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Wu, Jingyi

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Wu

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Jingyi

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Wu, Jingyi

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2020 - 20213

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Author's Publications: search.filters.isAuthorOfPublication.6e56c594-778c-4777-99d5-4dfc54a58a74

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    The landscape of RNA Pol II binding reveals a stepwise transition during ZGA
    (Springer Science and Business Media LLC, 2020-10-28) Liu, Bofeng; Xu, Qianhua; Wang, Qiujun; Feng, Su; Lai, Fangnong; Wang, Peizhe; Zheng, Fangyuan; Xiang, Yunlong; Wu, Jingyi; Nie, Junwei; Qiu, Cui; Xia, Weikun; Li, Lijia; Yu, Guang; Lin, Zili; Xu, Kai; Xiong, Zhuqing; Kong, Feng; Liu, Ling; Huang, Chunyi; Yu, Yang; Na, Jie; Xie, Wei
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    A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors
    (Springer Science and Business Media LLC, 2020-05-01) Slyper, Michal; Porter, Caroline; Ashenberg, Orr; Waldman, Julia; Drokhlyansky, Eugene; Wakiro, Isaac; Smilie, Christopher; Smith-Rosario, Gabriela; Wu, Jingyi; Dionne, Danielle; Vigneau, Sebastien; Jane-Valbuena, Judit; Tickle, Timothy; Napolitano, Sara; Su, Mei-Ju; Patel, Anand; Karlstrom, Asa; Gristch, Simon; Nomura, Masashi; Waghray, Avinash; Gohil, Satyen; Tsankov, Alexander; Jerby-Arnon, Livnat; Cohen, Ofir; Klughammer, Johanna; Rosen, Yanay; Gould, Joshua; Nguyen, Lan; Hofree, Matan; Tramontozzi, Peter; Levy, Rachel; Li, Bo; Wu, Catherine; Izar, Benjamin; Haq, Rizwan; Hodi, Stephen; Yoon, Charles; Hata, Aaron; Baker, Suzanne; Suva, Mario; Bueno, Raphael; Stover, Elizabeth; Clay, Michael; Dyer, M Aiven; Collins, Natalie; Matulonis, Ursula; Wagle, Nikhil; Johnson, Bruce; Rotem, Asaf; Rozenblatt-Rosen, Orit; Regev, Aviv
    Single-cell genomics is essential to chart tumor ecosystems. Although single-cell RNA-Seq (scRNA-Seq) profiles RNA from cells dissociated from fresh tumors, single-nucleus RNA-Seq (snRNA-Seq) is needed to profile frozen or hard-to-dissociate tumors. Each requires customization to different tissue and tumor types, posing a barrier to adoption. Here, we have developed a systematic toolbox for profiling fresh and frozen clinical tumor samples using scRNA-Seq and snRNA-Seq, respectively. We analyzed 216,490 cells and nuclei from 40 samples across 23 specimens spanning eight tumor types of varying tissue and sample characteristics. We evaluated protocols by cell and nucleus quality, recovery rate and cellular composition. scRNA-Seq and snRNA-Seq from matched samples recovered the same cell types, but at different proportions. Our work provides guidance for studies in a broad range of tumors, including criteria for testing and selecting methods from the toolbox for other tumors, thus paving the way for charting tumor atlases.
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    Publication
    Epigenetic silencing by SETDB1 suppresses tumour intrinsic immunogenicity
    (Springer Science and Business Media LLC, 2021-05-05) Griffin, Gabriel; Wu, Jingyi; Iracheta-Vellve, Arvin; Patti, James C.; Hsu, Jeffrey; Davis, Thomas; Dele-Oni, Deborah; Du, Peter P.; Halawi, Aya G.; Ishizuka, Jeffrey J.; Kim, Sarah Y.; Klaeger, Susan; Knudsen, Nelson H.; Miller, Brian C.; Nguyen, Tung H.; Olander, Kira E.; Papanastasiou, Malvina; Rachimi, Suzanna; Robitschek, Emily J.; Schneider, Emily; Yeary, Mitchell D.; Zimmer, Margaret; Jaffe, Jacob D.; Carr, Steven A.; Doench, John G.; Haining, William; Yates, Kathleen; Manguso, Robert T.; Bernstein, Bradley
    Epigenetic dysregulation is a defining feature of tumorigenesis that has been implicated in immune escape1,2. To identify epigenetic factors that modulate the immune sensitivity of cancer cells, we performed in vivo CRISPR-Cas9 screens targeting 936 chromatin regulators in mouse tumor models treated with immune checkpoint blockade (ICB). We identified the H3K9-methyltransferase SETDB1 and other members of the HUSH and KAP1 complexes as mediators of immune escape in tumor cells3–5. We also found that amplification of SETDB1 (1q21.3) in human tumors is associated with immune exclusion and resistance to ICB. SETDB1 represses broad genomic domains, many of which reside within the open genome compartment. These domains are enriched for transposable elements (TEs) and immune gene clusters associated with segmental duplication events, a central mechanism of genome evolution6. SETDB1 loss derepresses latent TE-derived regulatory elements, immunostimulatory genes, and TE-encoded retroviral antigens in these regions, and triggers TE-specific cytotoxic T-cell responses in vivo. Our study establishes SETDB1 as an epigenetic checkpoint that suppresses tumor cell immunogenicity by silencing TEs and evolving genomic loci, and thus represents a candidate target for immunotherapy.