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3. Expression-Based Cell Lineage Analysis in Drosophila Through a Course-Based Research Experience for Early Undergraduates.

Author

Olson, John M, Evans, Cory J, Ngo, Kathy T, Kim, Hee Jong, Nguyen, Joseph Duy, Gurley, Kayla GH, Ta, Truc, Patel, Vijay, Han, Lisa, Truong-N, Khoa T, Liang, Letty, Chu, Maggie K, Lam, Hiu, Ahn, Hannah G, Banerjee, Abhik Kumar, Choi, In Young, Kelley, Ross G, Moridzadeh, Naseem, Khan, Awais M, Khan, Omair, Lee, Szuyao, Johnson, Elizabeth B, Tigranyan, Annie, Wang, Jay, Gandhi, Anand D, Padhiar, Manish M, Calvopina, Joseph Hargan, Sumra, Kirandeep, Ou, Kristy, Wu, Jessie C, Dickan, Joseph N, Ahmadi, Sabrena M, Allen, Donald N, Mai, Van Thanh, Ansari, Saif, Yeh, George, Yoon, Earl, Gon, Kimberly, Yu, John Y, He, Johnny, Zaretsky, Jesse M, Lee, Noemi E, Kuoy, Edward, Patananan, Alexander N, Sitz, Daniel, Tran, PhuongThao, Do, Minh-Tu, Akhave, Samira J, Alvarez, Silverio D, Asem, Bobby, Asem, Neda, Azarian, Nicole A, Babaesfahani, Arezou, Bahrami, Ahmad, Bhamra, Manjeet, Bhargava, Ragini, Bhatia, Rakesh, Bhatia, Subir, Bumacod, Nicholas, Caine, Jonathan J, Caldwell, Thomas A, Calica, Nicole A, Calonico, Elise M, Chan, Carman, Chan, Helen H-L, Chang, Albert, Chang, Chiaen, Chang, Daniel, Chang, Jennifer S, Charania, Nauman, Chen, Jasmine Y, Chen, Kevin, Chen, Lu, Chen, Yuyu, Cheung, Derek J, Cheung, Jesse J, Chew, Jessica J, Chew, Nicole B, Chien, Cheng-An Tony, Chin, Alana M, Chin, Chee Jia, Cho, Youngho, Chou, Man Ting, Chow, Ke-Huan K, Chu, Carolyn, Chu, Derrick M, Chu, Virginia, Chuang, Katherine, Chugh, Arunit Singh, Cubberly, Mark R, Daniel, Michael Guillermo, Datta, Sangita, Dhaliwal, Raj, Dinh, Jenny, Dixit, Dhaval, Dowling, Emmylou, Feng, Melinda, From, Christopher M, Furukawa, Daisuke, and Gaddipati, Himaja

Subjects
Eye, Brain, Lymphatic System, Animals, Drosophila, Gene Expression, Cell Lineage, Research, Students, Universities, Wings, Animal, CURE, G-TRACE, STEM, education, gene expression, Wings, Animal, Genetics
Abstract

A variety of genetic techniques have been devised to determine cell lineage relationships during tissue development. Some of these systems monitor cell lineages spatially and/or temporally without regard to gene expression by the cells, whereas others correlate gene expression with the lineage under study. The GAL4 Technique for Real-time and Clonal Expression (G-TRACE) system allows for rapid, fluorescent protein-based visualization of both current and past GAL4 expression patterns and is therefore amenable to genome-wide expression-based lineage screens. Here we describe the results from such a screen, performed by undergraduate students of the University of California, Los Angeles (UCLA) Undergraduate Research Consortium for Functional Genomics (URCFG) and high school summer scholars as part of a discovery-based education program. The results of the screen, which reveal novel expression-based lineage patterns within the brain, the imaginal disc epithelia, and the hematopoietic lymph gland, have been compiled into the G-TRACE Expression Database (GED), an online resource for use by the Drosophila research community. The impact of this discovery-based research experience on student learning gains was assessed independently and shown to be greater than that of similar programs conducted elsewhere. Furthermore, students participating in the URCFG showed considerably higher STEM retention rates than UCLA STEM students that did not participate in the URCFG, as well as STEM students nationwide.

Published
2019

6. Regulation of ALT-associated homology-directed repair by polyADP-ribosylation

Author

Hoang, Song My, Kaminski, Nicole, Bhargava, Ragini, Barroso-González, Jonathan, Lynskey, Michelle L., García-Expósito, Laura, Roncaioli, Justin L., Wondisford, Anne R., Wallace, Callen T., Watkins, Simon C., James, Dominic I., Waddell, Ian D., Ogilvie, Donald, Smith, Kate M., da Veiga Leprevost, Felipe, Mellacharevu, Dattatreya, Nesvizhskii, Alexey I., Li, Jianfeng, Ray-Gallet, Dominique, Sobol, Robert W., Almouzni, Genevieve, and O’Sullivan, Roderick J.

Published
2020
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8. RAD51AP1 regulates ALT-HDR through chromatin-directed homeostasis of TERRA

Author

Kaminski, Nicole, primary, Wondisford, Anne R., additional, Kwon, Youngho, additional, Lynskey, Michelle Lee, additional, Bhargava, Ragini, additional, Barroso-González, Jonathan, additional, García-Expósito, Laura, additional, He, Boxue, additional, Xu, Meng, additional, Mellacheruvu, Dattatreya, additional, Watkins, Simon C., additional, Modesti, Mauro, additional, Miller, Kyle M., additional, Nesvizhskii, Alexey I., additional, Zhang, Huaiying, additional, Sung, Patrick, additional, and O’Sullivan, Roderick J., additional

Published
2022
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10. HIRA protects telomeres against R-loop-induced instability in ALT cancer cells

Author

Lynskey, Michelle Lee, Brown, Emily E., Bhargava, Ragini, Wondisford, Anne R., Ouriou, Jean-Baptiste, Freund, Oliver, Bowman, Ray W., Smith, Baylee A., Lardo, Santana M., Schamus-Hayes, Sandra, Hainer, Sarah J., and O’Sullivan, Roderick J.

Abstract

Inactivating mutations in chromatin modifiers, like the α-thalassemia/mental retardation, X-linked (ATRX)-death domain-associated protein (DAXX) chromatin remodeling/histone H3.3 deposition complex, drive the cancer-specific alternative lengthening of telomeres (ALT) pathway. Prior studies revealed that HIRA, another histone H3.3 chaperone, compensates for ATRX-DAXX loss at telomeres to sustain ALT cancer cell survival. How HIRA rescues telomeres from the consequences of ATRX-DAXX deficiency remains unclear. Here, using an assay for transposase-accessible chromatin using sequencing (ATAC-seq) and cleavage under targets and release using nuclease (CUT&RUN), we establish that HIRA-mediated deposition of new H3.3 maintains telomeric chromatin accessibility to prevent the detrimental accumulation of nucleosome-free single-stranded DNA (ssDNA) in ATRX-DAXX-deficient ALT cells. We show that the HIRA-UBN1/UBN2 complex deposits new H3.3 to prevent TERRA R-loop buildup and transcription-replication conflicts (TRCs) at telomeres. Furthermore, HIRA-mediated H3.3 incorporation into telomeric chromatin links productive ALT to the phosphorylation of serine 31, an H3.3-specific amino acid, by Chk1. Therefore, we identify a critical role for HIRA-mediated H3.3 deposition that ensures the survival of ATRX-DAXX-deficient ALT cancer cells.

Published
2024
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11. Genome rearrangements associated with aberrant telomere maintenance

Author

Bhargava, Ragini, Fischer, Matthias, O'Sullivan, Roderick J., Bhargava, Ragini, Fischer, Matthias, and O'Sullivan, Roderick J.

Abstract

There is unequivocal evidence that telomeres are crucial for cellular homeostasis and that telomere dysfunction can elicit genome instability and potentially initiate events that culminate in cancer. Mounting evidence points to telomeres having a crucial role in driving local and systemic structural rearrangements that drive cancer. These include the classical 'breakage-fusion-bridge' (BFB) cycles and more recently identified genome re-shaping events like kataegis and chromothripsis. In this brief review, we outline the established and most recent advances describing the roles that telomere dysfunction has in the origin of these catastrophic genome rearrangements. We discuss how local and systemic structural rearrangements enable telomere length maintenance, by either telomerase or the alternative lengthening of telomeres, that is essential to sustain cancer cell proliferation.

Published
2020

15. Expression-Based Cell Lineage Analysis inDrosophilaThrough a Course-Based Research Experience for Early Undergraduates

Author

Olson, John M, primary, Evans, Cory J, additional, Ngo, Kathy T, additional, Kim, Hee Jong, additional, Nguyen, Joseph Duy, additional, Gurley, Kayla G H, additional, Ta, Truc, additional, Patel, Vijay, additional, Han, Lisa, additional, Truong-N, Khoa T, additional, Liang, Letty, additional, Chu, Maggie K, additional, Lam, Hiu, additional, Ahn, Hannah G, additional, Banerjee, Abhik Kumar, additional, Choi, In Young, additional, Kelley, Ross G, additional, Moridzadeh, Naseem, additional, Khan, Awais M, additional, Khan, Omair, additional, Lee, Szuyao, additional, Johnson, Elizabeth B, additional, Tigranyan, Annie, additional, Wang, Jay, additional, Gandhi, Anand D, additional, Padhiar, Manish M, additional, Calvopina, Joseph Hargan, additional, Sumra, Kirandeep, additional, Ou, Kristy, additional, Wu, Jessie C, additional, Dickan, Joseph N, additional, Ahmadi, Sabrena M, additional, Allen, Donald N, additional, Mai, Van Thanh, additional, Ansari, Saif, additional, Yeh, George, additional, Yoon, Earl, additional, Gon, Kimberly, additional, Yu, John Y, additional, He, Johnny, additional, Zaretsky, Jesse M, additional, Lee, Noemi E, additional, Kuoy, Edward, additional, Patananan, Alexander N, additional, Sitz, Daniel, additional, Tran, PhuongThao, additional, Do, Minh-Tu, additional, Akhave, Samira J, additional, Alvarez, Silverio D, additional, Asem, Bobby, additional, Asem, Neda, additional, Azarian, Nicole A, additional, Babaesfahani, Arezou, additional, Bahrami, Ahmad, additional, Bhamra, Manjeet, additional, Bhargava, Ragini, additional, Bhatia, Rakesh, additional, Bhatia, Subir, additional, Bumacod, Nicholas, additional, Caine, Jonathan J, additional, Caldwell, Thomas A, additional, Calica, Nicole A, additional, Calonico, Elise M, additional, Chan, Carman, additional, Chan, Helen H-L, additional, Chang, Albert, additional, Chang, Chiaen, additional, Chang, Daniel, additional, Chang, Jennifer S, additional, Charania, Nauman, additional, Chen, Jasmine Y, additional, Chen, Kevin, additional, Chen, Lu, additional, Chen, Yuyu, additional, Cheung, Derek J, additional, Cheung, Jesse J, additional, Chew, Jessica J, additional, Chew, Nicole B, additional, Chien, Cheng-An Tony, additional, Chin, Alana M, additional, Chin, Chee Jia, additional, Cho, Youngho, additional, Chou, Man Ting, additional, Chow, Ke-Huan K, additional, Chu, Carolyn, additional, Chu, Derrick M, additional, Chu, Virginia, additional, Chuang, Katherine, additional, Chugh, Arunit Singh, additional, Cubberly, Mark R, additional, Daniel, Michael Guillermo, additional, Datta, Sangita, additional, Dhaliwal, Raj, additional, Dinh, Jenny, additional, Dixit, Dhaval, additional, Dowling, Emmylou, additional, Feng, Melinda, additional, From, Christopher M, additional, Furukawa, Daisuke, additional, Gaddipati, Himaja, additional, Gevorgyan, Lilit, additional, Ghaznavi, Zunera, additional, Ghosh, Tulika, additional, Gill, Jaskaran, additional, Groves, David J, additional, Gurara, Kalkidan K, additional, Haghighi, Ali R, additional, Havard, Alexandra L, additional, Heyrani, Nasser, additional, Hioe, Tanya, additional, Hong, Kirim, additional, Houman, Justin J, additional, Howland, Molly, additional, Hsia, Elaine L, additional, Hsueh, Justin, additional, Hu, Stacy, additional, Huang, Andrew J, additional, Huynh, Jasmine C, additional, Huynh, Jenny, additional, Iwuchukwu, Chris, additional, Jang, Michael J, additional, Jiang, An An, additional, Kahlon, Simran, additional, Kao, Pei-Yun, additional, Kaur, Manpreet, additional, Keehn, Matthew G, additional, Kim, Elizabeth J, additional, Kim, Hannah, additional, Kim, Michelle J, additional, Kim, Shawn J, additional, Kitich, Aleksandar, additional, Kornberg, Ross A, additional, Kouzelos, Nicholas G, additional, Kuon, Jane, additional, Lau, Bryan, additional, Lau, Roger K, additional, Law, Rona, additional, Le, Huy D, additional, Le, Rachael, additional, Lee, Carrou, additional, Lee, Christina, additional, Lee, Grace E, additional, Lee, Kenny, additional, Lee, Michelle J, additional, Lee, Regina V, additional, Lee, Sean H K, additional, Lee, Sung Kyu, additional, Lee, Sung-Ling D, additional, Lee, Yong Jun, additional, Leong, Megan J, additional, Li, David M, additional, Li, Hao, additional, Liang, Xingfu, additional, Lin, Eric, additional, Lin, Michelle M, additional, Lin, Peter, additional, Lin, Tiffany, additional, Lu, Stacey, additional, Luong, Serena S, additional, Ma, Jessica S, additional, Ma, Li, additional, Maghen, Justin N, additional, Mallam, Sravya, additional, Mann, Shivtaj, additional, Melehani, Jason H, additional, Miller, Ryan C, additional, Mittal, Nitish, additional, Moazez, Carmel M, additional, Moon, Susie, additional, Moridzadeh, Rameen, additional, Ngo, Kaley, additional, Nguyen, Hanh H, additional, Nguyen, Kambria, additional, Nguyen, Thien H, additional, Nieh, Angela W, additional, Niu, Isabella, additional, Oh, Seo-Kyung, additional, Ong, Jessica R, additional, Oyama, Randi K, additional, Park, Joseph, additional, Park, Yaelim A, additional, Passmore, Kimberly A, additional, Patel, Ami, additional, Patel, Amy A, additional, Patel, Dhruv, additional, Patel, Tirth, additional, Peterson, Katherine E, additional, Pham, An Huynh, additional, Pham, Steven V, additional, Phuphanich, Melissa E, additional, Poria, Neil D, additional, Pourzia, Alexandra, additional, Ragland, Victoria, additional, Ranat, Riki D, additional, Rice, Cameron M, additional, Roh, David, additional, Rojhani, Solomon, additional, Sadri, Lili, additional, Saguros, Agafe, additional, Saifee, Zainab, additional, Sandhu, Manjot, additional, Scruggs, Brooke, additional, Scully, Lisa M, additional, Shih, Vanessa, additional, Shin, Brian A, additional, Sholklapper, Tamir, additional, Singh, Harnek, additional, Singh, Sumedha, additional, Snyder, Sondra L, additional, Sobotka, Katelyn F, additional, Song, Sae Ho, additional, Sukumar, Siddharth, additional, Sullivan, Halley C, additional, Sy, Mark, additional, Tan, Hande, additional, Taylor, Sara K, additional, Thaker, Shivani K, additional, Thakore, Tulsi, additional, Tong, Gregory E, additional, Tran, Jacinda N, additional, Tran, Jonathan, additional, Tran, Tuan D, additional, Tran, Vivi, additional, Trang, Cindy L, additional, Trinh, Hung G, additional, Trinh, Peter, additional, Tseng, Han-Ching H, additional, Uotani, Ted T, additional, Uraizee, Akram V, additional, Vu, Kent K T, additional, Vu, Kevin K T, additional, Wadhwani, Komal, additional, Walia, Paluk K, additional, Wang, Rebecca S, additional, Wang, Shuo, additional, Wang, Stephanie J, additional, Wiredja, Danica D, additional, Wong, Andrew L, additional, Wu, Daniel, additional, Xue, Xi, additional, Yanez, Griselda, additional, Yang, Yung-Hsuan, additional, Ye, Zhong, additional, Yee, Victor W, additional, Yeh, Cynthia, additional, Zhao, Yue, additional, Zheng, Xin, additional, Ziegenbalg, Anke, additional, Alkali, Jon, additional, Azizkhanian, Ida, additional, Bhakta, Akash, additional, Berry, Luke, additional, Castillo, Ryen, additional, Darwish, Sonja, additional, Dickinson, Holly, additional, Dutta, Ritika, additional, Ghosh, Rahul Kumar, additional, Guerin, Riley, additional, Hofman, Jonathan, additional, Iwamoto, Garrick, additional, Kang, Sarah, additional, Kim, Andrew, additional, Kim, Brian, additional, Kim, Hanwool, additional, Kim, Kristine, additional, Kim, Suji, additional, Ko, Julie, additional, Koenig, Michael, additional, LaRiviere, Alejandro, additional, Lee, Clifton, additional, Lee, Jiwon, additional, Lung, Brandon, additional, Mittelman, Max, additional, Murata, Mark, additional, Park, Yujin, additional, Rothberg, Daniel, additional, Sprung-Keyser, Ben, additional, Thaker, Kunal, additional, Yip, Vivian, additional, Picard, Paul, additional, Diep, Francie, additional, Villarasa, Nikki, additional, Hartenstein, Volker, additional, Shapiro, Casey, additional, Levis-Fitzgerald, Marc, additional, Jaworski, Leslie, additional, Loppato, David, additional, Clark, Ira E, additional, and Banerjee, Utpal, additional

Published
2019
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21. Allelic Variation on Murine Chromosome 11 Modifies Host Inflammatory Responses and Resistance to Bacillus anthracis

Author

ARMY MEDICAL RESEARCH INST OF INFECTIOUS DISEASES FORT DETRICK MD BACTERIOLOGY DIV, Terra, Jill K, France, Bryan, Cote, Christopher K, Jenkins, Amy, Bozue, Joel A, Welkos, Susan L, Bhargava, Ragini, Ho, Chi-Lee, Mehrabian, Margarete, Pan, Calvin, ARMY MEDICAL RESEARCH INST OF INFECTIOUS DISEASES FORT DETRICK MD BACTERIOLOGY DIV, Terra, Jill K, France, Bryan, Cote, Christopher K, Jenkins, Amy, Bozue, Joel A, Welkos, Susan L, Bhargava, Ragini, Ho, Chi-Lee, Mehrabian, Margarete, and Pan, Calvin

Abstract

Anthrax is a potentially fatal disease resulting from infection with Bacillus anthracis. The outcome of infection is influenced by pathogen-encoded virulence factors such as lethal toxin (LT), as well as by genetic variation within the host. To identify host genes controlling susceptibility to anthrax, a library of congenic mice consisting of strains with homozygous chromosomal segments from the LT-responsive CAST/Ei strain introgressed on a LT-resistant C57BL/6 (B6) background was screened for response to LT. Three congenic strains containing CAST/Ei regions of chromosome 11 were identified that displayed a rapid inflammatory response to LT similar to, but more severe than that driven by a LT-responsive allele of the inflammasome constituent NRLP1B. Importantly, increased response to LT in congenic mice correlated with greater resistance to infection by the Sterne strain of B. anthracis. The genomic region controlling the inflammatory response to LT was mapped to 66.36?74.67 Mb on chromosome 11, a region that encodes the LT-responsive CAST/Ei allele of Nlrp1b. However, known downstream effects of NLRP1B activation, including macrophage pyroptosis, cytokine release, and leukocyte infiltration could not fully explain the response to LT or the resistance to B. anthracis Sterne in congenic mice. Further, the exacerbated response in congenic mice is inherited in a recessive manner while the Nlrp1b-mediated response to LT is dominant. Finally, congenic mice displayed increased responsiveness in a model of sepsis compared with B6 mice. In total, these data suggest that allelic variation of one or more chromosome 11 genes in addition to Nlrp1b controls the severity of host response to multiple inflammatory stimuli and contributes to resistance to B. anthracis Sterne. Expression quantitative trait locus analysis revealed 25 genes within this region as high priority candidates for contributing to the host response to LT, Published in PLoS Pathogens, v7 n12 p1-14 Dec 2011. Supported by NIH grants 2-T32-AI-07323 (JKT), AI077791 (KAB and SML), and HL28481 (AJL). The USAMRIID research described in this paper was supported by JSTO-CBD/DTRA project #CBM VAXBT-03-10-RDP004 (CKC, AJ, JB, and SLW). Immuno/BioSpot & Cytometrics Core in the UCLA Center for AIDS Research (CFAR) supported by NIH/NIAID AI028697.

Published
2011

22. Lethal phenotype in conditional late-onset arginase 1 deficiency in the mouse

Author

Kasten, Jennifer, primary, Hu, Chuhong, additional, Bhargava, Ragini, additional, Park, Hana, additional, Tai, Denise, additional, Byrne, James A., additional, Marescau, Bart, additional, De Deyn, Peter P., additional, Schlichting, Lisa, additional, Grody, Wayne W., additional, Cederbaum, Stephen D., additional, and Lipshutz, Gerald S., additional

Published
2013
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24. Allelic Variation on Murine Chromosome 11 Modifies Host Inflammatory Responses and Resistance to Bacillus anthracis

Author

Terra, Jill K., primary, France, Bryan, additional, Cote, Christopher K., additional, Jenkins, Amy, additional, Bozue, Joel A., additional, Welkos, Susan L., additional, Bhargava, Ragini, additional, Ho, Chi-Lee, additional, Mehrabian, Margarete, additional, Pan, Calvin, additional, Lusis, Aldons J., additional, Davis, Richard C., additional, LeVine, Steven M., additional, and Bradley, Kenneth A., additional

Published
2011
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25. TRIM24 directs replicative stress responses to maintain ALT telomeres via chromatin signaling.

Author

Kim D, Bhargava R, Wang SC, Lee D, Patel R, Oh S, Bowman RW, Na CH, O'Sullivan RJ, and Miller KM

Abstract

An inability to replicate the genome can cause replication stress and genome instability. Here, we develop BLOCK-ID, a proteomic method to identify and visualize proteins at stressed replication forks. This approach successfully identified novel mediators of the replication stress response, including the chromatin acetylation reader protein TRIM24. In validating TRIM24 function, we uncovered its crucial role in coordinating Alternative Lengthening of Telomeres (ALT), a cancer-specific telomere extension pathway involving replication stress. Our data reveal that TRIM24 is directed to telomeres via a p300/CBP-dependent acetylation chromatin signaling cascade, where it organizes ALT-associated PML bodies (APBs) to promote telomere DNA synthesis. Strikingly, we demonstrate that when artificially tethered at telomeres, TRIM24 can stimulate new telomere DNA synthesis in a SUMO-dependent manner, independently of p300/CBP or PML-dependent APBs. Thus, this study identifies a TRIM24 chromatin signaling pathway required for ALT telomere maintenance.

Published
2024
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