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      Characterization of noncoding regulatory DNA in the human genome

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      Journal: Nature Biotechnology
      Publisher: Springer Nature

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          Abstract

          Genome-wide mapping of regulatory elements will improve our understanding of how genetic variation in the noncoding genome affects disease phenotypes.

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          Most cited references62

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          Genome-wide association studies for complex traits: consensus, uncertainty and challenges.

          Mark McCarthy, Gonçalo R Abecasis, Lon Cardon … (2008)
          The past year has witnessed substantial advances in understanding the genetic basis of many common phenotypes of biomedical importance. These advances have been the result of systematic, well-powered, genome-wide surveys exploring the relationships between common sequence variation and disease predisposition. This approach has revealed over 50 disease-susceptibility loci and has provided insights into the allelic architecture of multifactorial traits. At the same time, much has been learned about the successful prosecution of association studies on such a scale. This Review highlights the knowledge gained, defines areas of emerging consensus, and describes the challenges that remain as researchers seek to obtain more complete descriptions of the susceptibility architecture of biomedical traits of interest and to translate the information gathered into improvements in clinical management.
          Article 0 comments Cited 812 times – based on 0 reviews     Review now
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            Efficient design and assembly of custom TALEN and other TAL effector-based constructs for DNA targeting

            Tomas Cermak, Erin L. Doyle, Michelle Christian … (2011)
            TALENs are important new tools for genome engineering. Fusions of transcription activator-like (TAL) effectors of plant pathogenic Xanthomonas spp. to the FokI nuclease, TALENs bind and cleave DNA in pairs. Binding specificity is determined by customizable arrays of polymorphic amino acid repeats in the TAL effectors. We present a method and reagents for efficiently assembling TALEN constructs with custom repeat arrays. We also describe design guidelines based on naturally occurring TAL effectors and their binding sites. Using software that applies these guidelines, in nine genes from plants, animals and protists, we found candidate cleavage sites on average every 35 bp. Each of 15 sites selected from this set was cleaved in a yeast-based assay with TALEN pairs constructed with our reagents. We used two of the TALEN pairs to mutate HPRT1 in human cells and ADH1 in Arabidopsis thaliana protoplasts. Our reagents include a plasmid construct for making custom TAL effectors and one for TAL effector fusions to additional proteins of interest. Using the former, we constructed de novo a functional analog of AvrHah1 of Xanthomonas gardneri. The complete plasmid set is available through the non-profit repository AddGene and a web-based version of our software is freely accessible online.
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              A TALE nuclease architecture for efficient genome editing.

              Jeffrey Miller, Siyuan Tan, Guijuan Qiao … (2011)
              Nucleases that cleave unique genomic sequences in living cells can be used for targeted gene editing and mutagenesis. Here we develop a strategy for generating such reagents based on transcription activator-like effector (TALE) proteins from Xanthomonas. We identify TALE truncation variants that efficiently cleave DNA when linked to the catalytic domain of FokI and use these nucleases to generate discrete edits or small deletions within endogenous human NTF3 and CCR5 genes at efficiencies of up to 25%. We further show that designed TALEs can regulate endogenous mammalian genes. These studies demonstrate the effective application of designed TALE transcription factors and nucleases for the targeted regulation and modification of endogenous genes.
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                Author and article information

                Journal
                Title: Nature Biotechnology
                Abbreviated Title: Nat Biotechnol
                Publisher: Springer Nature
                ISSN (Print): 1087-0156
                ISSN (Electronic): 1546-1696
                Publication date Created: August 8 2017
                Publication date (Print): August 8 2017
                Volume: 35
                Issue: 8
                Pages: 732-746
                Article
                DOI: 10.1038/nbt.3863
                PubMed ID: 28787426
                SO-VID: df408c45-ab08-4a57-a6cb-be369c6a533e
                Copyright © © 2017
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