the brain. The present review aimed to present and discuss the accumulating experimental data regarding the undesirable effects of sevoflurane on brain development as revealed by the laboratory studies. First, we summarized the long-lasting side effects of neonatal sevoflurane exposure on cognitive functions. Subsequently, we presented the structural changes, namely, neuroapoptosis, neurogenesis and synaptogenesis, following sevoflurane exposure in the immature brain. Finally, we also discussed the potential mechanisms underlying subsequent cognitive impairments later in life, which are induced by neonatal sevoflurane exposure and pointed out potential strategies for mitigating sevoflurane-induced long-term cognitive impairments. The type A gamma-amino butyric acid (GABAA) receptor, the main targets of sevoflurane, is excitatory rather than inhibitory in the immature neurons. The excitatory effects of the GABAA receptors have been linked to increased neuroapoptosis, elevated serum corticosterone levels and epigenetic modifications following neonatal sevoflurane exposure in rodents, which might contribute to sevoflurane-induced long-term cognitive abnormalities. We proposed that the excitatory GABAA receptor-mediated HPA axis activity might be a novel mechanism underlying sevoflurane-induced long-term cognitive impairments. More studies are needed to investigate the effectiveness and mechanisms by targeting the excitatory GABAA receptor as a prevention strategy to alleviate cognitive deficits induced by neonatal sevoflurane exposure in future.

The effect of acid activation and calcination of halloysite on the efficiency and selectivity of Pb(II), Cd(II), Zn(II) and As(V) uptake

Clay Minerals ◽  
2016 ◽  
Vol 51 (3) ◽  
pp. 385-394 ◽  
Author(s):  
Paulina Maziarz ◽  
Jakub Matusik
Keyword(s):  
Photoelectron Spectroscopy ◽  
Active Sites ◽  
Structural Changes ◽  
Selective Adsorption ◽  
Temperature Treatment ◽  
High Temperature Treatment ◽  
Acid Activation ◽  
Subsequent Formation ◽  
X Ray ◽  
Mineral Structure

AbstractThe present study investigated the efficiency and mechanisms of aqueous Pb(II), Cd(II), Zn(II) and As(V) adsorption on natural (H), calcined (HC), and acid-activated halloysite (HA). The XRD and FTIR measurements indicated that the aluminosilicate framework was not affected by high-temperature treatment, in contrast to acid activation, which led to structural changes mainly in the tetrahedral sheet. The sorption of cations on H sample was low, though it was most effective for As(V). The X-ray photoelectron spectroscopy results suggested that removal of As(V) might be related to its reduction to As(III) involving oxidation of Fe(II) present in the mineral structure and/or iron minerals. The calcination enhanced halloysite sorption capacity for cations, while the As(V) sorption decreased. This was due to partial dehydroxylation and the subsequent formation of additional active sites. The acid treatment induced selective adsorption of Pb(II).

The role of Pax-1 in axial skeleton development

Development ◽  
1994 ◽  
Vol 120 (5) ◽  
pp. 1109-1121 ◽  
Author(s):  
J. Wallin ◽  
J. Wilting ◽  
H. Koseki ◽  
R. Fritsch ◽  
B. Christ ◽  
...  
Keyword(s):  
Proximal Part ◽  
Axial Skeleton ◽  
Intervertebral Discs ◽  
Paraxial Mesoderm ◽  
Single Amino Acid ◽  
Lumbar Region ◽  
Entire Axis ◽  
Mouse Mutants ◽  
Column Formation

Previous studies have identified a single amino-acid substitution in the transcriptional regulator Pax-1 as the cause of the mouse skeletal mutant undulated (un). To evaluate the role of Pax-1 in the formation of the axial skeleton we have studied Pax-1 protein expression in early sclerotome cells and during subsequent embryonic development, and we have characterized the phenotype of three different Pax-1 mouse mutants, un, undulated-extensive (unex) and Undulated short-tail (Uns). In the Uns mutation the whole Pax-1 locus is deleted, resulting in the complete absence of Pax-1 protein in these mice. The other two genotypes are interpreted as hypomorphs. We conclude that Pax-1 is necessary for normal vertebral column formation along the entire axis, although the severity of the phenotype is strongest in the lumbar region and the tail. Pax-1-deficient mice lack vertebral bodies and intervertebral discs. The proximal part of the ribs and the rib homologues are also missing or severely malformed, whereas neural arches are nearly normal. Pax-1 is thus required for the development of the ventral parts of vertebrae. Embryonic analyses reveal that although sclerotomes are formed in mutant embryos, abnormalities can be detected from day 10.5 p.c. onwards. The phenotypic analyses also suggest that the notochord still influences vertebral body formation some days after the sclerotomes are formed. Furthermore, the notochord diameter is larger in mutant embryos from day 12 p.c., due to increased cell proliferation. In the strongly affected genotypes the notochord persists as a rod-like structure and the nucleus pulposus is never properly formed. Since the notochord is Pax-1-negative these findings suggest a bidirectional interaction between notochord and paraxial mesoderm. The availability of these Pax-1 mutant alleles permitted us to define an early role for Pax-1 in sclerotome patterning as well as a late role in intervertebral disc development. Our observations suggest that Pax-1 function is required for essential steps in ventral sclerotome differentiation, i.e. for the transition from the mesenchymal stage to the onset of chondrogenesis.

Conflicting Diagnosis of Dermal Sinus Tract and Tethered Cord

2013 ◽  
Vol 40 (6) ◽  
pp. 889-891
Author(s):  
Chris J. Hong ◽  
Saleh A. Almenawer ◽  
Boleslaw Lach ◽  
Nina Stein ◽  
Benedicto Baronia ◽  
...  
Keyword(s):  
Spinal Dysraphism ◽  
Tethered Cord ◽  
Sinus Tract ◽  
Neural Tube Closure ◽  
Dermal Sinus ◽  
Lumbar Region ◽  
Occult Spinal Dysraphism ◽  
Developmental Abnormalities ◽  
Skin Tags ◽  
Dermal Sinus Tract

Dermal sinus tracts (DSTs) are an uncommon form of occult spinal dysraphism that is attributed to incomplete neural tube closure during fetal development. Dermal sinus tracts are found along the midline neuroaxis from the nasion to the coccyx, but they most commonly appear in the lumbar region. Dermal sinus tracts are more commonly associated with other developmental abnormalities such as skin tags, naevi, spinal dermoid cysts, meningocoele, lipomas and spinal cord tethering, and can be complicated by cerebrospinal fluid drainage, shedding of keratin from the epithelialized tract, and infection such as meningitis.

Induction photopériodique de l'organogenèse et de la floraison in vitro chez le Cichorium intybus: aspects histologiques

1992 ◽  
Vol 70 (6) ◽  
pp. 1302-1311 ◽  
Author(s):  
Karima Mikou ◽  
Philippe Badila
Keyword(s):  
Structural Changes ◽  
Cichorium Intybus ◽  
Fluorescent Light ◽  
Flower Formation ◽  
Root Explants ◽  
Subsequent Formation ◽  
Flower Primordia ◽  
Short Day ◽  
Long Day

In root explants of a long-day plant, Cichorium intybus L., grown in vitro, inflorescences were produced under short-day conditions (9 h) if long days were applied on days 10 to 18 of culture. Long days consisted of either 16 h fluorescent light (5.6 W∙m−2) or daily cycles of 9 h white fluorescent plus 15 h red (660 nm, 0.3 W∙m−2) or blue (440 nm, 0.5 W∙m−2) light. The structural changes in the meristems of buds regenerated under these conditions were studied. The influence of photoperiod appeared to be critical between the 10th and 16th days, during the progressive transition from vegetative to prefloral stage, which occurred more rapidly under photoperiodic conditions with red or blue light. In noninductive short days, intermediate meristems could be observed tardily on day 24, but no flower formation took place after transfer to long days. Increasing the quantity of light under short-day conditions up to a level comparable to long-day conditions resulted in a rise in mitotic activity, mainly in the peripheral zone of the meristem, but the vegetative zonation was retained. These data therefore indicate that the duration of light really commits the meristem to the subsequent formation of flower primordia; in contrast, the quantity of light controls the bud formation during the first part of development. Key words: Cichorium, tissue cultures, flowering, meristems, organogenesis, photoperiodism.

scholarly journals Linking Oxidative Stress and Proteinopathy in Alzheimer’s Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1231
Author(s):  
Chanchal Sharma ◽  
Sang Ryong Kim
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Structural Changes ◽  
Aging Brain ◽  
Ros Production ◽  
Subsequent Loss ◽  
Β Amyloid ◽  
Neuroprotective Therapies

Proteinopathy and excessive production of reactive oxygen species (ROS), which are the principal features observed in the Alzheimer’s disease (AD) brain, contribute to neuronal toxicity. β-amyloid and tau are the primary proteins responsible for the proteinopathy (amyloidopathy and tauopathy, respectively) in AD, which depends on ROS production; these aggregates can also generate ROS. These mechanisms work in concert and reinforce each other to drive the pathology observed in the aging brain, which primarily involves oxidative stress (OS). This, in turn, triggers neurodegeneration due to the subsequent loss of synapses and neurons. Understanding these interactions may thus aid in the identification of potential neuroprotective therapies that could be clinically useful. Here, we review the role of β-amyloid and tau in the activation of ROS production. We then further discuss how free radicals can influence structural changes in key toxic intermediates and describe the putative mechanisms by which OS and oligomers cause neuronal death.

scholarly journals Morphological features of bone in calcium and vitamin D deficiency

2013 ◽  
Vol 19 (4) ◽  
pp. 212-217
Author(s):  
Lidia Chircor ◽  
G. Iordan ◽  
Loredana Surdu
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Structural Changes ◽  
Morphological Features ◽  
Abnormal Development ◽  
Sex Distribution ◽  
Bone Deformity ◽  
Developmental Abnormalities ◽  
Bone Changes ◽  
Independent Entity

Abstract The authors aim to identify morphological features of the bone abnormal development caused by calcium and vitamin D deficiency (CDD) and possible risk factors in the occurrence of these changes. The study is conducted on a selected group of 102 children aged 10-12 years with bone changes due to CDD, diagnosed and treated in Constanţa City from 2000 - 2010. For cases where the same child presented several bone deformities, we considered every bone deformity as an independent entity. In this study we observed deformation of the bones of the skull, prominent frontal bone 62 cases (60.78%); “beads rib” 49 cases (48.03%) sub mammary grooves 31 cases (30.32%), increasing the volume of knee joint 75 cases (73.52%) and wrist 68 cases (66.66%). The changes visible under direct examination are accompanied by structural changes visible by radiological exam, so the epiphysis plate has an irregular appearance (35 cases), serrated (35 cases), are enlarged (34 cases) or cup (31 cases). Analysis of sex distribution shows higher involvement of male children, sex ratio 3/1. Age group most affected in the studied group is 3-36 months. Skeletal deformities in CDD conditions are associated with peculiar situations of risk: monthly income below Average 72 cases (70.5%), increased pigmentation of the skin 61 (59.8%), prematurity 20 (19.6%). Increased incidence of developmental abnormalities of the bones due to CDD in the studied group and in different regions (England, Turkey, USA, etc) in recent years coincides with modern life style, which involves skin protection against solar radiation and a lack of exposure to sunlight.

scholarly journals Pathways of Ca2+ entry and cytoskeletal damage following eccentric contractions in mouse skeletal muscle

2012 ◽  
Vol 112 (12) ◽  
pp. 2077-2086 ◽  
Author(s):  
Bao-Ting Zhang ◽  
Nicholas P. Whitehead ◽  
Othon L. Gervasio ◽  
Trent F. Reardon ◽  
Molly Vale ◽  
...  
Keyword(s):  
Structural Changes ◽  
Transient Receptor Potential ◽  
Isometric Force ◽  
Force Production ◽  
Receptor Potential ◽  
Cytoskeletal Proteins ◽  
Eccentric Contractions ◽  
Antibody Staining ◽  
Transient Receptor ◽  
Stretch Activated Channels

Muscles that are stretched during contraction (eccentric contractions) show deficits in force production and a variety of structural changes, including loss of antibody staining of cytoskeletal proteins. Extracellular Ca2+ entry and activation of calpains have been proposed as mechanisms involved in these changes. The present study used isolated mouse extensor digitorum longus (EDL) muscles subjected to 10 eccentric contractions and monitored force production, immunostaining of cytoskeletal proteins, and resting stiffness. Possible pathways for Ca2+ entry were tested with streptomycin (200 μM), a blocker of stretch-activated channels, and with muscles from mice deficient in the transient receptor potential canonical 1 gene (TRPC1 KO), a candidate gene for stretch-activated channels. At 30 min after the eccentric contractions, the isometric force was decreased to 75 ± 3% of initial control and this force loss was reduced by streptomycin but not in the TRPC1 KO. Desmin, titin, and dystrophin all showed patchy loss of immunostaining 30 min after the eccentric contractions, which was substantially reduced by streptomycin and in the TRPC1 KO muscles. Muscles showed a reduction of resting stiffness following eccentric contractions, and this reduction was eliminated by streptomycin and absent in the TRPC1 KO muscles. Calpain activation was determined by the appearance of a lower molecular weight autolysis product and μ-calpain was activated at 30 min, whereas the muscle-specific calpain-3 was not. To test whether the loss of stiffness was caused by titin cleavage, protein gels were used but no significant titin cleavage was detected. These results suggest that Ca2+ entry following eccentric contractions is through a stretch-activated channel that is blocked by streptomycin and encoded or modulated by TRPC1.

scholarly journals SOME ASPECTS OF THE STRUCTURAL ORGANIZATION OF THE MYOFIBRIL AS REVEALED BY ANTIBODY-STAINING METHODS

1966 ◽  
Vol 28 (3) ◽  
pp. 505-525 ◽  
Author(s):  
Frank A. Pepe
Keyword(s):  
Structural Changes ◽  
Fluorescent Antibody ◽  
Thick Filament ◽  
Myosin Molecule ◽  
Weakly Bound ◽  
Antibody Staining ◽  
Thick Filaments ◽  
Antigenic Sites ◽  
Myosin Filaments ◽  
Staining Methods

From observations of fluorescent antibody staining and antibody staining in electron microscopy, evidence is presented for the following: (a) Direct contact of the actin and myosin filaments occurs at all stages of contraction. This results in inhibition of antibody staining of the H-meromyosin portion of the myosin molecule in the region of overlap of the thin and thick filaments. (b) Small structural changes occur in the thick filaments during contraction. This leads to exposure of antigenic sites of the L-meromyosin portion of the myosin molecule. The accessibility of these antigenic sites is dependent upon the sarcomere length. (c) The M line is composed of a protein which is weakly bound to the center of the thick filament and is not actin, myosin, or tropomyosin. (d) Tropomyosin as well as actin is present in the I band. (e) If actin or tropomyosin is present in the Z line, it is masked and unavailable for staining with antibody.

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