ASCOCARPIC DEVELOPMENT IN DIPOROTHECA RHIZOPHILA

1964 ◽  
Vol 42 (11) ◽  
pp. 1525-1530 ◽  
Author(s):  
C. C. Gordon ◽  
C. Gardner Shaw
Keyword(s):  
Apical Cell ◽  
Vegetative Hypha ◽  
The Third ◽  
Final Maturation ◽  
A Cell ◽  
Generative Cells

In Diporotheca rhizophila Gordon & Shaw upright unicellular perithecial initials are produced on the superficial mycelium covering the host's roots. By septation the initial becomes a three-celled primordium. Two cells, produced laterally from the penultimate cell of the primordium, by division in two planes, form the perithecial wall. During final maturation two to three divisions in the third plane make the wall three to five cells thick. The centrum originates from the apical cell of the primordium. Dikaryotization of an immature perithecium involves the production of one to many hyaline receptive hyphae from the dark, pigmented, peridial cells. These receptive hyphae fuse with superficial vegetative hyphae, and a nucleus from a cell of the vegetative hypha apparently migrates into the centrum. No structure within the centrum of the perithecium could be interpreted as an ascogonium. The same hyaline, pseudoparenchymatous filaments which form the ascal generative cells in the basal and central areas of the centrum give rise to periphyses within the perithecial neck.

“The Greatest Thrill I Get is When I Hear a Criminal Say, ‘Yes, I Did it’”: Race and the Third Degree in New Orleans, 1920–1945

2016 ◽  
Vol 34 (1) ◽  
pp. 1-44
Author(s):  
Jeffrey S. Adler
Keyword(s):  
African American ◽  
Medical Care ◽  
New Orleans ◽  
Police Officer ◽  
Police Officers ◽  
Constitutional Protection ◽  
The Third ◽  
The Face ◽  
A Cell ◽  
Short Time

On May 11, 1938, two New Orleans policemen entered the Astoria Restaurant, marched to the kitchen, and approached Loyd D. T. Washington, a 41-year-old African American cook. They informed Washington that they would be taking him to the First Precinct station for questioning, although they assured the cook that he need not change his clothes and “should be right back” to the “Negro restaurant,” where he had worked for 3 years. Immediately after arriving at the station house, police officers “surrounded” Washington, showed him a photograph of a man, and announced that he had killed a white man in Yazoo City, Mississippi, 20 years earlier. When Washington insisted that he did not know the man in the photograph, that he had never been to (or even heard of) Yazoo City, and that he had been in the army at the time of the murder, the law enforcers confined him in a cell, although they had no warrant for his arrest and did not charge him with any crime. The following day, a detective brought him to the “show-up room” in the precinct house, where he continued the interrogation and, according to Washington, “tried to make me sign papers stating that I had killed a white man” in Mississippi. As every African American New Orleanian knew, the show-up (or line-up) room was the setting where detectives tortured suspects and extracted confessions. “You know you killed him, Nigger,” the detective roared. Washington, however, refused to confess, and the detective began punching him in the face, knocking out five of his teeth. After Washington crumbled to the floor, the detective repeatedly kicked him and broke one of his ribs. The beating continued for an hour, until other policemen restrained the detective, saying “give him a chance to confess and if he doesn't you may start again.” But Washington did not confess, and the violent interrogation began anew. A short time later, another police officer interrupted the detective, telling him “do not kill this man in here, after all he is wanted in Yazoo City.” Bloodied and writhing in pain, Washington asked to contact his family, but the request was ignored. Because he had not been formally charged with a crime, New Orleans law enforcers believed that Washington had no constitutional protection again self-incrimination or coercive interrogation and no right to an arraignment or bail, and they had no obligation to contact his relatives or to provide medical care for him.

A Cell in the Third Dimension: Tetrakaidecahedron Realized

1969 ◽  
Vol 31 (8) ◽  
pp. 517-518 ◽  
Author(s):  
Robert A. Lehman
Keyword(s):  
The Third ◽  
A Cell ◽  
Third Dimension

The putative sponge aggregation receptor. Isolation and characterization of a molecule composed of scavenger receptor cysteine-rich domains and short consensus repeats

1998 ◽  
Vol 111 (17) ◽  
pp. 2635-2644 ◽  
Author(s):  
B. Blumbach ◽  
Z. Pancer ◽  
B. Diehl-Seifert ◽  
R. Steffen ◽  
J. Munkner ◽  
...  
Keyword(s):  
Cell Surface ◽  
Scavenger Receptor ◽  
Cell Surface Receptor ◽  
Functional Assay ◽  
Cdna Clones ◽  
The Third ◽  
Short Consensus Repeats ◽  
Isolation And Characterization ◽  
A Cell ◽  
Cell Cell

Porifera (sponges) are the oldest extant metazoan phylum. Dissociated sponge cells serve as a classic system to study processes of cell reaggregation. The reaggregation of dissociated cells is mediated by an extracellularly localized aggregation factor (AF), based on heterophilic interactions of the third order; the AF bridges two cells by ligating a cell-surface-bound aggregation receptor (AR). In the present study we report cloning, expression and immunohistochemical localization of a polypeptide from the marine sponge Geodia cydonium, which very likely represents the AR. The presumed AR gene gives rise to at least three forms of alternatively spliced transcripts of 6.5, 4.9 and 3.9 kb, as detected by northern blotting. Two cDNA clones corresponding to the shorter forms were already reported earlier; here we present an analysis of the largest. All three putative polypeptides feature scavenger receptor cysteine-rich (SRCR) domains. The largest form, SRCR-SCR-Car, is a cell-surface receptor of molecular mass 220 kDa, which is assumed to be the cell-adhesion receptor AR; the second form, SRCR-Re, is also a putative receptor of 166 kDa, while the third form, SRCR-Mo, is a soluble molecule of 129 kDa. The SRCR-SCR-Car molecule consists of fourteen SRCR domains, six short consensus repeats (SCRs), a C-terminal transmembrane domain and a cytoplasmic tail; its fourteenth SRCR domain features an Arg-Gly-Asp tripeptide. To obtain monoclonal antibodies, a 170-amino-acid-long polypeptide that is found in all three forms of the SRCR-containing proteins was expressed in E. coli. In a western blot of sponge cells lysate the monoclonal antibody raised against the recombinant polypeptide recognized two major immuno-reacting polypeptides (220 and 117 kDa) and two minor bands (36 and 32 kDa). The antibody was found to react with antigen(s) predominantly localized on the plasma membranes of cells, especially those of spherulous cells. In a functional assay Fab' fragments of the antibodies suppressed AF-mediated cell-cell reaggregation. Additionally, a recombinant SRCR-soluble fragment effectively inhibited AF-mediated cell-cell reaggregation. We conclude that the 220 kDa SRCR-containing protein of the sponge G. cydonium is very likely the AR.

Multiple developmental defects in Engrailed-1 mutant mice: an early mid-hindbrain deletion and patterning defects in forelimbs and sternum

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 2065-2075 ◽  
Author(s):  
W. Wurst ◽  
A.B. Auerbach ◽  
A.L. Joyner
Keyword(s):  
Spinal Cord ◽  
Embryonic Development ◽  
Normal Development ◽  
Cranial Nerves ◽  
Mutant Mice ◽  
Mouse Development ◽  
Developmental Defects ◽  
Targeted Deletion ◽  
The Third ◽  
A Cell

During mouse development, the homeobox-containing gene En-1 is specifically expressed across the mid-hindbrain junction, the ventral ectoderm of the limb buds, and in regions of the hindbrain, spinal cord, somites and somite-derived tissues. To address the function of En-1 during embryogenesis, we have generated mice homozygous for a targeted deletion of the En-1 homeobox. En-1 mutant mice died shortly after birth and exhibited multiple developmental defects. In the brains of newborn mutants, most of the colliculi and cerebellum were missing and the third and fourth cranial nerves were absent. A deletion of midhindbrain tissue was observed as early as 9.5 days of embryonic development and the phenotype resembles that previously reported for Wnt-1 mutant mice. In addition, patterning of the forelimb paws and sternum was disrupted, and the 13th ribs were truncated. The results of these studies suggest a cell autonomous role for En-1 in generation and/or survival of mid-hindbrain precursor cells and also a non-cell autonomous role in signalling normal development of the limbs and possibly sternum.

Improved unroofing protocols for cryo-electron microscopy, atomic force microscopy and freeze-etching electron microscopy and the associated mechanisms

Microscopy ◽  
2020 ◽  
Vol 69 (6) ◽  
pp. 350-359
Author(s):  
Nobuhiro Morone ◽  
Eiji Usukura ◽  
Akihiro Narita ◽  
Jiro Usukura
Keyword(s):  
Electron Microscopy ◽  
Atomic Force Microscopy ◽  
Cell Membrane ◽  
Apical Cell ◽  
Force Microscopy ◽  
Atomic Force ◽  
Cryo Electron Microscopy ◽  
Cytoplasmic Surface ◽  
A Cell ◽  
Freeze Etching

Abstract Unroofing, which is the mechanical shearing of a cell to expose the cytoplasmic surface of the cell membrane, is a unique preparation method that allows membrane cytoskeletons to be observed by cryo-electron microscopy, atomic force microscopy, freeze-etching electron microscopy and other methods. Ultrasound and adhesion have been known to mechanically unroof cells. In this study, unroofing using these two means was denoted sonication unroofing and adhesion unroofing, respectively. We clarified the mechanisms by which cell membranes are removed in these unroofing procedures and established efficient protocols for each based on the mechanisms. In sonication unroofing, fine bubbles generated by sonication adhered electrostatically to apical cell surfaces and then removed the apical (dorsal) cell membrane with the assistance of buoyancy and water flow. The cytoplasmic surface of the ventral cell membrane remaining on the grids became observable by this method. In adhesion unroofing, grids charged positively by coating with Alcian blue were pressed onto the cells, thereby tightly adsorbing the dorsal cell membrane. Subsequently, a part of the cell membrane strongly adhered to the grids was peeled from the cells and transferred onto the grids when the grids were lifted. This method thus allowed the visualization of the cytoplasmic surface of the dorsal cell membrane. This paper describes robust, improved protocols for the two unroofing methods in detail. In addition, micro-unroofing (perforation) likely due to nanobubbles is introduced as a new method to make cells transparent to electron beams.

A computational model of the effect of symplastic growth on cell mechanics in a linear leaf blade

2015 ◽  
Vol 13 (01) ◽  
pp. 1540005 ◽  
Author(s):  
Ulyana Zubairova ◽  
Sergey Golushko ◽  
Aleksey Penenko ◽  
Sergey Nikolaev
Keyword(s):  
Cell Mechanics ◽  
Leaf Blade ◽  
Computational Simulation ◽  
Growth Function ◽  
Leaf Base ◽  
Growing Cell ◽  
Linear Leaf ◽  
A Cell ◽  
Symplastic Growth ◽  
Generative Cells

The epidermis of a linear leaf, as in Poaceae, is established by parallel files of cells originating from the leaf base. Their feature is symplastic growth where neighboring cell walls adhere and do not slide along each other. We developed a simple mechanical cell-based model for symplastic growth of linear leaf blade. The challenge is to determine what restrictions on cell size symplastic growth creates compared to the free growing cells. We assume an unidirectional growing cell ensemble starting from a meristem-like layer of generative cells and then generating parallel cell rows from every cell of the initial layer. Each cell is characterized by its growth function, and growth of the whole leaf blade is accompanied by mutual adjustment between all the cells. Cells divide once they have reached a threshold area. A mathematical model and its implementation are proposed for computational simulation of 1D symplastic growth of tissues. The question analyzed is how a cell grows in a plant tissue if there is a mechanism for regulating the growth of an isolated growing cell and the behavior of the cell wall matter is elastoplastic. The results of the simulation of linear leaf blade growth are compared to those for a free-growing cell population.

scholarly journals Antibodies to the major insoluble milk fat globule membrane-associated protein: specific location in apical regions of lactating epithelial cells.

1981 ◽  
Vol 89 (3) ◽  
pp. 485-494 ◽  
Author(s):  
W W Franke ◽  
H W Heid ◽  
C Grund ◽  
S Winter ◽  
C Freudenstein ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Milk Fat ◽  
Lipid Production ◽  
Apical Cell ◽  
Cell Types ◽  
Specific Marker ◽  
Milk Lipid ◽  
Apical Surface ◽  
Milk Fat Globule ◽  
A Cell

Milk lipid globules of various species are surrounded by a membrane structure that is separated from the triglyceride core of the globule by a densely staining fuzzy coat layer of 10- to 50-nm thickness. This internal coat structure remains attached to the membrane during isolation and extraction with low- and high-salt buffers, is insoluble in nondenaturing detergents, and is enriched in an acidic glycoprotein (butyrophilin) with an apparent Mr of 67,000. Guinea pig antibodies against this protein, which show cross-reaction with the corresponding protein in some (goat) but not other (human, rat) species, have been used for localization of butyrophilin on frozen sections of various tissues from cow by immunofluorescence and electron microscopy. Significant reaction is found only in milk-secreting epithelial cells and not in other cell types of mammary gland and various epithelial tissues. In milk-secreting cells, the staining is restricted to the apical cell surface, including budding milk lipid globules, and to the periphery of the milk lipid globules contained in the alveolar lumina. These findings indicate that butyrophilin, which is constitutively secreted by surface budding in coordination with milk lipid production, is located at the apical surface and is not detected at basolateral surfaces, in endoplasmic reticulum, and in Golgi apparatus. This protein structure represents an example of a cell type-specific cytoskeletal component in a cell apex. It is suggested that this antigen provides a specific marker for the apical surface of milk-secreting cells and that butyrophilin is involved in the vectorial discharge of milk lipid globules.

scholarly journals Dopamine reduces cell surface Na+/H+ exchanger-3 protein by decreasing NHE3 exocytosis and cell membrane recycling

2017 ◽  
Vol 313 (4) ◽  
pp. F1018-F1025 ◽  
Author(s):  
Ming Chang Hu ◽  
I. Alexandru Bobulescu ◽  
Henry Quiñones ◽  
Serge M. Gisler ◽  
Orson W. Moe
Keyword(s):  
Cell Membrane ◽  
Cell Surface ◽  
Proximal Tubule ◽  
Apical Cell ◽  
Brefeldin A ◽  
Dependent Manner ◽  
Culture Model ◽  
A Cell ◽  
The Many ◽  
Dose Dependent

The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of Na+ transporters to effect sodium excretion, including the proximal tubule Na+/H+ exchanger-3 (NHE3). DA represent a single hormone that regulates NHE3 at multiple levels, including translation, degradation, endocytosis, and protein phosphorylation. Because cell surface NHE3 protein is determined by the balance between exocytotic insertion and endocytotic retrieval, we examined whether DA acutely affects the rate of NHE3 exocytosis in a cell culture model. DA inhibited NHE3 exocytosis at a dose-dependent manner with a half maximal around 10−6 M. The DA effect on NHE3 exocytosis was blocked by inhibition of protein kinase A and by brefeldin A, which inhibits endoplasmic reticulum-to-Golgi transport. NHE3 directly interacts with the ε-subunit of coatomer protein based on yeast-two-hybrid and coimmunoprecipitation. Because NHE3 has been shown to be recycled back to the cell membrane after endocytosis, we measured NHE3 recycling using a biochemical reinsertion assay and showed that reinsertion of NHE3 back to the membrane is also inhibited by DA. In conclusion, among the many mechanisms by which DA reduces apical membrane NHE3 and induces proximal tubule natriuresis, one additional mechanism is inhibition of exocytotic insertion and reinsertion of NHE3 in the apical cell surface.

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