The broad goal of the Computational Biology Core (Core C) is to support each of the Program Projects by providing computational support for the high-throughput genomic methods required by the Program. Specifically, the Core will focus on 3 main areas of support: data tracking/management/distribution, high- throughput sequencing analysis, and functional characterization of genes/motifs. Importantly, all Projects will generate significant amounts of genome-scale data, including the recombination and double stranded break (DSB) maps of Project A Paigen, the PRDMS-ChlP-seq and Affinity-seq of Project B Petkov, and the RNA- seq and H3K4me3-ChlP-seq of Projects C Hibbs and D Handel. The analysis of these diverse and voluminous data requires sophisticated techniques for data processing and analysis that the individual projects cannot provide. The ability of each project and of the overall Program to achieve our goals relies on accurate and reliable data management and analyses, which the Core will provide by accomplishing 3 specific aims: 1) The Core will manage the faithful tracking of information from mouse through final genomic data point by utilizing JAX's Laboratory Information Management System (LIMS). 2) The Core will provide high-quality analysis of high-throughput sequencing (HTS) data by applying cutting-edge analysis methods. 3) The Core will facilitate biological interpretation of analysis results by providing Project Leaders with functional enrichment and motif analyses of their genomic data. All of these analyses will be delivered in a timely manner by coordinating with the other Program Cores and JAX's Gene Expression Service, which provides facilities and expertise in support of high-throughput sequencing and gene expression studies. Core C will be under the direction of Dr. Matthew Hibbs, who holds bachelors and doctoral degrees in Computer Science and is well qualified to direct these computational tasks.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Program Projects (P01)
Project #
5P01GM099640-02
Application #
8723855
Study Section
Special Emphasis Panel (ZRG1-GGG-F)
Project Start
Project End
Budget Start
2014-08-01
Budget End
2015-07-31
Support Year
2
Fiscal Year
2014
Total Cost
$215,745
Indirect Cost
$92,462
Name
Jackson Laboratory
Department
Type
DUNS #
042140483
City
Bar Harbor
State
ME
Country
United States
Zip Code
04609
Paigen, Kenneth; Petkov, Petko M (2018) PRDM9 and Its Role in Genetic Recombination. Trends Genet 34:291-300
Powers, Natalie R; Parvanov, Emil D; Baker, Christopher L et al. (2016) The Meiotic Recombination Activator PRDM9 Trimethylates Both H3K36 and H3K4 at Recombination Hotspots In Vivo. PLoS Genet 12:e1006146
Ball, Robyn L; Fujiwara, Yasuhiro; Sun, Fengyun et al. (2016) Regulatory complexity revealed by integrated cytological and RNA-seq analyses of meiotic substages in mouse spermatocytes. BMC Genomics 17:628
Narasimhan, Vagheesh M; Hunt, Karen A; Mason, Dan et al. (2016) Health and population effects of rare gene knockouts in adult humans with related parents. Science 352:474-7
Huang, Fang; Sirinakis, George; Allgeyer, Edward S et al. (2016) Ultra-High Resolution 3D Imaging of Whole Cells. Cell 166:1028-1040
Walker, Michael; Billings, Timothy; Baker, Christopher L et al. (2015) Affinity-seq detects genome-wide PRDM9 binding sites and reveals the impact of prior chromatin modifications on mammalian recombination hotspot usage. Epigenetics Chromatin 8:31
Didion, John P; Morgan, Andrew P; Clayshulte, Amelia M-F et al. (2015) A multi-megabase copy number gain causes maternal transmission ratio distortion on mouse chromosome 2. PLoS Genet 11:e1004850
Baker, Christopher L; Petkova, Pavlina; Walker, Michael et al. (2015) Multimer Formation Explains Allelic Suppression of PRDM9 Recombination Hotspots. PLoS Genet 11:e1005512
Sun, Fengyun; Fujiwara, Yasuhiro; Reinholdt, Laura G et al. (2015) Nuclear localization of PRDM9 and its role in meiotic chromatin modifications and homologous synapsis. Chromosoma 124:397-415
Baker, Christopher L; Kajita, Shimpei; Walker, Michael et al. (2015) PRDM9 drives evolutionary erosion of hotspots in Mus musculus through haplotype-specific initiation of meiotic recombination. PLoS Genet 11:e1004916

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