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For the last decade, the Burgess lab has focused on developing technologies to systematically annotate the functions for all the genes in a vertebrate genome. After completion of the human genome sequence, approximately 70 percent of the protein-coding genes could be assigned a putative function based on at least one identified Pfam domain. However, for the vast majority of these genes, assigned functions are inferred and their true in vivo functions have never been directly tested. Because the genomes of the vertebrate model organisms mouse (Mus musculus) and zebrafish (Danio rerio) have also been sequenced, they offer the opportunity to test the function of every vertebrate gene, and by extension, the function of their human homologs.
In previous work, Dr. Burgess participated in a large-scale genetic screen for embryonic lethal phenotypes in the zebrafish. This effort used proviral insertions as the mutagen, allowing for rapid cloning of the mutated gene. To date, this effort represents the largest number of mutations identified, phenotyped, and cloned from a vertebrate genetic screen (Golling et al., Nat Gen 2002). Upon his arrival at NHGRI, Dr. Burgess' Developmental Genomics Section (DGS) simultaneously began both characterizing in detail a number of mutants causing developmental defects in the zebrafish inner ear, and preparing the groundwork for a more systematic approach to mutating and phenotyping all zebrafish genes. The Burgess group developed new techniques for high-throughput identification of retroviral integration sites, and rapidly identified proviral insertion sites as a first step in developing a pipeline to mutate all the genes in the zebrafish genome. They then successfully mutagenized zebrafish embryos, mapped thousands of insertion sites and created a large pool of mutant zebrafish lines (Wang et al., PNAS 2007, Varshney et al., Genome Res, 2014). Using this approach, the DGS generated mutations in over 5,000 zebrafish genes, or approximately 25% of the total genes in the zebrafish genome. Dr. Burgess has arranged for the Zebrafish International Stock Center (ZIRC) to distribute these mutants to the research community, essentially free of charge.
In previous work, Dr. Burgess participated in a large-scale genetic screen for embryonic lethal phenotypes in the zebrafish. This effort used proviral insertions as the mutagen, allowing for rapid cloning of the mutated gene. To date, this effort represents the largest number of mutations identified, phenotyped, and cloned from a vertebrate genetic screen (Golling et al., Nat Gen 2002). Upon his arrival at NHGRI, Dr. Burgess' Developmental Genomics Section (DGS) simultaneously began both characterizing in detail a number of mutants causing developmental defects in the zebrafish inner ear, and preparing the groundwork for a more systematic approach to mutating and phenotyping all zebrafish genes. The Burgess group developed new techniques for high-throughput identification of retroviral integration sites, and rapidly identified proviral insertion sites as a first step in developing a pipeline to mutate all the genes in the zebrafish genome. They then successfully mutagenized zebrafish embryos, mapped thousands of insertion sites and created a large pool of mutant zebrafish lines (Wang et al., PNAS 2007, Varshney et al., Genome Res, 2014). Using this approach, the DGS generated mutations in over 5,000 zebrafish genes, or approximately 25% of the total genes in the zebrafish genome. Dr. Burgess has arranged for the Zebrafish International Stock Center (ZIRC) to distribute these mutants to the research community, essentially free of charge.
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Molecular Neurobiologyno. 3 (2024): 1753-1768
Nature Communicationsno. 1 (2023)
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Nature Communicationsno. 1 (2023): 1-13
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Erika Fodor,Javan Okendo,Nóra Szabó, Kata Szabó,Dávid Czimer, Anita Tarján-Rácz, Ildikó Szeverényi,Bi Wei Low,Jia Huan Liew,Sergey Koren,Arang Rhie,László Orbán,
bioRxiv : the preprint server for biology (2023)
Tetsuo Kon,Kentaro Fukuta,Zelin Chen,Koto Kon-Nanjo, Kota Suzuki, Masakazu Ishikawa, Hikari Tanaka,Shawn M. Burgess,Hideki Noguchi,Atsushi Toyoda,Yoshihiro Omori
Judith Habicher,Gaurav K. Varshney,Laura Waldmann,Daniel Snitting,Amin Allalou,Hanqing Zhang, Abdurrahman Ghanem, Caroline Öhman Mägi,Tabea Dierker,Lena Kjellén,Shawn M. Burgess,Johan Ledin
PLOS Geneticsno. 2 (2022): e1010067-e1010067
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