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Results for “mutation scanning”

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At least 811 records · Page 45Linked to original sources
PubMed1990

Chemical treatments of the cell packets induced from a Micrococcus luteus mutant and teichuronic acids on the packet surface.

Cell packets (MT packets) induced from a tetrads-forming mutant (strain MT) of Micrococcus luteus, both treated with chemical reagents and non-treated, were observed with a scanning electron microscope (SEM). The agglutinability of MT packets with antiserum containing anti-teichuronic acid antibody was examined. The binding of protein A-gold particles to the MT packets, mediated with the antiserum, was also observed with SEM. Gold particles were observed uniformly on the whole packet surface and also on the bridging structure formed by the outermost layer of the cell wall. Mild acid treatment, NaIO4-NaBH4 treatment and mild Smith degradation of the MT packets extremely decreased the agglutinability and binding of protein A-gold particles. The treatments gave a little influence on the surface feature and appreciably destroyed the regular packet structure. It was supposed that teichuronic acids distributed uniformly on the whole packet surface, naturally on the surface of the bridging structure too, and appreciably participated in the maintenance of the regular packet structure.

Cell Membrane↗
PubMed1989

Studies of heart development in normal and cardiac lethal mutant axolotls: a review.

The morphology of developing hearts in axolotls, Ambystoma mexicanum, has been studied by scanning electron microscopy in order to provide a chronology of morphogenesis that can be correlated with ongoing biochemical and immunocytochemical studies. In addition to normal embryos we have studied homozygous recessive cardiac lethal mutant axolotls. The mutant myocardium undergoes aberrant sarcomere development and lacks a normal heartbeat. Morphogenesis of mutant hearts appears to be nearly normal with respect to myocardial cell shape changes, epicardial formation, and the distribution of extracellular matrix fibrils in the cardiac jelly. This suggests that the deficient arrangement of contractile proteins in mutant myocardial cells does not prevent the normal organization or function of cytoskeletal isoforms of these proteins in the developing myocardium and epicardium. The implications of biochemical and morphological investigations of axolotl hearts are considered in the context of the entire developmental history of the cardiogenic mesoderm.

Ambystoma↗
PubMed1987

[Significance of rec A-gene activity in altering the ultrastructure of Escherichia coli].

The pathogenic E. coli strain, serovar 0124 studied in this investigation and its mutants rec A 56 and rec A 441 differ in their ultrastructural organization. In strains having defects in gene rec A, the appearance of intracytoplasmic membranous structures and a great number of extracellular membranous vesicles, as well as the formation of the filamentous forms of cells in the colonies, can be observed. These data indicate that the product of gene rec A plays an active role in the metabolism of bacterial membranes.

Escherichia coli↗
PubMed1988

Scale development in talpid3 mutant chick embryos.

The fact that dermal condensations are not, as they are in feather development, involved in early scale morphogenesis in birds suggests that in the mutant talpid3, where mesenchymal cell surface and motility properties are impaired, scales might develop relatively normally though feathers do not. This prediction has been checked using chorioallantoic membrane grafts of talpid and normal hind limbs, and found to be substantially justified although the abnormal overall shape of the talpid limb has a distorting effect on scale patterning. However, the abnormal talpid dermis seems to have effects on the direction and extent of epidermal invagination at scale margins. Since the control of epidermal invagination is a relatively unexplored area, this is a particularly useful finding.

Animals↗
PubMed1987

[Ultrastructural characteristics of Proteus vulgaris and Proteus mirabilis cells differing in the capacity for swarming].

Specific differences in the structure of colonies and the location of microbial cells in colonies, characteristic for aggregating and nonaggregating genetically related pairs of P. vulgaris and P. mirabilis strains, have been demonstrated by means of transmission and scanning electron microscopy. In calculating the number of flagellae per 100 outlines of microbial bodies revealed in negatively stained preparations, the fact that both aggregating and nonaggregating bacteria possess practically the same number of flagellae, on the average 4-8 flagellae per microbial cell outline, has been established. This fact indicates that the presence of flagellae in microbial cells is unrelated to their capacity for swarming.

Cell Movement↗
PubMed1986

Eyelid development and fusion induced by cortisone treatment in mutant, lidgap-Miller, foetal mice. A scanning electron microscope study.

In normal mice the eyelids grow across the eye and fuse together during days 15 and 16 of gestation, and the mice are born with their eyes closed. In mutant lgMl)/lgMl) (lidgap-Miller) foetuses this growth and fusion does not occur and the mice are born with their eyes open. A single prenatal treatment with cortisone on day 14 of gestation masks the genetic defect, and the mice are born with their eyes closed. In the present study, a scanning electron microscope was used to investigate: whether eyelid closure in cortisone-treated lgMl/lgMl foetuses differs from that in normal foetuses of the CBA/J and ICR/Ml strains and, if so, how; and off developing eyelids of untreated lgMl/lgMl foetuses differ from normal. The induced closure differs from normal. During their growth, eyelids of treated mutant foetuses have a deficiency of rounded periderm cells at their margins; the margin cells agglomerate and flatten prematurely. In closed eyes of treated mutants there is a gap between periderm cells of the upper and lower eyelids along part of the fusion line. Fusion is completed late, during day 17. Maturation of the head periderm is advanced in treated lgMl/lgMl foetuses on day 16, relative to normal CBA/J and untreated lgMl/lgMl foetuses. Untreated lgMl/lgMl foetuses differ from normal in that the eyelids never cover the eye and lack rounded periderm cells at their perimeter. The periderm cells present form a flattened band along the eyelid margin rather than, as in normal eyelids, along the fusion line. The results of the cortisone study suggest that the route to eyelid closure in mice may not be narrowly canalized either in cell morphology or number, or in timing, and that closed eyes may be achieved after cortisone treatment in lgMl/lgMl foetuses as part of an induced maturation of the periderm.

Animals↗
PubMed1983

The effect of miconazole on ergosterol-less mutant of Candida albicans.

The effect of miconazole in fungistatic concentration on an ergosterol-competent Candida albicans strain and its ergosterol-nonproducing mutant was investigated by scanning and transmission electron microscopy. The ergosterol-less mutant showed pronounced alterations by scanning electron microscopy. The increased sensitivity to miconazole of the ergosterol-less mutant was attributed to an altered plasma membrane composition and rigidity.

Candida albicans↗
PubMed1984

Abnormal corneal and eyelid development in the repeated epilation mouse.

Development of the eyelids and cornea in repeated epilation (Er/Er) mice is characterized by fusion of the tarsal conjunctiva to the epithelia of the bulbar conjunctiva and cornea. We investigated the ultrastructural features of this malformation and tested for abnormal expression of filaggrin by immunofluorescence. Heterozygous (Er/+) breeding stock were mated and 13,14,15, and 19-day-old embryos were studied by light and electron microscopy. Fusion occurred in all Er/Er specimens and was associated with abnormal migration of surface ectodermal cells onto the cornea. Immunofluorescence studies with antimouse filaggrin antibody on day 13 and day 15 revealed the presence of filaggrin precursors in the fused epithelia of mutants, but not in normal corneal or conjunctival epithelia. The results suggest defective regulation of the synthesis of cellular proteins and altered cell surface properties in the Er/Er ocular epithelia.

Abnormalities, Multiple↗
PubMed1984

Characterization of a reduced-eye mutant of the grasshopper, Melanoplus sanguinipes.

A reduced-eye (re) mutant grasshopper of Melanoplus sanguinipes has been characterized by small flat compound eyes lacking facets, no lateral ocelli and only a remnant of the median ocellus. The re grasshoppers walk, jump, fly and feed in a normal manner, but do not respond to visual and auditory stimuli, suggesting they may be blind and deaf. Extracellular recordings from the ventral nerve cord of re mutants verified the lack of neural activity in response to visual and auditory inputs, yet the mutants detected mechanical and tactile stimuli. Electroretinograms implied that a visual deficit may be within the photoreceptors of the compound eye. Histological examination of the compound eyes and ocelli indicated that the cells of the mutant compound eye incompletely differentiate. The optic lamina underlying the retina is missing, as is the outer optic chiasma. The medulla and lobula of the mutant optic lobe are present, however, the neuropil of the medulla lacks the characteristic axonal projection patterns of wild-type grasshoppers. The re grasshopper also lacks all ocellar nerves. Ocellar nerves are normally formed from processes of second order ocellar neurons (SONs), suggesting that if the mutant SONs are present within the protocerebrum, their morphology is drastically altered. Comparison of embryos and juvenile nymphs supports the suggestion that the alterations in the re visual system are the result of abnormal differentiation during development. Even though there is clear evidence of morphological alterations in second and third order optic lobe interneurons, one higher order visual interneuron of the midbrain, the descending contralateral movement detector (DCMD), has the same morphology as the DCMD in a wild-type brain. In this instance, the complete deprivation of the primary sensory input does not appear to alter cellular development.

Animals↗
PubMed1982

Scanning electron microscopy of cartilage in mice with hereditary chondrodysplasia.

Mice born with hereditary, recessive chondrodysplasia (cho/cho) are dwarfed because the cartilage model upon which the endochondral osseous skeleton develops is defective. The mutant's cartilage matrix lacks cohesiveness which apparently contributes to the absence of columnar alignment of proliferating epiphyseal chondrocytes in developing tubular (long) bones. The present communication reviews our current understanding of skeletal dysplasia as it relates to defective chondrogenesis, and presents observations made with the scanning electron microscope of cellular disarray and nonuniform size and distribution of collagen fibrils which confirm the existence of a matrix defect. Autoradiographic experiments on tibial cartilage, similar to those performed on sternal cartilage, confirm the normal pattern of sulfate labeling by mutant epiphyses.

Animals↗
PubMed1983

An SEM analysis of neural crest migration in the mouse.

The cellular morphology and migratory pathways of the trunk neural crest are described in normal mouse embryos, and in embryos homozygous for Patch in which neural crest derivatives develop abnormally. Trunk neural crest cells initially appear in 8 1/2-day embryos as a unique cell population on the dorsal neural tube surface and are relatively rounded. Once they begin to migrate the cells flatten and orient somewhat tangentially to the neural tube, and advance ventrad between the somites and neural tube. At the onset of migration neural crest cells extend lamellipodia onto the surface of the tube while detaching their trailing processes from the lumenal surface. The basal lamina on the dorsal neural tube is discontinuous when cell migration begins in this region. As development proceeds, the basal lamina gradually becomes continuous from a lateral to dorsal direction and neural crest emigration is progressively confined to the narrowing region of discontinuous basal lamina. Cell separation from the neural tube ceases concomitant with completion of a continuous basement membrane. Preliminary observations of the mutant embryos reveal that abnormal extracellular spaces appear and patterns of crest migration are subsequently altered. We conclude that the extracellular matrix, extracellular spaces and basement membranes may delimit crest migration in the mouse.

Animals↗