Regional localisation of tri- and tetranucleotide repeat sequence-containing cosmids on chromosome 13

1995 ◽  
Vol 70 (1-2) ◽  
pp. 102-103
Author(s):  
L.A. Hawthorn ◽  
B. Kapanadse ◽  
N. Yankovsky ◽  
J.K. Cowell
2000 ◽  
Vol 38 (4) ◽  
pp. 1516-1519 ◽  
Author(s):  
D. M. Adair ◽  
P. L. Worsham ◽  
K. K. Hill ◽  
A. M. Klevytska ◽  
P. J. Jackson ◽  
...  

We have identified a tetranucleotide repeat sequence, (CAAA)N, in the genome of Yersinia pestis, the causative agent of plague. This variable-number tandem repeat (VNTR) region has nine alleles and great diversity (calculated as 1 minus the sum of the squared allele frequencies) (diversity value, 0.82) within a set of 35 diverse Y. pestis strains. In contrast, the nucleotide sequence of the lcrV (low-calcium-response) gene differed only slightly among these strains, having a haplotype diversity value of 0.17. Replicated cultures, phenotypic variants of particular strains, and extensively cultured replicates within strains did not differ in VNTR allele type. Thus, while a high mutation rate must contribute to the great diversity of this locus, alleles appear stable under routine laboratory culture conditions. The classic three plague biovars did not have single identifying alleles, although there were allelic biases within biovar categories. The antiqua biovar was the most diverse, with four alleles observed in 5 strains, while the orientalis and mediaevalis biovars exhibited five alleles in 21 strains and three alleles in 8 strains, respectively. The CAAA VNTR is located immediately adjacent to the transcriptional promoters for flanking open reading frames and may affect their activity. This VNTR marker may provide a high-resolution tool for epidemiological analyses of plague.


1994 ◽  
Vol 71 (06) ◽  
pp. 731-736 ◽  
Author(s):  
M W Mansfield ◽  
M H Stickland ◽  
A M Carter ◽  
P J Grant

SummaryTo identify whether genotype contributes to the difference in PAI-1 levels in type 1 and type 2 diabetic subjects and whether genotype relates to the development of retinopathy, a Hind III restriction fragment length polymorphism and two dinucleotide repeat polymorphisms were studied. In 519 Caucasian diabetic subjects (192 type 1, 327 type 2) and 123 Caucasian control subjects there were no differences in the frequency of the Hind III restriction alleles (type 1 vs type 2 vs control: allele 1 0.397 vs 0.420 vs 0.448; allele 2 0.603 vs 0.580 vs 0.552) nor in the allelic frequency at either dinucleotide repeat sequence. In 86 subjects with no retinopathy at 15 years or more from diagnosis of diabetes and 190 subjects with diabetic retinopathy there was no difference in the frequency of Hind III restriction alleles (retinopathy present vs retinopathy absent: allele 1 0.400 vs 0.467; allele 2 0.600 vs 0.533) nor in the allelic frequencies at either dinucleotide repeat sequence. The results indicate that there is no or minimal influence of the PAI-1 gene on either PAI-1 levels or the development of diabetic retinopathy in patients with diabetes mellitus.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Narumol Bhummaphan ◽  
Piyapat Pin-on ◽  
Preeyaporn Plaimee Phiboonchaiyanan ◽  
Jirattha Siriluksana ◽  
Chatchawit Aporntewan ◽  
...  

Abstract Background Intratumour heterogeneous gene expression among cancer and cancer stem cells (CSCs) can cause failure of current targeted therapies because each drug aims to target the function of a single gene. Long mononucleotide A-T repeats are cis-regulatory transcriptional elements that control many genes, increasing the expression of numerous genes in various cancers, including lung cancer. Therefore, targeting A-T repeats may dysregulate many genes driving cancer development. Here, we tested a peptide nucleic acid (PNA) oligo containing a long A-repeat sequence [A(15)] to disrupt the transcriptional control of the A-T repeat in lung cancer and CSCs. Methods First, we separated CSCs from parental lung cancer cell lines. Then, we evaluated the role of A-T repeat gene regulation by counting the number of repeats in differentially regulated genes between CSCs and the parental cells of the CSCs. After testing the dosage and effect of PNA-A15 on normal and cancer cell toxicity and CSC phenotypes, we analysed genome-wide expression to identify dysregulated genes in CSCs. Results The number of A-T repeats in genes differentially regulated between CSCs and parental cells differed. PNA-A15 was toxic to lung cancer cells and CSCs but not to noncancer cells. Finally, PNA-A15 dysregulated a number of genes in lung CSCs. Conclusion PNA-A15 is a promising novel targeted therapy agent that targets the transcriptional control activity of multiple genes in lung CSCs.


Genetics ◽  
2002 ◽  
Vol 161 (3) ◽  
pp. 1065-1075
Author(s):  
David K Butler ◽  
David Gillespie ◽  
Brandi Steele

Abstract Large DNA palindromes form sporadically in many eukaryotic and prokaryotic genomes and are often associated with amplified genes. The presence of a short inverted repeat sequence near a DNA double-strand break has been implicated in the formation of large palindromes in a variety of organisms. Previously we have established that in Saccharomyces cerevisae a linear DNA palindrome is efficiently formed from a single-copy circular plasmid when a DNA double-strand break is introduced next to a short inverted repeat sequence. In this study we address whether the linear palindromes form by an intermolecular reaction (that is, a reaction between two identical fragments in a head-to-head arrangement) or by an unusual intramolecular reaction, as it apparently does in other examples of palindrome formation. Our evidence supports a model in which palindromes are primarily formed by an intermolecular reaction involving homologous recombination of short inverted repeat sequences. We have also extended our investigation into the requirement for DNA double-strand break repair genes in palindrome formation. We have found that a deletion of the RAD52 gene significantly reduces palindrome formation by intermolecular recombination and that deletions of two other genes in the RAD52-epistasis group (RAD51 and MRE11) have little or no effect on palindrome formation. In addition, palindrome formation is dramatically reduced by a deletion of the nucleotide excision repair gene RAD1.


2021 ◽  
Vol 60 (4) ◽  
pp. 771-774
Author(s):  
Chih-Ping Chen ◽  
Chen-Yu Chen ◽  
Schu-Rern Chern ◽  
Shin-Wen Chen ◽  
Fang-Tzu Wu ◽  
...  

2009 ◽  
Vol 62 (10) ◽  
pp. 1339 ◽  
Author(s):  
Candy K. Y. Chun ◽  
Richard J. Payne

Several dendrimers possessing multiple copies of peptides and glycopeptides belonging to the MUC1 eicosapeptide tandem repeat sequence have been prepared. Fmoc-strategy solid-phase peptide synthesis was used to construct the peptides and glycopeptides, which were conjugated to suitably functionalized dendrimer cores using the copper-catalyzed azide-alkyne cycloaddition reaction to produce multivalent peptide and glycopeptide dendrimers.


Hereditas ◽  
2004 ◽  
Vol 119 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Renuka Chaudhary ◽  
Bhanu P. Chowdhary ◽  
Ingrid Harbitz ◽  
Ingemar Gustavsson

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