The Genome Technology Unit has been actively involved in a large number of NIAMS research projects, including: -Analysis of genomic organization of T lymphocytes to understand gene regulatory mechanisms for T helper cell fate specification and function. ATAC-seq, RNA-Seq and ChIP-Seq have been used to draw maps of chromatin states, chromatin accessibility and transcriptome revealing molecular mechanism for cell fate specification and function. - Study of specific regions of the bone sialoprotein (BSP) to determine specific regions of the BSP molecule responsible for promoting tooth root formation, through interacting with integrins, and regulating mineral formation during cementogenesis. - Identification of novel pathophysiologic pathways involved in myositis by comparing the transcriptomes of muscle biopsies from myositis patients with defined myositis autoantibodies. - Dynamic of changes in the epigenetic features observed during cellular activation of B-cells and its impacts on cellular activation by comparison of histone marks, nucleosome binding, transcription factor binding, DNA (de)methylation and 3-D nuclear structure using different sequencing technologies (ChIP-Seq, mRNA-seq, whole genome methyl-seq, 4C, Hi-C). - impact of RNA binding proteins (RBPs) on posttranscriptional gene regulation (PTGR) - Impact of select RBPs on translation initiation and elongation. - Mutual crosstalk that occur between the skin, the microbiota and resident leukocytes during steady-state and inflammation - Specification and maintenance of cell lineages in the skin, study of the regulation of stem cells in the skin. - Understanding the activity of chromatin regulators such as Polycomb proteins, the transcription factor Pst1, Ago2 and eRNAs in regulating gene expression during muscle differentiation. - Discovering the molecular mechanisms regulating metabolism and epigenetics during specification, differentiation, and regeneration of skeletal muscle cells. -Analysis of chromatin accessibility and genomic organization of quiescent and differentiating muscle stem cells (satellite cells) by ATAC-seq. - Analysis of single cell transcriptome in several human and mouse models of disease and differentiation/cell fate specification

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Support Year
3
Fiscal Year
2018
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Indirect Cost
Name
Arthritis, Musculoskeletal, Skin Dis
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Puchner, Antonia; Saferding, Victoria; Bonelli, Michael et al. (2018) Non-classical monocytes as mediators of tissue destruction in arthritis. Ann Rheum Dis 77:1490-1497
Carlucci, Philip M; Purmalek, Monica M; Dey, Amit K et al. (2018) Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus. JCI Insight 3:
Mikami, Yohei; Scarno, Gianluca; Zitti, Beatrice et al. (2018) NCR+ ILC3 maintain larger STAT4 reservoir via T-BET to regulate type 1 features upon IL-23 stimulation in mice. Eur J Immunol 48:1174-1180
Feng, Xuesong; Naz, Faiza; Juan, Aster H et al. (2018) Identification of Skeletal Muscle Satellite Cells by Immunofluorescence with Pax7 and Laminin Antibodies. J Vis Exp :
Giannelou, Angeliki; Wang, Hongying; Zhou, Qing et al. (2018) Aberrant tRNA processing causes an autoinflammatory syndrome responsive to TNF inhibitors. Ann Rheum Dis 77:612-619
Linehan, Jonathan L; Harrison, Oliver J; Han, Seong-Ji et al. (2018) Non-classical Immunity Controls Microbiota Impact on Skin Immunity and Tissue Repair. Cell 172:784-796.e18
Tsai, Pei-Fang; Dell'Orso, Stefania; Rodriguez, Joseph et al. (2018) A Muscle-Specific Enhancer RNA Mediates Cohesin Recruitment and Regulates Transcription In trans. Mol Cell 71:129-141.e8
Juan, Aster H; Wang, Stan; Ko, Kyung Dae et al. (2017) Roles of H3K27me2 and H3K27me3 Examined during Fate Specification of Embryonic Stem Cells. Cell Rep 18:297
Mowel, Walter K; McCright, Sam J; Kotzin, Jonathan J et al. (2017) Group 1 Innate Lymphoid Cell Lineage Identity Is Determined by a cis-Regulatory Element Marked by a Long Non-coding RNA. Immunity 47:435-449.e8
Afzali, Behdad; Grönholm, Juha; Vandrovcova, Jana et al. (2017) BACH2 immunodeficiency illustrates an association between super-enhancers and haploinsufficiency. Nat Immunol 18:813-823

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