scholarly journals THE EFFECT OF CRUDE PREPARATIONS OF VACCINIA ON MITOSIS AND DNA SYNTHESIS OF KB CELLS

1966 ◽  
Vol 124 (2) ◽  
pp. 199-208 ◽  
Author(s):  
Jadwiga Koziorowska ◽  
Krzysztof Włodarski
Keyword(s):  
Dna Synthesis ◽  
Mitotic Cell ◽  
Kb Cells ◽  
Cytologic Examination ◽  
Morphologic Study ◽  
One Stage ◽  
Cell Pool ◽  
Infected Cells ◽  
Mitotic Cells

A morphologic study has been made on KB cells infected with various doses of vaccinia as to DNA synthesis and mitosis. Determination of mitotic indices revealed that the mitotic cell pool depended on the proportion of infected cells and the time after infection. By cytologic examination neither mitotic lesions were found nor an accumulation of mitotic cells at any one stage of mitosis was demonstrated. Radioautographs of infected cultures have shown that the frequency of cells labeled over nuclei was significantly increased as compared with control cultures. Following the greatest dose of virus (multiplicity of 20 PFU/cell) the ratio of cells synthesizing DNA to mitotic cells increased from 45:5 at 5 hr to 50:0 at 50 hr. Concommittant with the appearance of this disparity between the DNA-synthesizing cell pool and mitotic cell pool the nuclei of cells became "lightly" labeled. Following the lowest dose of virus (multiplicity of 0.0002 PFU/cell) the increase of the fraction of mitotic cells was proportional to the increase of the fraction of cells which were labeled over nuclei.

Two-Stage Procedure for the Quantitative Determination of Autoprothrombin III Concentration and Some Applications

1967 ◽  
Vol 18 (01/02) ◽  
pp. 198-210 ◽  
Author(s):  
Ronald S Reno ◽  
Walter H Seegers
Keyword(s):  
Prothrombin Time ◽  
Factor Vii ◽  
Two Stage ◽  
Pronounced Increase ◽  
One Stage ◽  
Assay Procedure ◽  
Bovine Plasma ◽  
The One ◽  
Autoprothrombin C

SummaryA two-stage assay procedure was developed for the determination of the autoprothrombin C titre which can be developed from prothrombin or autoprothrombin III containing solutions. The proenzyme is activated by Russell’s viper venom and the autoprothrombin C activity that appears is measured by its ability to shorten the partial thromboplastin time of bovine plasma.Using the assay, the autoprothrombin C titre was determined in the plasma of several species, as well as the percentage of it remaining in the serum from blood clotted in glass test tubes. Much autoprothrombin III remains in human serum. With sufficient thromboplastin it was completely utilized. Plasma from selected patients with coagulation disorders was assayed and only Stuart plasma was abnormal. In so-called factor VII, IX, and P.T.A. deficiency the autoprothrombin C titre and thrombin titre that could be developed was normal. In one case (prethrombin irregularity) practically no thrombin titre developed but the amount of autoprothrombin C which generated was in the normal range.Dogs were treated with Dicumarol and the autoprothrombin C titre that could be developed from their plasmas decreased until only traces could be detected. This coincided with a lowering of the thrombin titre that could be developed and a prolongation of the one-stage prothrombin time. While the Dicumarol was acting, the dogs were given an infusion of purified bovine prothrombin and the levels of autoprothrombin C, thrombin and one-stage prothrombin time were followed for several hours. The tests became normal immediately after the infusion and then went back to preinfusion levels over a period of 24 hrs.In other dogs the effect of Dicumarol was reversed by giving vitamin K1 intravenously. The effect of the vitamin was noticed as early as 20 min after administration.In response to vitamin K the most pronounced increase was with that portion of the prothrombin molecule which yields thrombin. The proportion of that protein with respect to the precursor of autoprothrombin C increased during the first hour and then started to go down and after 3 hrs was equal to the proportion normally found in plasma.

Replicative bacteriophage DNA synthesis in plasmolyzed T4-infected cells: evidence for two independent pathways to DNA.

1976 ◽  
Vol 20 (1) ◽  
pp. 142-156 ◽  
Author(s):  
M G Wovcha ◽  
C S Chiu ◽  
P K Tomich ◽  
G R Greenberg
Keyword(s):  
Dna Synthesis ◽  
Infected Cells

scholarly journals Human Cytomegalovirus Inhibits Cellular DNA Synthesis and Arrests Productively Infected Cells in Late G1

Virology ◽  
1996 ◽  
Vol 224 (1) ◽  
pp. 150-160 ◽  
Author(s):  
Wade A. Bresnahan ◽  
Istvan Boldogh ◽  
E.Aubrey Thompson ◽  
Thomas Albrecht
Keyword(s):  
Dna Synthesis ◽  
Human Cytomegalovirus ◽  
Infected Cells ◽  
Cellular Dna

scholarly journals Arginine deprivation in KB cells: I. Effect on cell cycle progress

1977 ◽  
Vol 75 (3) ◽  
pp. 881-888 ◽  
Author(s):  
AS Weissfeld ◽  
H Rouse
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Tritiated Thymidine ◽  
Experimental Period ◽  
Cell Multiplication ◽  
Starvation Period ◽  
Kb Cells ◽  
Insoluble Material ◽  
Cell Cycle Inhibition ◽  
Cellular Dna

When exponentially growing KB cells were deprived of arginine, cell multiplication ceased after 12 h but viability was maintained throughout the experimental period (42-48 h). Although tritiated thymidine ([(3)H]TdR) incorporation into acid-insoluble material declined to 5 percent of the initial rate, the fraction of cells engaged in DNA synthesis, determined by autoradiography, remained constant throughout the starvation period and approximately equal to the synthesizing fraction in exponentially growing controls (40 percent). Continous [(3)H]TdR-labeling indicated that 80 percent of the arginine-starved cells incorporated (3)H at some time during a 48-h deprivation period. Thus, some cells ceased DNA synthesis, whereas some initially nonsynthesizing cells initiated DNA synthesis during starvation. Flow microfluorometric profiles of distribution of cellular DNA contents at the end of the starvation period indicated that essentially no cells had a 4c or G2 complement. If arginine was restored after 30 h of starvation, cultures resumed active, largely asynchronous division after a 16-h lag. Autoradiographs of metaphase figures from cultures continuously labeled with [(3)H]TdR after restoration indicated that all cells in the culture underwent DNA synthesis before dividing. It was concluded that the majority of cells in arginine-starved cultures are arrested in neither a normal G1 nor G2. It is proposed that for an exponential culture, i.e. from most positions in the cell cycle, inhibition of cell growth after arginine with withdrawal centers on the ability of cells to complete replication of their DNA.

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Signal Interference ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Mitotic Cells

AbstractDuring development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early Drosophila embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

scholarly journals An asymmetric junctional mechanoresponse coordinates mitotic rounding with epithelial integrity

2021 ◽  
Vol 220 (5) ◽  
Author(s):  
Jooske L. Monster ◽  
Lisa Donker ◽  
Marjolein J. Vliem ◽  
Zaw Win ◽  
Helen K. Matthews ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Morphological Changes ◽  
Mitotic Cell ◽  
Cell Junctions ◽  
Actin Binding ◽  
Epithelial Barrier ◽  
Epithelial Integrity ◽  
Tensile Forces ◽  
Shape Changes ◽  
Mitotic Cells

Epithelia are continuously self-renewed, but how epithelial integrity is maintained during the morphological changes that cells undergo in mitosis is not well understood. Here, we show that as epithelial cells round up when they enter mitosis, they exert tensile forces on neighboring cells. We find that mitotic cell–cell junctions withstand these tensile forces through the mechanosensitive recruitment of the actin-binding protein vinculin to cadherin-based adhesions. Surprisingly, vinculin that is recruited to mitotic junctions originates selectively from the neighbors of mitotic cells, resulting in an asymmetric composition of cadherin junctions. Inhibition of junctional vinculin recruitment in neighbors of mitotic cells results in junctional breakage and weakened epithelial barrier. Conversely, the absence of vinculin from the cadherin complex in mitotic cells is necessary to successfully undergo mitotic rounding. Our data thus identify an asymmetric mechanoresponse at cadherin adhesions during mitosis, which is essential to maintain epithelial integrity while at the same time enable the shape changes of mitotic cells.

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