Expression of p53-Regulated Genes in Cultured Mammalian Cells After Exposure to A Space Environment
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Abstract:
The space environment contains two major biologically significant influences; space radiation and microgravity. The tumor suppressor gene product p53 is generally thought to contribute to the genetic stability of cells with DNA damage through the activity of p53 initiated signal transduction pathways. We propose to investigate the expression of p53-regulated genes in cultured mammalian cells after exposure to a space environment. We expect that the data from this proposal will be useful for designing physiological protection against the serious effects of space radiation during long-term stays in space.Keywords:
Space Radiation
Suppressor mutation
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Cellular senescence
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Abstract We identified and characterized 14 extragenic mutations that suppressed the dominant egg-laying defect of certain lin-12 gain-of-function mutations. These suppressors defined seven genes: sup-l7, lag-2, sel-4, sel-5, sel-6, sel-7 and sel-8. Mutations in six of the genes are recessive suppressors, whereas the two mutations that define the seventh gene, lag-2, are semi-dominant suppressors. These suppressor mutations were able to suppress other lin-12 gain-of-function mutations. The suppressor mutations arose at a very low frequency per gene, 10-50 times below the typical loss-of-function mutation frequency. The suppressor mutations in sup1 7 and lag-2 were shown to be rare non-null alleles, and we present evidence that null mutations in these two genes cause lethality. Temperature-shift studies for two suppressor genes, sup1 7and lag-2, suggest that both genes act at approximately the same time as lin-12in specifying a cell fate. Suppressor alleles of six of these genes enhanced a temperature-sensitive loss-of-function allele of glp-1, a gene related to lin-12 in structure and function. Our analysis of these suppressors suggests that the majority of these genes are part of a shared lin-12/glp-1 signal transduction pathway, or act to regulate the expression or stability of lin-12 and glp-1.
Null allele
Suppressor mutation
Loss function
Genetic screen
Caenorhabditis
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Changes in gene expression after treatment of Escherichia coli cultures with mitomycin C were assessed using gene array technology. Unexpectedly, a large number of genes (nearly 30% of all genes) displayed significant changes in their expression level. Analysis and classification of expression profiles of the corresponding genes allowed us to assign this large number of genes into one or two dozen small clusters of genes with similar expression profiles. This assignment allowed us to describe systematically the changes in the level of gene expression in response to DNA damage. Among the damage-induced genes, more than 100 are novel. From those genes involved in DNA metabolism that have not previously been shown to be induced by DNA damage, the mutS gene involved in mismatch repair is especially noteworthy. In addition to the SOS response, we observed the induction of other stress response pathways, such as those of oxidative stress and osmotic protection. Among the genes that are downregulated in response to DNA damage are numerous protein biosynthesis genes. Analysis of the gene expression data highlighted the essential involvement of sigma(s)-regulated genes and the general stress response network in the response to DNA damage.
SOS response
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Abstract The phenotype of some spontaneous mutations in Drosophila can be modified by mutations at unlinked loci. The affected alleles are caused by the insertion of retroviral transposable elements. The idiosyncratic functional and structural properties of these elements play a key role in determining the expression characteristics of the genes into which they are inserted. These phenotypes are reversed or intensified by the allelic state of suppressor and enhancer loci through changes in the transcriptional properties of the transposable elements.
DNA Transposable Elements
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Abstract The distal part of 1p is frequently deleted in aggressive neuroblastoma, and the region is believed to harbor one or more tumor suppressor genes relevant to tumor development. To analyze differences among neuroblastoma tumors, an expression profile was established for the genes mapped within a previously described shortest region of overlap of deletions at 1p36.2. The gene expression levels were quantified by TaqMan real‐time (RT)‐PCR for 30 transcripts using 55 primary neuroblastoma tumors. Here we report on a significant decrease in gene expression of the genes RERE, PIK3CD , LZIC, PGD, and PEX14 and an increase of SLC2A5 when comparing tumors of favorable biology to Stage 4 neuroblastomas. When comparing 1p‐deleted tumors of all stages to tumors with an intact 1p, a significant difference at gene‐by‐gene level in TNFRSF9 , RERE , PIK3CD , CLSTN1 , CTNNBIP1, and CASZ1 was detected. A complete loss of expression could not be seen for any single gene analyzed. Several of the genes with diminished expression in unfavorable or 1p‐deleted tumors have functions that could contribute to tumor development. It is also possible that a combination of lowly expressed genes at 1p, rather than one single classical tumor suppressor gene, causes the unfavorable outcome associated with 1p‐deletion in neuroblastoma. © 2006 Wiley‐Liss, Inc.
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N-Myc
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Although it is now well known that some diseased areas, such as cancer nests, inflammation loci, and infarction areas, are acidified, little is known about cellular signal transduction, gene expression, and cellular functions under acidic conditions. Our group showed that different signal proteins were activated under acidic conditions compared with those observed in a typical medium of around pH 7.4 that has been used until now. Investigations of gene expression under acidic conditions may be crucial to our understanding of signal transduction in acidic diseased areas. In this study, we investigated gene expression in mesothelioma cells cultured at an acidic pH using a DNA microarray technique. After 24 h culture at pH 6.7, expressions of 379 genes were increased more than twofold compared with those in cells cultured at pH 7.5. Genes encoding receptors, signal proteins including transcription factors, and cytokines including growth factors numbered 35, 32, and 17 among the 379 genes, respectively. Since the functions of 78 genes are unknown, it can be argued that cells may have other genes for signaling under acidic conditions. The expressions of 37 of the 379 genes were observed to increase after as little as 2 h. After 24 h culture at pH 6.7, expressions of 412 genes were repressed more than twofold compared with those in cells cultured at pH 7.5, and the 412 genes contained 35, 76, and 7 genes encoding receptors, signal proteins including transcription factors, and cytokines including growth factors, respectively. These results suggest that the signal pathways in acidic diseased areas are different, at least in part, from those examined with cells cultured at a pH of around 7.4.
TBX1
Transcription
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Objective: To screen signal transduction -regulated genes in nasopharyngeal carcinoma using gene chips. Methods: A preliminary selection of abnormal expression genes from the gene chips of the Shenzhen Weixin company which detected the seven nasopharyngeal carcinoma and one rhinopharyngitis. And then to integrate the data of signal transduction -regulated by Gene Ontology, screen signal transduction -regulated genes from gene chips in NPC from BioCarta. Result: 1.In the basic of gene chips, there are 871 high expression genes and 343 low expression genes in the nasopharyngeal carcinoma tissue. 2.There are 27 differential expression relate gene of signal conducting. 21 of them are high expressing and 7 are low express. 3.We accepted 7 signal transduction -regulated genes from BioCarta which could play important role in the development of NPC. And we got several signal pathways. Conclusion: We found a new way how to screen signal transduction-regulated genes from gene chips in NPC and then make a preliminary identification of the Candidate Gene.
Transduction (biophysics)
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