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Precise Manipulation of Chromosomes in Vivo Enables Genome-Wide Codon Replacement
Isaacs, Farren J.,Carr, Peter A.,Wang, Harris H.,Lajoie, Marc J.,Sterling, Bram,Kraal, Laurens,Tolonen, Andrew C.,Gianoulis, Tara A.,Goodman, Daniel B.,Reppas, Nikos B.,Emig, Christopher J.,Bang, Duhe American Association for the Advancement of Scienc 2011 Science Vol.333 No.6040
<P>We present genome engineering technologies that are capable of fundamentally reengineering genomes from the nucleotide to the megabase scale. We used multiplex automated genome engineering (MAGE) to site-specifically replace all 314 TAG stop codons with synonymous TAA codons in parallel across 32 Escherichia coli strains. This approach allowed us to measure individual recombination frequencies, confirm viability for each modification, and identify associated phenotypes. We developed hierarchical conjugative assembly genome engineering (CAGE) to merge these sets of codon modifications into genomes with 80 precise changes, which demonstrate that these synonymous codon substitutions can be combined into higher-order strains without synthetic lethal effects. Our methods treat the chromosome as both an editable and an evolvable template, permitting the exploration of vast genetic landscapes.</P>
The Somatic Genomic Landscape of Chromophobe Renal Cell Carcinoma
The Cancer Genome Atlas Research Network,Davis, Caleb F.,Ricketts, C.J.,Wang, M.,Yang, L.,Cherniack, Andrew D.,Shen, H.,Buhay, C.,Kang, H.,Kim, S.,Fahey, Catherine C.,Hacker, Kathryn E.,Bhanot, G.,Gor Cell Press 2014 Cancer Cell Vol.26 No.3
We describe the landscape of somatic genomic alterations of 66 chromophobe renal cell carcinomas (ChRCCs) on the basis of multidimensional and comprehensive characterization, including mtDNA and whole-genome sequencing. The result is consistent that ChRCC originates from the distal nephron compared with other kidney cancers with more proximal origins. Combined mtDNA and gene expression analysis implicates changes in mitochondrial function as a component of the disease biology, while suggesting alternative roles for mtDNA mutations in cancers relying on oxidative phosphorylation. Genomic rearrangements lead to recurrent structural breakpoints within TERT promoter region, which correlates with highly elevated TERT expression and manifestation of kataegis, representing a mechanism of TERT upregulation in cancer distinct from previously observed amplifications and point mutations.