PubMed HealthSearch

PubMed · 6344023

Search algorithm for pattern match analysis of nucleic acid sequences.

Abstract

A new type of search algorithm to find biological information inherited in nucleic acid sequences was developed. The algorithm is of pattern match type and is based on the fact that genetic information often is a function of a predictable statistical occurrence of the four bases within parts of the sequence. The search algorithm compares the known statistical pattern of bases in e.g. a promoter, with an unknown sequence and calculates the statistical significance of the match at all positions in the unknown sequence. The program was tested on 54 published prokaryotic promoters. 44 or 49 could be found with 1 or 4 false answers, respectively. The program was also used on plasmid pBR322. All promoters functioning in an in vitro transcription system were found (tet, anti-tet, p4, bla and ori) except the so called p5 promoter. A search for donor and acceptor sites was performed in a human HLA genomic sequence that contains six introns. Five of the possible six donor and acceptor sites were found.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R Harr, M Häggström, P Gustafsson. 1983-05-11. Search algorithm for pattern match analysis of nucleic acid sequences.. https://doi.org/10.1093/nar%2F11.9.2943

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

miR-503-3p promotes epithelial-mesenchymal transition in breast cancer by directly targeting SMAD2 and E-cadherin.

Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of miR-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined. Here, we found that miR-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified miR-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of miR-503-3p in breast cancer cells inhibited expression of epithelial-mesenchymal transition (EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their mRNA 3' untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer.

Base Sequence

Identification and characterization of Prp45p and Prp46p, essential pre-mRNA splicing factors.

Through exhaustive two-hybrid screens using a budding yeast genomic library, and starting with the splicing factor and DEAH-box RNA helicase Prp22p as bait, we identified yeast Prp45p and Prp46p. We show that as well as interacting in two-hybrid screens, Prp45p and Prp46p interact with each other in vitro. We demonstrate that Prp45p and Prp46p are spliceosome associated throughout the splicing process and both are essential for pre-mRNA splicing. Under nonsplicing conditions they also associate in coprecipitation assays with low levels of the U2, U5, and U6 snRNAs that may indicate their presence in endogenous activated spliceosomes or in a postsplicing snRNP complex.

Base Sequence

Rap1p is a negative regulator of the RAP1 gene.

The promoter of the RAP1 gene contains four potential binding sites for Rap1p, located between the UAS and the RNA initiation site. We have confirmed that three of these sites are recognised by Rap1p in vitro. Different combinations of the three sites were then mutated to abolish Rap1p binding, and the effect of these mutations on promoter activity was determined. When all three Rap1p sites were mutated, the activity of the promoter increased by about 130%, indicating that at least one of the sites is a negative element. Analysis of promoters with different combinations of the mutant sites revealed that the 5'-most site (A) is the principal target for repression. To test the involvement of Rap1p in controlling RAP1 expression, we have measured transcription of the chromosomal RAP1 gene in a RAP1 wild-type strain and two strains containing rap1ts mutations. At a semi-permissive temperature, the RAP1 promoter was more active in the rap1ts strains than in the RAP1 wild-type strain, suggesting that expression of the chromosomal RAP1 gene is greater when the activity of Rap1p in the cell is compromised. The activities of the wild-type promoter, and the promoter with mutations in the three Rap1p-binding sites, were compared in sir1, sir2, sir3 and sir4 mutant strains. In each case, the mutated promoter was significantly more active than the wild-type promoter, implying that the repression mechanism is not dependent on any one of the SIR gene products.

Base Sequence