scholarly journals DNA CONTENT OF PLACENTAL NUCLEI

1962 ◽  
Vol 13 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Michael Galton

The DNA content of individual nuclei in four immature human placentas was determined by microspectrophotometric analysis of Feulgen-stained sections. The absence of mitosis in the syncytiotrophoblast, taken together with the finding of a diploid unimodal distribution, at a time of rapid placental growth, indicated that the syncytiotrophoblast possessed little or no intrinsic reproductive capacity. In contrast, the cytotrophoblast displayed considerable mitotic activity and was found to contain a high proportion of nuclei with DNA values in excess of the diploid amount, corresponding to DNA synthesis in interphase nuclei preparatory to division. From the complementary behavior of the two layers of trophoblast, with respect to evidence of reproductive ability, it is concluded that the rapid accumulation of nuclei in the syncytiotrophoblast, during the early development of the placenta, is accounted for by cell proliferation within the cytotrophoblast followed by alignment and coalescence of some daughter cells in the syncytiotrophoblast.

1983 ◽  
Vol 244 (5) ◽  
pp. G469-G474 ◽  
Author(s):  
J. P. Buts ◽  
R. De Meyer ◽  
J. Kolanowski

This study was undertaken to determine whether the rat colon exhibits ontogenic changes in epithelial cell proliferation and DNA synthesis during growth. DNA synthesis was measured at intervals after birth in four colonic segments by the incorporation rates of [3H]thymidine. The labeled crypt cell index was determined by radioautography. New findings from our study are that 1) in each colonic segment of suckling rats, [3H]thymidine incorporation rate overshot the adult levels (49-119%) with a peak occurring at day 14 postpartum, 2) between days 14 and 20, the incorporation rates declined sharply to adult values and remained thereafter unchanged until adulthood; during the same period, the labeled and mitotic index decreased, respectively, from 52 to 19% and from 3.58 to 1.43%, 3) the decrease in DNA synthesis and in cell proliferation rates was concomitant with an upsurge in plasma total corticosterone initiated on day 14, and 4) treatment of 10-day-old sucklings with physiological doses of hydrocortisone for 4 consecutive days significantly depressed (P less than 0.01) colonic DNA content and DNA synthesis rates to levels about 45-67% of the control values. These data indicate that growth of the colon may be under the control of glucocorticoid secretion at the weaning period.


1982 ◽  
Vol 9 (2) ◽  
pp. 179 ◽  
Author(s):  
T.L Setter ◽  
H Greenway ◽  
J Kuo

Effects of high external NaCl concentrations on growth were examined in the unicellular freshwater alga Cldorella emevsonii during different phases of cell development, using synchronized cultures obtained by alternating light-dark cycles. Growth of cultures synchronized at 1 mM NaCl [external osmotic pressure (next=) 0.08 MPa] was compared with (i) cultures synchronized at 200 mM NaCl (n,,, = 1.01 MPa) and (ii) cultures synchronized at 1 mM NaCl from which the daughter cells were suddenly transferred to 100, 150 or 200 mM NaCl. The effects of these two treatments on synthesis of protein, RNA and DNA during cell cycles were similar, and are attributed to the high nexta nd not to specific effects of Na+ and C1-. Growth inhibitions in cells at 200 mM NaCl relative to 1 mM NaCl occurred mainly via effects on cell division; this was confirmed by electron microscopy. There was a lag before net DNA synthesis commenced, and there were reductions in rates of net DNA synthesis in cells at 200 mM NaCl relative to 1 mM NaC1. Rates of increase in cell volume and in protein and RNA content per cell were little affected by high external NaCl concentrations. Consequently, daughter cells at 200 mM NaCl were approximately twice the volume and contained twice as much protein and RNA as daughter cells at 1 mM NaCl, while DNA content was equal in daughter cells at 1 and 200 mM NaCl.


Science ◽  
2021 ◽  
Vol 372 (6547) ◽  
pp. 1176-1181
Author(s):  
Marco D’Ario ◽  
Rafael Tavares ◽  
Katharina Schiessl ◽  
Bénédicte Desvoyes ◽  
Crisanto Gutierrez ◽  
...  

How eukaryotic cells assess and maintain sizes specific for their species and cell type remains unclear. We show that in the Arabidopsis shoot stem cell niche, cell size variability caused by asymmetric divisions is corrected by adjusting the growth period before DNA synthesis. KIP-related protein 4 (KRP4) inhibits progression to DNA synthesis and associates with mitotic chromosomes. The F BOX-LIKE 17 (FBL17) protein removes excess KRP4. Consequently, daughter cells are born with comparable amounts of KRP4. Inhibitor dilution models predicted that KRP4 inherited through chromatin would robustly regulate size, whereas inheritance of excess free KRP4 would disrupt size homeostasis, as confirmed by mutant analyses. We propose that a cell cycle regulator, stabilized by association with mitotic chromosomes, reads DNA content as a cell size–independent scale.


1990 ◽  
Vol 97 (3) ◽  
pp. 509-516 ◽  
Author(s):  
S. Sazer ◽  
S.W. Sherwood

Cell growth and division require the doubling of cellular constituents followed by their equal distribution to the two daughter cells. Within a growing population, the ratio of mitochondrial to cellular volume is maintained, as is the number of mitochondrial genomes per cell. The mechanisms responsible for coordinating nuclear and mitochondrial DNA synthesis, and for balancing increases in cell and mitochondrial size are not well understood. In studies of the fission yeast Schizosaccharomyces pombe we quantified cellular and mitochondrial DNA content by both Southern blot analysis and flow cytometry of cells stained with a variety of DNA-binding fluorochromes, which we show are able to detect nuclear and mitochondrial DNA with different efficiencies. In the conditional cell division cycle mutant cdc10, which is unable to initiate nuclear DNA synthesis, we found that there was an increase in the mitochondrial DNA content in the absence of nuclear DNA replication. This demonstrates that mitochondrial and nuclear DNA synthesis are not obligately linked. We also show that mitochondrial DNA replication is not required for the increase in mitochondrial size that occurs as cells elongate, although this results in a decrease in the ratio of mitochondrial DNA to mitochondrial volume.


1992 ◽  
Vol 25 (11) ◽  
pp. 341-345 ◽  
Author(s):  
C. Furihata ◽  
M. Yamashita ◽  
N. Kinae ◽  
T. Matsushima

MX is a strong direct acting mutagen on Salmonella typhimurium TA100 and is present in chlorinated tap water which contains organic compounds. MX was administered orally to 7-week-old male F344 rats, and its geno-toxicity in the pyloric mucosa of stomach was examined by analysis of DNA single strand scissions by the alkaline elution method. The effect of MX on cell proliferation was examined by assays of the inductions of replicative DNA synthesis and ornithine decarboxylase. MX at closes of 20-48 mg/kg body weight induced DNA single strand scissions dose-dependently (p<0.02) in the pyloric mucosa of the stomach 2 h after its administration. Moreover at doses of 10-60 mg/kg body weight, it induced up to 21-fold increase in replicative DNA synthesis (p<0.01) 16 h after its administration. At doses of 10-60 mg/kg body weight, it induced up to 100-fold increase in ornithine decarboxylase activity with a maximum 16 h after its administration. These results suggest that MX is genotoxic and induces cell proliferation in the glandular stomach of rats.


2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Qian Liu ◽  
Lijuan Guo ◽  
Hongyan Qi ◽  
Meng Lou ◽  
Rui Wang ◽  
...  

AbstractRibonucleotide reductase (RR) is a unique enzyme for the reduction of NDPs to dNDPs, the building blocks for DNA synthesis and thus essential for cell proliferation. Pan-cancer profiling studies showed that RRM2, the small subunit M2 of RR, is abnormally overexpressed in multiple types of cancers; however, the underlying regulatory mechanisms in cancers are still unclear. In this study, through searching in cancer-omics databases and immunohistochemistry validation with clinical samples, we showed that the expression of MYBL2, a key oncogenic transcriptional factor, was significantly upregulated correlatively with RRM2 in colorectal cancer (CRC). Ectopic expression and knockdown experiments indicated that MYBL2 was essential for CRC cell proliferation, DNA synthesis, and cell cycle progression in an RRM2-dependent manner. Mechanistically, MYBL2 directly bound to the promoter of RRM2 gene and promoted its transcription during S-phase together with TAF15 and MuvB components. Notably, knockdown of MYBL2 sensitized CRC cells to treatment with MK-1775, a clinical trial drug for inhibition of WEE1, which is involved in a degradation pathway of RRM2. Finally, mouse xenograft experiments showed that the combined suppression of MYBL2 and WEE1 synergistically inhibited CRC growth with a low systemic toxicity in vivo. Therefore, we propose a new regulatory mechanism for RRM2 transcription for CRC proliferation, in which MYBL2 functions by constituting a dynamic S-phase transcription complex following the G1/early S-phase E2Fs complex. Doubly targeting the transcription and degradation machines of RRM2 could produce a synthetic inhibitory effect on RRM2 level with a novel potential for CRC treatment.


2006 ◽  
Vol 107 (2) ◽  
pp. 211-221 ◽  
Author(s):  
Mieczysław Kuraś ◽  
Julita Nowakowska ◽  
Elwira Śliwińska ◽  
Radosław Pilarski ◽  
Renata Ilasz ◽  
...  

1995 ◽  
Vol 36 (4) ◽  
pp. 325-334 ◽  
Author(s):  
Richard Hoffman ◽  
Walter Woodrow Burns ◽  
Dietrich H. Paper

BIOspektrum ◽  
2021 ◽  
Vol 27 (3) ◽  
pp. 246-249
Author(s):  
Elisabeth Kruse ◽  
Stephan Hamperl

AbstractTimely and accurate duplication of DNA prior to cell division is a prerequisite for propagation of the genetic material to both daughter cells. DNA synthesis initiates at discrete sites, termed replication origins, and proceeds in a bidirectional manner until all genomic DNA is replicated. Despite the fundamental nature of these events, a uniform method that identifies origins of replication in a comprehensive manner is still missing. Here, we present currently available and discuss new approaches to map replication origins in mammalian genomes.


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