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      6mA-Finder: a novel online tool for predicting DNA N6-methyladenine sites in genomes

      Author(s): 1 , 1 , 1 , 1 , 2 , 3
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      Publication date Created:
      Publication date (Electronic):
      Journal: Bioinformatics
      Publisher: Oxford University Press (OUP)

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          Abstract

          Motivation

          DNA N6-methyladenine (6 mA) has recently been found as an essential epigenetic modification, playing its roles in a variety of cellular processes. The abnormal status of DNA 6 mA modification has been reported in cancer and other disease. The annotation of 6 mA marks in genome is the first crucial step to explore the underlying molecular mechanisms including its regulatory roles.

          Results

          We present a novel online DNA 6 mA site tool, 6 mA-Finder, by incorporating seven sequence-derived information and three physicochemical-based features through recursive feature elimination strategy. Our multiple cross-validations indicate the promising accuracy and robustness of our model. 6 mA-Finder outperforms its peer tools in general and species-specific 6 mA site prediction, suggesting it can provide a useful resource for further experimental investigation of DNA 6 mA modification.

          Availability and implementation

          https://bioinfo.uth.edu/6mA_Finder.

          Supplementary information

          Supplementary data are available at Bioinformatics online.

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          CD-HIT: accelerated for clustering the next-generation sequencing data

          Limin Fu, Beifang Niu, Zhengwei Zhu … (2012)
          Summary: CD-HIT is a widely used program for clustering biological sequences to reduce sequence redundancy and improve the performance of other sequence analyses. In response to the rapid increase in the amount of sequencing data produced by the next-generation sequencing technologies, we have developed a new CD-HIT program accelerated with a novel parallelization strategy and some other techniques to allow efficient clustering of such datasets. Our tests demonstrated very good speedup derived from the parallelization for up to ∼24 cores and a quasi-linear speedup for up to ∼8 cores. The enhanced CD-HIT is capable of handling very large datasets in much shorter time than previous versions. Availability: http://cd-hit.org. Contact: liwz@sdsc.edu Supplementary information: Supplementary data are available at Bioinformatics online.
          Article 0 comments Cited 2260 times – based on 0 reviews     Review now
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            N 6 -Methyladenine DNA Modification in the Human Genome

            Jinbao Liu, Shang-Qian Xie, Feng Luo … (2018)
            DNA N6-methyladenine (6mA) modification is the most prevalent DNA modification in prokaryotes, but whether it exists in human cells and whether it plays a role in human diseases remain enigmatic. Here, we showed that 6mA is extensively present in the human genome, and we cataloged 881,240 6mA sites accounting for ∼0.051% of the total adenines. [G/C]AGG[C/T] was the most significantly associated motif with 6mA modification. 6mA sites were enriched in the coding regions and mark actively transcribed genes in human cells. DNA 6mA and N6-demethyladenine modification in the human genome were mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The abundance of 6mA was significantly lower in cancers, accompanied by decreased N6AMT1 and increased ALKBH1 levels, and downregulation of 6mA modification levels promoted tumorigenesis. Collectively, our results demonstrate that DNA 6mA modification is extensively present in human cells and the decrease of genomic DNA 6mA promotes human tumorigenesis.
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              DNA Methylation on N6-Adenine in C. elegans.

              Eric Lieberman Greer, Mario Andres Blanco, Lei Gu … (2015)
              In mammalian cells, DNA methylation on the fifth position of cytosine (5mC) plays an important role as an epigenetic mark. However, DNA methylation was considered to be absent in C. elegans because of the lack of detectable 5mC, as well as homologs of the cytosine DNA methyltransferases. Here, using multiple approaches, we demonstrate the presence of adenine N(6)-methylation (6mA) in C. elegans DNA. We further demonstrate that this modification increases trans-generationally in a paradigm of epigenetic inheritance. Importantly, we identify a DNA demethylase, NMAD-1, and a potential DNA methyltransferase, DAMT-1, which regulate 6mA levels and crosstalk between methylations of histone H3K4 and adenines and control the epigenetic inheritance of phenotypes associated with the loss of the H3K4me2 demethylase spr-5. Together, these data identify a DNA modification in C. elegans and raise the exciting possibility that 6mA may be a carrier of heritable epigenetic information in eukaryotes. Copyright © 2015 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Title: Bioinformatics
                Publisher: Oxford University Press (OUP)
                ISSN (Print): 1367-4803
                ISSN (Electronic): 1460-2059
                Publication date Created: May 15 2020
                Publication date Created: May 01 2020
                Publication date Created: February 24 2020
                Publication date Other: May 15 2020
                Publication date (Print): May 01 2020
                Publication date (Electronic): February 24 2020
                Volume: 36
                Issue: 10
                Pages: 3257-3259
                Affiliations
                [1 ]School of Biomedical Informatics, Center for Precision Health
                [2 ]MD Anderson Cancer Center, UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030, USA
                [3 ]Department of Biomedical Informatics, Vanderbilt University Medical Center, Nashville, TN 37203, USA
                Article
                DOI: 10.1093/bioinformatics/btaa113
                PubMed ID: 32091591
                SO-VID: d869ed52-52ae-40dd-b083-607e28a8d933
                Copyright © © 2020
                License:

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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