Embryonic lethal mutation in mouse collagen I gene causes rupture of blood vessels and is associated with erythropoietic and mesenchymal cell death

Cell ◽  
1984 ◽  
Vol 38 (2) ◽  
pp. 597-607 ◽  
Author(s):  
Jürgen Löhler ◽  
Rupert Timpl ◽  
Rudolf Jaenisch
Keyword(s):  
Cell Death ◽  
Blood Vessels ◽  
Mesenchymal Cell ◽  
Lethal Mutation ◽  
Collagen I ◽  
Embryonic Lethal ◽  
I Gene

scholarly journals Collagen synthesis by cell lines derived from Mov-13 mouse embryos which have a lethal mutation in the collagen α 1(I) gene

1987 ◽  
Vol 244 (2) ◽  
pp. 375-379 ◽  
Author(s):  
M Dziadek ◽  
R Timpl ◽  
R Jaenisch
Keyword(s):  
Cell Lines ◽  
Collagen Synthesis ◽  
Mouse Embryos ◽  
Lethal Mutation ◽  
Collagen I ◽  
Wild Type ◽  
Collagen Types ◽  
Total Collagen ◽  
I Gene ◽  
Procollagen Iii

Mouse embryos homozygous for the Mov-13 mutation produce no collagen I, owing to transcriptional blockage of the collagen alpha 1(I) gene by a retroviral insert. Fibroblast-like cell lines derived from these embryos were compared with similar lines derived from heterozygous and wild-type embryos with respect to the total amounts, and types, of collagen synthesized. Total collagen synthesized by either cloned or uncloned cell lines correlated with their genotype, demonstrating no compensation for absence of collagen I production by an increase in synthesis of other collagen types. Procollagen alpha 2(I) chains were not detected in the homozygous cell lines, demonstrating that these chains do not form homotrimers, nor do they form heterotrimers with alpha-chains of other collagen types. Procollagen III levels were quantified by radioimmunoassay and found to be similar in all cell lines.

Retrovirus-induced lethal mutation in collagen I gene of mice is associated with an altered chromatin structure

Cell ◽  
1984 ◽  
Vol 38 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Michael Breindl ◽  
Klaus Harbers ◽  
Rudolf Jaenisch
Keyword(s):  
Chromatin Structure ◽  
Lethal Mutation ◽  
Collagen I ◽  
I Gene

Vascular regression during the formation of the free digits in the avian limb bud: a comparative study in chick and duck embryos

Development ◽  
1985 ◽  
Vol 85 (1) ◽  
pp. 239-250
Author(s):  
J. M. Hurle ◽  
E. Colvee ◽  
M. A. Fernandez-Teran
Keyword(s):  
Cell Death ◽  
Blood Vessels ◽  
Mesenchymal Cell ◽  
Limb Bud ◽  
Death Process ◽  
Electron Microscopic ◽  
Transmission Electron ◽  
Transmission Electron Microscopic ◽  
Microscopic Studies ◽  
Cell Death Process

The pattern and structure of the blood vessels of the interdigital spaces of the leg bud have been studied by means of Indian ink injections and transmission electron microscopy in the chick and duck embryos. The results show that in the chick the interdigital necrotic process responsible for the freeing of the digits is followed by regression of the blood vessels. In the webbed foot of the duck, the interdigital necrotic processes are not followed by vascular regression. Transmission electron microscopic studies show that both in the chick and in the duck, interdigital blood vessels are immature structures lacking basal lamina. Dead cells of presumably endothelial origin were detected in the lumen of the regressing blood vessels of the chick but not in the duck. However, the intensity of this cell death process does not appear to be high enough to account by itself for the disappearance of the interdigital blood vessels. The possible relationships between interdigital mesenchymal cell death and vascular regression are discussed.

Interdigital tissue chondrogenesis induced by surgical removal of the ectoderm in the embryonic chick leg bud

Development ◽  
1986 ◽  
Vol 94 (1) ◽  
pp. 231-244
Author(s):  
J. M. Hurle ◽  
Y. Gañan
Keyword(s):  
Cell Death ◽  
Vital Staining ◽  
Mesenchymal Cell ◽  
Neutral Red ◽  
Surgical Removal ◽  
Experimental Conditions ◽  
Local Inhibition ◽  
Dorsal Ectoderm ◽  
Interdigital Cell Death ◽  
Proximal Zone

In the present work, we have analysed the possible involvement of ectodermal tissue in the control of interdigital mesenchymal cell death. Two types of experiments were performed in the stages previous to the onset of interdigital cell death: (i) removal of the AER of the interdigit; (ii) removal of the dorsal ectoderm of the interdigit. After the operation embryos were sacrificed at 10–12h intervals and the leg buds were studied by whole-mount cartilage staining, vital staining with neutral red and scanning electron microscopy. Between stages 27 and 30, ridge removal caused a local inhibition of the growth of the interdigit. In a high percentage of the cases, ridge removal at these stages was followed 30–40 h later by the formation of ectopic nodules of cartilage in the interdigit. The incidence of ectopic cartilage formation was maximum at stage 29 (60%). In all cases, cell death took place on schedule although the intensity and extent of necrosis appeared diminished in relation to the intensity of inhibition of interdigital growth and to the presence of interdigital cartilages. Ridge removal at stage 31 did not cause inhibition of the growth of the interdigit and ectopic chondrogenesis was only detected in 3 out of 35 operated embryos. Dorsal ectoderm removal from the proximal zone of the interdigit at stage 29 caused the chondrogenesis of the proximal interdigital mesenchyme in 6 out of 18 operated embryos. The pattern of neutral red vital staining was consistent with these results revealing a partial inhibition of interdigital cell death in the proximal zone of the interdigit. It is proposed that under the present experimental conditions the mesenchymal cells are diverted from the death programme by a primary transformation into cartilage.

Studies on the female-sterile phenotype of 1(1)su(f) ts76a, a temperature-sensitive allele of the suppressor of forked mutation in Drosophila melanogaster

Development ◽  
1980 ◽  
Vol 55 (1) ◽  
pp. 247-256
Author(s):  
Thomas G. Wilson
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Follicle Cell ◽  
Lethal Mutation ◽  
Female Sterility ◽  
Temperature Sensitive ◽  
Egg Chambers ◽  
A Cell ◽  
Sensitive Allele

A new allele of the suppressor of forked [su(f)] mutation in Drosophila melanogaster has been found and designated 1(1)su(f)ts76a. It is temperature-sensitive for suppression of forked (f) and has additional temperature-sensitive phenotypes of lethality, female sterility, and abnormal bristle formation at 29 °C. It closely resembles two other conditional alleles of su(f), 1(1)su(f)ts67g and 1(1)ts726. Female sterility at 29 °C is characterized by both disorganized egg chambers in the ovarioles and also chorion-deficient oocytes. Both of these abnormalities may be the result of premature follicle cell death. The observations on 1(1)su(f)ts76a are consistent with the proposal that the similar allele, 1(1)ts726, is a cell-lethal mutation specifically affecting mitotically active cells.

Cell death and the development of limb form and skeletal pattern in normal and wingless (ws) chick embryos

Development ◽  
1973 ◽  
Vol 30 (3) ◽  
pp. 753-772
Author(s):  
J. R. Hinchliffe ◽  
D. A. Ede
Keyword(s):  
Cell Death ◽  
Phenotypic Expression ◽  
Mesenchymal Cell ◽  
Limb Bud ◽  
Death Process ◽  
Electron Microscopic ◽  
Wide Range ◽  
Skeletal Pattern ◽  
Autoradiographic Analysis ◽  
Mutant Phenotypes

The wingless condition resulting from the action of the sex-linked wingless (ws) gene arises from the precocious appearance of cell death in the anterior necrotic zone (ANZ) of the forelimb-bud at stage 19 (3 days) and its progressive extension beyond its normal area during stages 20–23. A similar though less pronounced effect occurs in the hindlimb-bud. Although some wingless hindlimb-buds are normal, others are affected by the precocious appearance of cell death in the ANZ. The ws wingless mutant resembles the different wingless mutant investigated by Zwilling (1956) in that the apical ectodermal ridge (AER) is absent in most ws wing-buds. AER absence could be due to ws mesenchymal cell death interfering with the production of apical ectodermal maintenance factor (AEMF), which Zwilling claims is necessary to maintain the AER which plays an essential role in inducing limb outgrowth. Wingless mutant phenotypes range from birds with rudimentary wings and normal legs through a modal type with forelimbs absent and hindlimbs normal to wingless and legless forms showing a high degree of expressivity. Individual wingless embryos vary in the degree to which the precocious ANZ appearing at 3 days is extended into the limb-bud and the wide range of wingless phenotypic expression is attributed to this variation. Electron microscopic and histochemical analysis of the cell death process in wingless wing-buds revealed the presence of both isolated dead cells and macrophages, which contained intense acid phosphatase activity. These findings are interpreted as showing that isolated dead cells are ingested by neighbouring mesenchymal cells which thus become transformed into macrophages, first ingesting and then digesting further dead cells. A study was made of the origin of the anomalous hindlimb condition, including absence or reduction of the tibia and digits, characteristic of severely affected wingless embryos. Autoradiographic analysis of the pattern of 35SO4 uptake revealed that at stage 24/5 (4½ days) wingless hindlimb-buds which were smaller than normal had a normal prospective fibula region, but that the prospective tibia region was small or absent. Thus the effect of a precocious hindlimb ANZ at stages 19–22 is to reduce or delete the pre-axial prospective tibia at stage 24/5.

scholarly journals Characterization of morphology in healthy, traumatized and aged knee meniscus of different species: A pilot study

2019 ◽  
Vol 28 (1) ◽  
pp. 96-110
Author(s):  
Marija Podļesnaja ◽  
Mara Pilmane ◽  
Modris Ciems
Keyword(s):  
Cell Death ◽  
Pilot Study ◽  
Knee Joint ◽  
Comparative Morphology ◽  
Anatomical Structure ◽  
Collagen I ◽  
Knee Meniscus ◽  
Moderate Number ◽  
Number Of Cells

Meniscus is a fibrocartilaginous anatomical structure that realizes complicated biomechanical functions in the knee joint. However, no comparative morphology studies have been done on different species and conditions regarding the meniscus. Thus, the aim of our pilot study was to compare the morphology of traumatized and aged human and healthy deer meniscus to reveal the tissue ground, growth, degeneration, cell death and inflammation factors. The study included surgery materials from one deer and two humans. Biotin-streptavidin immunohistochemistry was performed for detection of tissue TGFβ1, MMP2, MMP9, collagen I, caspase, Il-1, Il-6, Il-10. The results were evaluated semiquantitatively. An abundant number of Collagen I positive cells were detected in the disordered human meniscus but not in the deer one. TGFβ1 was seen in numerous to abundant number of cells in all the three cases. MMPs and caspase were distributed with numerous to abundant cells in both human and deer meniscus. Numerous to abundant cells of traumatized and aged human menisci showed IL-1 and IL-6, while the deer meniscus demonstrated cytokine expression in a moderate number of cells only in limited zones. The traumatized human meniscus possessed an abundant number of IL-10 positive cells, while the deer and the aged human meniscus showed mainly a moderate number of IL-10 cells with some elevation of cytokine in superficial and deepest layers of the meniscus.

Multiple collagen I gene regulatory elements have sites of stress-induced DNA duplex destabilization and nuclear scaffold/matrix association potential

2002 ◽  
Vol 84 (3) ◽  
pp. 484-496 ◽  
Author(s):  
Christian Mielke ◽  
Morten O. Christensen ◽  
Ole Westergaard ◽  
J�rgen Bode ◽  
Craig J. Benham ◽  
...  
Keyword(s):  
Regulatory Elements ◽  
Collagen I ◽  
Dna Duplex ◽  
Nuclear Scaffold ◽  
Gene Regulatory Elements ◽  
Gene Regulatory ◽  
Duplex Destabilization ◽  
I Gene
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