High Throughput Next Generation Sequencing: supports genomics and epigenomics research in muscle, skin, bone and autoimmune diseases.

基因组技术部门积极参与了NIAMS的大量研究项目，包括： -分析 T 淋巴细胞的基因组组织，以了解 T 辅助细胞命运规范和功能的基因调控机制。 ATAC-seq、RNA-Seq 和 ChIP-Seq 已用于绘制染色质状态、染色质可及性和转录组图谱，揭示细胞命运规范和功能的分子机制。 - 研究骨唾液蛋白 (BSP) 的特定区域，以确定 BSP 分子的特定区域，通过与整合素相互作用，促进牙根形成，并在牙骨质形成过程中调节矿物质形成。 - UBA1 体细胞突变和严重成人发病自身炎症性疾病的研究 - 使用不同测序技术（ChIP-Seq、mRNA-seq、全基因组甲基-seq、4C、Hi-C）比较组蛋白标记、核小体结合、转录因子结合、DNA（去）甲基化和 3-D 核结构，观察 B 细胞细胞激活期间观察到的表观遗传特征变化的动态及其对细胞激活的影响。 - RNA 结合蛋白 (RBP) 对转录后基因调控 (PTGR) 的影响。 - 选定的 RBP 对翻译起始和延伸的影响。 - 在稳态和炎症期间皮肤、微生物群和常驻白细胞之间发生的相互串扰。 - 皮肤细胞谱系的规范和维护，以及皮肤干细胞调节的研究。 - 了解染色质调节因子（例如 Polycomb 蛋白、转录因子 Pst1、Ago2 和 eRNA）在肌肉分化过程中调节基因表达的活性。 - 发现骨骼肌细胞规范、分化和再生过程中调节代谢和表观遗传学的分子机制。 - 转录组、表观遗传学和功能分析表明中性粒细胞多样性与系统性红斑狼疮的发病机制有关。 - 先天淋巴细胞对皮脂腺的稳态控制调节共生细菌平衡。 -通过 ATAC-seq 分析静态和分化肌肉干细胞（卫星细胞）的染色质可及性和基因组组织。 - 几种人类和小鼠疾病模型中的单细胞转录组分析以及分化/细胞命运规范。 -了解皮肤微生物组在湿疹性皮肤病（包括特应性皮炎）中的作用。 -中性粒细胞生物学中的性别差异调节对 I 型干扰素和免疫代谢的反应。 -MicroRNA-221和-222作为IL-23下游的负反馈调节剂调节肠道炎症Th17细胞反应。 -快速增强子重塑和转录因子重新利用可在 NK 细胞急性激活时实现高强度基因诱导。 -从稀有肌肉干细胞群或有限数量的小鼠胚胎干细胞开始制备RNA-seq文库的方案。 -FoxO 保持真正的肌肉干细胞静止状态直至老年。 -CTCF 协调长程粘连蛋白驱动的 V(D)J 重组扫描。 -来自骆驼科动物小鼠和美洲驼的纳米抗体可中和 SARS-CoV-2 变体 -非放射性、改进的 PAR-CLIP 和小 RNA cDNA 文库制备方案。 -RNA结合基序蛋白4、RBM4对人内源性逆转录病毒的转录后调控 -DLX3肿瘤抑制功能的丧失通过EGFRERBB2途径促进鳞状细胞癌的进展

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. - Study of somatic mutations in UBA1 and severe adult-onset Autoinflammarory Disease - 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 occurs between the skin, the microbiota and resident leukocytes during steady-state and inflammation. - Specification and maintenance of cell lineages in the skin, and 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. - Transcriptomic, epigenetic, and functional analyses implicate neutrophil diversity in the pathogenesis of systemic lupus erythematosus. - Homeostatic Control of Sebaceous Glands by Innate Lymphoid Cells Regulates Commensal Bacteria Equilibrium. -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. -Understanding the roll of cutaneous microbiome in eczematous skin diseases, including atopic dermatitis. -Sex differences in neutrophil biology modulate response to type I interferons and immunometabolism. -MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of interleukin-23. -Rapid Enhancer Remodeling and Transcription Factor Repurposing Enable High Magnitude Gene Induction upon Acute Activation of NK Cells. -Protocol for RNA-seq library preparation starting from a rare muscle stem cell population or a limited number of mouse embryonic stem cells. -FoxO maintains a genuine muscle stem-cell quiescent state until geriatric age. -CTCF orchestrates long-range cohesin-driven V(D)J recombinational scanning. -Nanobodies from camelid mice and llamas neutralize SARS-CoV-2 variants -A non-radioactive, improved PAR-CLIP and small RNA cDNA library preparation protocol. -Posttranscriptional regulation of human endogenous retroviruses by RNA-binding motif protein 4, RBM4 -Loss of DLX3 tumor suppressive function promotes progression of SCC through EGFRERBB2 pathway