ABSENCE OF DIFFERENTIAL RNA SYNTHESIS BY THE X CHROMOSOMES OF COW LEUCOCYTES

1970 ◽  
Vol 12 (1) ◽  
pp. 44-51 ◽  
Author(s):  
K. Mann ◽  
B. B. Mukherjee

The patterns of ribonucleic acid synthesis by the two X chromosomes during mitotic interphase were studied at metaphase. Cultured cow leucocytes were pulsed with H3-uridine for 15 minutes, washed, resuspended in tracer-free medium and collected at different times after the end of the pulse. Autoradiography of the cells failed to show any significant differences in the number of grains located over the two X chromosomes. The incorporation of H3-uridine into RNA by both X chromosomes indicates that at least part of the 'inactive' X chromosome must be actively synthesizing some RNA.

2021 ◽  
Vol 22 (3) ◽  
pp. 1114
Author(s):  
Ali Youness ◽  
Charles-Henry Miquel ◽  
Jean-Charles Guéry

Women represent 80% of people affected by autoimmune diseases. Although, many studies have demonstrated a role for sex hormone receptor signaling, particularly estrogens, in the direct regulation of innate and adaptive components of the immune system, recent data suggest that female sex hormones are not the only cause of the female predisposition to autoimmunity. Besides sex steroid hormones, growing evidence points towards the role of X-linked genetic factors. In female mammals, one of the two X chromosomes is randomly inactivated during embryonic development, resulting in a cellular mosaicism, where about one-half of the cells in a given tissue express either the maternal X chromosome or the paternal one. X chromosome inactivation (XCI) is however not complete and 15 to 23% of genes from the inactive X chromosome (Xi) escape XCI, thereby contributing to the emergence of a female-specific heterogeneous population of cells with bi-allelic expression of some X-linked genes. Although the direct contribution of this genetic mechanism in the female susceptibility to autoimmunity still remains to be established, the cellular mosaicism resulting from XCI escape is likely to create a unique functional plasticity within female immune cells. Here, we review recent findings identifying key immune related genes that escape XCI and the relationship between gene dosage imbalance and functional responsiveness in female cells.


1974 ◽  
Vol 20 (7) ◽  
pp. 977-980 ◽  
Author(s):  
David K. Horowitz ◽  
Peter J. Russell

Sexual differentiation in male strains of the aquatic fungus Achlya ambisexualis Raper is induced by antheridiol, a sexual steroid hormone secreted by female strains. Antheridiol-induced initiation of the morphologically distinct antheridial branches in male Achlya is completely prevented when DNA-dependent RNA synthesis is inhibited by actinomycin D. In addition antheridial branch elongation is inhibited to a degree proportional to the concentration of actinomycin D added. Thus, evidence indicates that RNA synthesis is required for antheridiol-induced initiation of antheridial branching and that continued RNA synthesis is required for elongation of antheridial branches.


Author(s):  
Alessandra Spaziano ◽  
Dr Irene Cantone

Mammalian females (XX) silence transcription on one of the two X chromosomes to compensate the expression dosage with males (XY). This process — named X-chromosome inactivation — entails a variety of epigenetic modifications that act synergistically to maintain silencing and make it heritable through cell divisions. Genes along the inactive X chromosome are, indeed, refractory to reactivation. Nonetheless, X-chromosome reactivation can occur alongside with epigenome reprogramming or by perturbing multiple silencing pathways. Here we review the events associated with X-chromosome reactivation during in vivo and in vitro reprogramming and highlight recent efforts in inducing Xi reactivation by molecular perturbations. This provides us with a first understanding of the mechanisms underlying X-chromosome reactivation, which could be tackled for therapeutic purposes.


1970 ◽  
Vol 120 (2) ◽  
pp. 381-384 ◽  
Author(s):  
D. Rickwood ◽  
H. G. Klemperer

1. Isolated nuclei from starved rats showed a lowered incorporation of [14C]UMP into RNA. 2. The Mg2+-dependent incorporation was decreased by 30% after 1 day of starvation, but incorporation in the presence of Mn2+ and ammonium sulphate decreased only after longer periods of starvation. 3. RNA synthesis by nuclei in the presence of excess of added RNA polymerase was unchanged after 1 day of starvation and was inhibited by 20% after 4 days. 4. The capacity of nuclei to bind actinomycin D was unchanged after 1 day and was decreased by 20% after 4 days of starvation.


1968 ◽  
Vol 23 (2) ◽  
pp. 268-271 ◽  
Author(s):  
D. Werner

When the centric diatom Cyclotella cryptica is grown in a Si (OH) 4-free medium, the glutamic acid pool decreases within 3 hours to a third of the original value, whereas the aspartic acid pool is reduced by only about 20 per cent. The pools of nucleosid-triphosphates and of glycerol-1-phosphate remain unaffected during this time. The nucleosid-diphosphates pool decreases in the same way as that of aspartic acid. The decrease in the glutamic acid pool precedes the inhibition of total protein synthesis in Si (OH) 4-deficient cells, and a significant decrease in the a-ketoglutarate pool precedes the decrease of the glutamic acid content. Already within 60 minutes ofter incubation in a Si (OH) 4-free medium, the content of a-ketoglutarate is decreased to one third of the normal value. On the other hand, the acetyl CoA pathway (enhanced fatty acid synthesis) is not inhibited. The results suggest, that the Si (OH) 4-metabolism interferes with reactions between the condensing enzyme (acetyl-CoA and oxalacetate) and a-ketoglutarate. The delay between inhibition of protein- and RNA-synthesis and the different changes in the pools of amino acids and nucleosid-triphosphates resemble the regulation of the nucleosid-triphosphate pool and RNA-synthesis in amino acid starved strains of E. coli (EDLIN and NEUHARD) 1, though the primary causes are quite different.


1979 ◽  
Vol 178 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Torsten Yngner ◽  
Claes Engelbrecht ◽  
Lillemor Lewan ◽  
Jan-Erik Annerfeldt

The balance between anabolism and catabolism of [5-3H]uridine was studied in the mouse after partial hepatectomy. Labelling of RNA and UDP-glucose was determined and evaluated in relation to changes in the specific radioactivity of UTP. The amounts of labelled catabolic products of uridine were increased several-fold in liver and blood after partial hepatectomy. The specific radioactivity of RNA decreased to about 60% of the control value at 6h and was in the same range as that of control liver at 24h after operation. Decreased labelling of RNA and UDP-glucose was attributable to decreased specific radioactivity of UTP. No changes in the size of the UTP pool or in the balance between uridine anabolism and catabolism were found that could explain the decreased specific radioactivity of UTP. Rather, the alterations in the labelling of this metabolite induced by the partial hepatectomy may be related to decreased phosphorylating capacity in the liver cells and/or dilution of the labelled precursor in an expanded uridine pool. The enhanced amounts of uridine catabolic products in liver and blood were probably a consequence of accumulation and altered incorporation of the metabolites from the blood into the liver cells. Despite the increased amounts of labelled catabolic products and the decreased labelling of RNA, the results reported here actually suggest decreased uridine catabolism and slightly increased RNA synthesis in mouse liver after partial hepatectomy. The results stress the importance of proper controls in determination of nucleic acid synthesis and in metabolic studies by use of labelled precursors.


Genetics ◽  
2006 ◽  
Vol 174 (3) ◽  
pp. 1115-1133 ◽  
Author(s):  
Silvia V. Diaz-Perez ◽  
David O. Ferguson ◽  
Chen Wang ◽  
Gyorgyi Csankovszki ◽  
Chengming Wang ◽  
...  

1966 ◽  
Vol 44 (6) ◽  
pp. 739-745 ◽  
Author(s):  
R. A. Fletcher ◽  
Daphne J. Osborne

The addition of gibberellin A3 (GA) to leaf discs of Taraxacum officinale Weber retards their senescence and delays the decline in the levels of chlorophyll, protein, and RNA. Incorporation of 14C leucine and 14C adenine into protein and RNA respectively was increased by GA. This enhancement of protein and RNA synthesis did not occur if the discs were supplied with actinomycin D before treatment with gibberellin. If, however, actinomycin D was added after the gibberellin treatment then the stimulatory effect of the hormone was maintained. These results suggest that the retarding action of gibberellins on leaf senescence could be mediated through a regulation of RNA synthesis that is DNA dependent.


2005 ◽  
Vol 25 (7) ◽  
pp. 2757-2769 ◽  
Author(s):  
Nicholas Stavropoulos ◽  
Rebecca K. Rowntree ◽  
Jeannie T. Lee

ABSTRACT X chromosome inactivation silences one of two X chromosomes in the mammalian female cell and is controlled by a binary switch that involves interactions between Xist and Tsix, a sense-antisense pair of noncoding genes. On the future active X chromosome, Tsix expression suppresses Xist upregulation, while on the future inactive X chromosome, Tsix repression is required for Xist-mediated chromosome silencing. Thus, understanding the binary switch mechanism depends on ascertaining how Tsix expression is regulated. Here we have taken an unbiased approach toward identifying Tsix regulatory elements within the X chromosome inactivation center. First, we defined the major Tsix promoter and found that it cannot fully recapitulate the developmental dynamics of Tsix expression, indicating a requirement for additional regulatory elements. We then delineated two enhancers, one classical enhancer mapping upstream of Tsix and a bipartite enhancer that flanks the major Tsix promoter. These experiments revealed the intergenic transcription element Xite as an enhancer of Tsix and the repeat element DXPas34 as a component of the bipartite enhancer. Each enhancer contains DNase I-hypersensitive sites and appears to confer developmental specificity to Tsix expression. Characterization of these enhancers will facilitate the identification of trans-acting regulatory factors for X chromosome counting and choice.


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