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3. The Human Tumor Atlas Network: Charting Tumor Transitions across Space and Time at Single-Cell Resolution

Author

Aberle, Denise, Achilefu, Samuel I., Ademuyiwa, Foluso O., Adey, Andrew C., Aft, Rebecca L., Agarwal, Rachana, Aguilar, Ruben A., Alikarami, Fatemeh, Allaj, Viola, Amos, Christopher, Anders, Robert A., Angelo, Michael R., Anton, Kristen, Ashenberg, Orr, Aster, Jon C., Babur, Ozgun, Bahmani, Amir, Balsubramani, Akshay, Barrett, David, Beane, Jennifer, Bender, Diane E., Bernt, Kathrin, Berry, Lynne, Betts, Courtney B., Bletz, Julie, Blise, Katie, Boire, Adrienne, Boland, Genevieve, Borowsky, Alexander, Bosse, Kristopher, Bott, Matthew, Boyden, Ed, Brooks, James, Bueno, Raphael, Burlingame, Erik A., Cai, Qiuyin, Campbell, Joshua, Caravan, Wagma, Cerami, Ethan, Chaib, Hassan, Chan, Joseph M., Chang, Young Hwan, Chatterjee, Deyali, Chaudhary, Ojasvi, Chen, Alyce A., Chen, Bob, Chen, Changya, Chen, Chia-hui, Chen, Feng, Chen, Yu-An, Chheda, Milan G., Chin, Koei, Chiu, Roxanne, Chu, Shih-Kai, Chuaqui, Rodrigo, Chun, Jaeyoung, Cisneros, Luis, Coffey, Robert J., Colditz, Graham A., Cole, Kristina, Collins, Natalie, Contrepois, Kevin, Coussens, Lisa M., Creason, Allison L., Crichton, Daniel, Curtis, Christina, Davidsen, Tanja, Davies, Sherri R., de Bruijn, Ino, Dellostritto, Laura, De Marzo, Angelo, Demir, Emek, DeNardo, David G., Diep, Dinh, Ding, Li, Diskin, Sharon, Doan, Xengie, Drewes, Julia, Dubinett, Stephen, Dyer, Michael, Egger, Jacklynn, Eng, Jennifer, Engelhardt, Barbara, Erwin, Graham, Esplin, Edward D., Esserman, Laura, Felmeister, Alex, Feiler, Heidi S., Fields, Ryan C., Fisher, Stephen, Flaherty, Keith, Flournoy, Jennifer, Ford, James M., Fortunato, Angelo, Frangieh, Allison, Frye, Jennifer L., Fulton, Robert S., Galipeau, Danielle, Gan, Siting, Gao, Jianjiong, Gao, Long, Gao, Peng, Gao, Vianne R., Geiger, Tim, George, Ajit, Getz, Gad, Ghosh, Sharmistha, Giannakis, Marios, Gibbs, David L., Gillanders, William E., Goecks, Jeremy, Goedegebuure, Simon P., Gould, Alanna, Gowers, Kate, Gray, Joe W., Greenleaf, William, Gresham, Jeremy, Guerriero, Jennifer L., Guha, Tuhin K., Guimaraes, Alexander R., Guinney, Justin, Gutman, David, Hacohen, Nir, Hanlon, Sean, Hansen, Casey R., Harismendy, Olivier, Harris, Kathleen A., Hata, Aaron, Hayashi, Akimasa, Heiser, Cody, Helvie, Karla, Herndon, John M., Hirst, Gilliam, Hodi, Frank, Hollmann, Travis, Horning, Aaron, Hsieh, James J., Hughes, Shannon, Huh, Won Jae, Hunger, Stephen, Hwang, Shelley E., Iacobuzio-Donahue, Christine A., Ijaz, Heba, Izar, Benjamin, Jacobson, Connor A., Janes, Samuel, Jané-Valbuena, Judit, Jayasinghe, Reyka G., Jiang, Lihua, Johnson, Brett E., Johnson, Bruce, Ju, Tao, Kadara, Humam, Kaestner, Klaus, Kagan, Jacob, Kalinke, Lukas, Keith, Robert, Khan, Aziz, Kibbe, Warren, Kim, Albert H., Kim, Erika, Kim, Junhyong, Kolodzie, Annette, Kopytra, Mateusz, Kotler, Eran, Krueger, Robert, Krysan, Kostyantyn, Kundaje, Anshul, Ladabaum, Uri, Lake, Blue B., Lam, Huy, Laquindanum, Rozelle, Lau, Ken S., Laughney, Ashley M., Lee, Hayan, Lenburg, Marc, Leonard, Carina, Leshchiner, Ignaty, Levy, Rochelle, Li, Jerry, Lian, Christine G., Lim, Kian-Huat, Lin, Jia-Ren, Lin, Yiyun, Liu, Qi, Liu, Ruiyang, Lively, Tracy, Longabaugh, William J.R., Longacre, Teri, Ma, Cynthia X., Macedonia, Mary Catherine, Madison, Tyler, Maher, Christopher A., Maitra, Anirban, Makinen, Netta, Makowski, Danika, Maley, Carlo, Maliga, Zoltan, Mallo, Diego, Maris, John, Markham, Nick, Marks, Jeffrey, Martinez, Daniel, Mashl, Robert J., Masilionais, Ignas, Mason, Jennifer, Massagué, Joan, Massion, Pierre, Mattar, Marissa, Mazurchuk, Richard, Mazutis, Linas, Mazzilli, Sarah A., McKinley, Eliot T., McMichael, Joshua F., Merrick, Daniel, Meyerson, Matthew, Miessner, Julia R., Mills, Gordon B., Mills, Meredith, Mondal, Suman B., Mori, Motomi, Mori, Yuriko, Moses, Elizabeth, Mosse, Yael, Muhlich, Jeremy L., Murphy, George F., Navin, Nicholas E., Nawy, Tal, Nederlof, Michel, Ness, Reid, Nevins, Stephanie, Nikolov, Milen, Nirmal, Ajit Johnson, Nolan, Garry, Novikov, Edward, Oberdoerffer, Philipp, O’Connell, Brendan, Offin, Michael, Oh, Stephen T., Olson, Anastasiya, Ooms, Alex, Ossandon, Miguel, Owzar, Kouros, Parmar, Swapnil, Patel, Tasleema, Patti, Gary J., Pe’er, Dana, Pe'er, Itsik, Peng, Tao, Persson, Daniel, Petty, Marvin, Pfister, Hanspeter, Polyak, Kornelia, Pourfarhangi, Kamyar, Puram, Sidharth V., Qiu, Qi, Quintanal-Villalonga, Álvaro, Raj, Arjun, Ramirez-Solano, Marisol, Rashid, Rumana, Reeb, Ashley N., Regev, Aviv, Reid, Mary, Resnick, Adam, Reynolds, Sheila M., Riesterer, Jessica L., Rodig, Scott, Roland, Joseph T., Rosenfield, Sonia, Rotem, Asaf, Roy, Sudipta, Rozenblatt-Rosen, Orit, Rudin, Charles M., Ryser, Marc D., Santagata, Sandro, Santi-Vicini, Maria, Sato, Kazuhito, Schapiro, Denis, Schrag, Deborah, Schultz, Nikolaus, Sears, Cynthia L., Sears, Rosalie C., Sen, Subrata, Sen, Triparna, Shalek, Alex, Sheng, Jeff, Sheng, Quanhu, Shoghi, Kooresh I., Shrubsole, Martha J., Shyr, Yu, Sibley, Alexander B., Siex, Kiara, Simmons, Alan J., Singer, Dinah S., Sivagnanam, Shamilene, Slyper, Michal, Snyder, Michael P., Sokolov, Artem, Song, Sheng-Kwei, Sorger, Peter K., Southard-Smith, Austin, Spira, Avrum, Srivastava, Sudhir, Stein, Janet, Storm, Phillip, Stover, Elizabeth, Strand, Siri H., Su, Timothy, Sudar, Damir, Sullivan, Ryan, Surrey, Lea, Suvà, Mario, Tan, Kai, Terekhanova, Nadezhda V., Ternes, Luke, Thammavong, Lisa, Thibault, Guillaume, Thomas, George V., Thorsson, Vésteinn, Todres, Ellen, Tran, Linh, Tyler, Madison, Uzun, Yasin, Vachani, Anil, Van Allen, Eliezer, Vandekar, Simon, Veis, Deborah J., Vigneau, Sébastien, Vossough, Arastoo, Waanders, Angela, Wagle, Nikhil, Wang, Liang-Bo, Wendl, Michael C., West, Robert, Williams, Elizabeth H., Wu, Chi-yun, Wu, Hao, Wu, Hung-Yi, Wyczalkowski, Matthew A., Xie, Yubin, Yang, Xiaolu, Yapp, Clarence, Yu, Wenbao, Yuan, Yinyin, Zhang, Dadong, Zhang, Kun, Zhang, Mianlei, Zhang, Nancy, Zhang, Yantian, Zhao, Yanyan, Zhou, Daniel Cui, Zhou, Zilu, Zhu, Houxiang, Zhu, Qin, Zhu, Xiangzhu, Zhu, Yuankun, Zhuang, Xiaowei, Hupalowska, Anna, Rood, Jennifer E., Hanlon, Sean E., Hughes, Shannon K., Hwang, E. Shelley, Johnson, Bruce E., Shalek, Alex K., Spira, Avrum E., and West, Robert B.

Published
2020
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5. A marmoset brain cell census reveals regional specialization of cellular identities

Author

Krienen, Fenna M., primary, Levandowski, Kirsten M., additional, Zaniewski, Heather, additional, del Rosario, Ricardo C.H., additional, Schroeder, Margaret E., additional, Goldman, Melissa, additional, Wienisch, Martin, additional, Lutservitz, Alyssa, additional, Beja-Glasser, Victoria F., additional, Chen, Cindy, additional, Zhang, Qiangge, additional, Chan, Ken Y., additional, Li, Katelyn X., additional, Sharma, Jitendra, additional, McCormack, Dana, additional, Shin, Tay Won, additional, Harrahill, Andrew, additional, Nyase, Eric, additional, Mudhar, Gagandeep, additional, Mauermann, Abigail, additional, Wysoker, Alec, additional, Nemesh, James, additional, Kashin, Seva, additional, Vergara, Josselyn, additional, Chelini, Gabriele, additional, Dimidschstein, Jordane, additional, Berretta, Sabina, additional, Deverman, Benjamin E., additional, Boyden, Ed, additional, McCarroll, Steven A., additional, and Feng, Guoping, additional

Published
2023
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6. Transcriptomic reprogramming for neuronal age reversal

Author

Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Howard Hughes Medical Institute, Plesa, Alexandru M., Shadpour, Michael, Boyden, Ed, Church, George M., Massachusetts Institute of Technology. Department of Biological Engineering, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Howard Hughes Medical Institute, Plesa, Alexandru M., Shadpour, Michael, Boyden, Ed, and Church, George M.

Abstract

Aging is a progressive multifaceted functional decline of a biological system. Chronic age-related conditions such as neurodegenerative diseases are leading causes of death worldwide, and they are becoming a pressing problem for our society. To address this global challenge, there is a need for novel, safe, and effective rejuvenation therapies aimed at reversing age-related phenotypes and improving human health. With gene expression being a key determinant of cell identity and function, and in light of recent studies reporting rejuvenation effects through genetic perturbations, we propose an age reversal strategy focused on reprogramming the cell transcriptome to a youthful state. To this end, we suggest using transcriptomic data from primary human cells to predict rejuvenation targets and develop high-throughput aging assays, which can be used in large perturbation screens. We propose neural cells as particularly relevant targets for rejuvenation due to substantial impact of neurodegeneration on human frailty. Of all cell types in the brain, we argue that glutamatergic neurons, neuronal stem cells, and oligodendrocytes represent the most impactful and tractable targets. Lastly, we provide experimental designs for anti-aging reprogramming screens that will likely enable the development of neuronal age reversal therapies, which hold promise for dramatically improving human health.

Published
2023

7. Cell-type specific developmental defects inPTEN-mutant cortical organoids converge on abnormal circuit activity

Author

Pigoni, Martina, primary, Uzquiano, Ana, additional, Paulsen, Bruna, additional, Kedaigle, Amanda, additional, Yang, Sung Min, additional, Symvoulidis, Panagiotis, additional, Adiconis, Xian, additional, Velasco, Silvia, additional, Sartore, Rafaela, additional, Kim, Kwanho, additional, Tucewicz, Ashley, additional, Tsafou, Kalliopi, additional, Jin, Xin, additional, Barrett, Lindy, additional, Chen, Fei, additional, Boyden, Ed, additional, Regev, Aviv, additional, Levin, Joshua Z., additional, and Arlotta, Paola, additional

Published
2022
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8. A marmoset brain cell census reveals persistent influence of developmental origin on neurons

Author

Krienen, Fenna M., primary, Levandowski, Kirsten M., additional, Zaniewski, Heather, additional, del Rosario, Ricardo C.H., additional, Schroeder, Margaret E., additional, Goldman, Melissa, additional, Lutservitz, Alyssa, additional, Zhang, Qiangge, additional, Li, Katelyn X., additional, Beja-Glasser, Victoria F., additional, Sharma, Jitendra, additional, Shin, Tay Won, additional, Mauermann, Abigail, additional, Wysoker, Alec, additional, Nemesh, James, additional, Kashin, Seva, additional, Vergara, Josselyn, additional, Chelini, Gabriele, additional, Dimidschstein, Jordane, additional, Berretta, Sabina, additional, Boyden, Ed, additional, McCarroll, Steven A., additional, and Feng, Guoping, additional

Published
2022
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13. Targeted Expansion Sequencing Protocols v1

Author

not provided Sinha, Anubhav, primary, Cui, Yi, additional, not provided not provided not provided Alon, Shahar, additional, Chen, Fei, additional, not provided not provided T. Wassie, Asmamaw, additional, and Boyden, Ed, additional

Published
2021
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14. Sensory gamma frequency stimulation in cognitively healthy and AD individuals safely induces highly coordinated 40 hz neural oscillation: A preliminary study of non‐invasive sensory stimulation for treating Alzheimer’s disease

Author

Suk, Ho‐Jun, primary, Chan, Diane, additional, Jackson, Brennan, additional, Fernandez, Vanesa, additional, Stark, Danielle, additional, Milman, Noah, additional, Beach, Sara, additional, Uitermarkt, Brandt, additional, Gander, Phillip, additional, Boes, Aaron D, additional, Brown, Emery, additional, Boyden, Ed, additional, and Tsai, Li‐Huei, additional

Published
2020
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20. The Human Tumor Atlas Network: Charting Tumor Transitions across Space and Time at Single-Cell Resolution

Author

Rozenblatt-Rosen, Orit, primary, Regev, Aviv, additional, Oberdoerffer, Philipp, additional, Nawy, Tal, additional, Hupalowska, Anna, additional, Rood, Jennifer E., additional, Ashenberg, Orr, additional, Cerami, Ethan, additional, Coffey, Robert J., additional, Demir, Emek, additional, Ding, Li, additional, Esplin, Edward D., additional, Ford, James M., additional, Goecks, Jeremy, additional, Ghosh, Sharmistha, additional, Gray, Joe W., additional, Guinney, Justin, additional, Hanlon, Sean E., additional, Hughes, Shannon K., additional, Hwang, E. Shelley, additional, Iacobuzio-Donahue, Christine A., additional, Jané-Valbuena, Judit, additional, Johnson, Bruce E., additional, Lau, Ken S., additional, Lively, Tracy, additional, Mazzilli, Sarah A., additional, Pe’er, Dana, additional, Santagata, Sandro, additional, Shalek, Alex K., additional, Schapiro, Denis, additional, Snyder, Michael P., additional, Sorger, Peter K., additional, Spira, Avrum E., additional, Srivastava, Sudhir, additional, Tan, Kai, additional, West, Robert B., additional, Williams, Elizabeth H., additional, Aberle, Denise, additional, Achilefu, Samuel I., additional, Ademuyiwa, Foluso O., additional, Adey, Andrew C., additional, Aft, Rebecca L., additional, Agarwal, Rachana, additional, Aguilar, Ruben A., additional, Alikarami, Fatemeh, additional, Allaj, Viola, additional, Amos, Christopher, additional, Anders, Robert A., additional, Angelo, Michael R., additional, Anton, Kristen, additional, Aster, Jon C., additional, Babur, Ozgun, additional, Bahmani, Amir, additional, Balsubramani, Akshay, additional, Barrett, David, additional, Beane, Jennifer, additional, Bender, Diane E., additional, Bernt, Kathrin, additional, Berry, Lynne, additional, Betts, Courtney B., additional, Bletz, Julie, additional, Blise, Katie, additional, Boire, Adrienne, additional, Boland, Genevieve, additional, Borowsky, Alexander, additional, Bosse, Kristopher, additional, Bott, Matthew, additional, Boyden, Ed, additional, Brooks, James, additional, Bueno, Raphael, additional, Burlingame, Erik A., additional, Cai, Qiuyin, additional, Campbell, Joshua, additional, Caravan, Wagma, additional, Chaib, Hassan, additional, Chan, Joseph M., additional, Chang, Young Hwan, additional, Chatterjee, Deyali, additional, Chaudhary, Ojasvi, additional, Chen, Alyce A., additional, Chen, Bob, additional, Chen, Changya, additional, Chen, Chia-hui, additional, Chen, Feng, additional, Chen, Yu-An, additional, Chheda, Milan G., additional, Chin, Koei, additional, Chiu, Roxanne, additional, Chu, Shih-Kai, additional, Chuaqui, Rodrigo, additional, Chun, Jaeyoung, additional, Cisneros, Luis, additional, Colditz, Graham A., additional, Cole, Kristina, additional, Collins, Natalie, additional, Contrepois, Kevin, additional, Coussens, Lisa M., additional, Creason, Allison L., additional, Crichton, Daniel, additional, Curtis, Christina, additional, Davidsen, Tanja, additional, Davies, Sherri R., additional, de Bruijn, Ino, additional, Dellostritto, Laura, additional, De Marzo, Angelo, additional, DeNardo, David G., additional, Diep, Dinh, additional, Diskin, Sharon, additional, Doan, Xengie, additional, Drewes, Julia, additional, Dubinett, Stephen, additional, Dyer, Michael, additional, Egger, Jacklynn, additional, Eng, Jennifer, additional, Engelhardt, Barbara, additional, Erwin, Graham, additional, Esserman, Laura, additional, Felmeister, Alex, additional, Feiler, Heidi S., additional, Fields, Ryan C., additional, Fisher, Stephen, additional, Flaherty, Keith, additional, Flournoy, Jennifer, additional, Fortunato, Angelo, additional, Frangieh, Allison, additional, Frye, Jennifer L., additional, Fulton, Robert S., additional, Galipeau, Danielle, additional, Gan, Siting, additional, Gao, Jianjiong, additional, Gao, Long, additional, Gao, Peng, additional, Gao, Vianne R., additional, Geiger, Tim, additional, George, Ajit, additional, Getz, Gad, additional, Giannakis, Marios, additional, Gibbs, David L., additional, Gillanders, William E., additional, Goedegebuure, Simon P., additional, Gould, Alanna, additional, Gowers, Kate, additional, Greenleaf, William, additional, Gresham, Jeremy, additional, Guerriero, Jennifer L., additional, Guha, Tuhin K., additional, Guimaraes, Alexander R., additional, Gutman, David, additional, Hacohen, Nir, additional, Hanlon, Sean, additional, Hansen, Casey R., additional, Harismendy, Olivier, additional, Harris, Kathleen A., additional, Hata, Aaron, additional, Hayashi, Akimasa, additional, Heiser, Cody, additional, Helvie, Karla, additional, Herndon, John M., additional, Hirst, Gilliam, additional, Hodi, Frank, additional, Hollmann, Travis, additional, Horning, Aaron, additional, Hsieh, James J., additional, Hughes, Shannon, additional, Huh, Won Jae, additional, Hunger, Stephen, additional, Hwang, Shelley E., additional, Ijaz, Heba, additional, Izar, Benjamin, additional, Jacobson, Connor A., additional, Janes, Samuel, additional, Jayasinghe, Reyka G., additional, Jiang, Lihua, additional, Johnson, Brett E., additional, Johnson, Bruce, additional, Ju, Tao, additional, Kadara, Humam, additional, Kaestner, Klaus, additional, Kagan, Jacob, additional, Kalinke, Lukas, additional, Keith, Robert, additional, Khan, Aziz, additional, Kibbe, Warren, additional, Kim, Albert H., additional, Kim, Erika, additional, Kim, Junhyong, additional, Kolodzie, Annette, additional, Kopytra, Mateusz, additional, Kotler, Eran, additional, Krueger, Robert, additional, Krysan, Kostyantyn, additional, Kundaje, Anshul, additional, Ladabaum, Uri, additional, Lake, Blue B., additional, Lam, Huy, additional, Laquindanum, Rozelle, additional, Laughney, Ashley M., additional, Lee, Hayan, additional, Lenburg, Marc, additional, Leonard, Carina, additional, Leshchiner, Ignaty, additional, Levy, Rochelle, additional, Li, Jerry, additional, Lian, Christine G., additional, Lim, Kian-Huat, additional, Lin, Jia-Ren, additional, Lin, Yiyun, additional, Liu, Qi, additional, Liu, Ruiyang, additional, Longabaugh, William J.R., additional, Longacre, Teri, additional, Ma, Cynthia X., additional, Macedonia, Mary Catherine, additional, Madison, Tyler, additional, Maher, Christopher A., additional, Maitra, Anirban, additional, Makinen, Netta, additional, Makowski, Danika, additional, Maley, Carlo, additional, Maliga, Zoltan, additional, Mallo, Diego, additional, Maris, John, additional, Markham, Nick, additional, Marks, Jeffrey, additional, Martinez, Daniel, additional, Mashl, Robert J., additional, Masilionais, Ignas, additional, Mason, Jennifer, additional, Massagué, Joan, additional, Massion, Pierre, additional, Mattar, Marissa, additional, Mazurchuk, Richard, additional, Mazutis, Linas, additional, McKinley, Eliot T., additional, McMichael, Joshua F., additional, Merrick, Daniel, additional, Meyerson, Matthew, additional, Miessner, Julia R., additional, Mills, Gordon B., additional, Mills, Meredith, additional, Mondal, Suman B., additional, Mori, Motomi, additional, Mori, Yuriko, additional, Moses, Elizabeth, additional, Mosse, Yael, additional, Muhlich, Jeremy L., additional, Murphy, George F., additional, Navin, Nicholas E., additional, Nederlof, Michel, additional, Ness, Reid, additional, Nevins, Stephanie, additional, Nikolov, Milen, additional, Nirmal, Ajit Johnson, additional, Nolan, Garry, additional, Novikov, Edward, additional, O’Connell, Brendan, additional, Offin, Michael, additional, Oh, Stephen T., additional, Olson, Anastasiya, additional, Ooms, Alex, additional, Ossandon, Miguel, additional, Owzar, Kouros, additional, Parmar, Swapnil, additional, Patel, Tasleema, additional, Patti, Gary J., additional, Pe'er, Itsik, additional, Peng, Tao, additional, Persson, Daniel, additional, Petty, Marvin, additional, Pfister, Hanspeter, additional, Polyak, Kornelia, additional, Pourfarhangi, Kamyar, additional, Puram, Sidharth V., additional, Qiu, Qi, additional, Quintanal-Villalonga, Álvaro, additional, Raj, Arjun, additional, Ramirez-Solano, Marisol, additional, Rashid, Rumana, additional, Reeb, Ashley N., additional, Reid, Mary, additional, Resnick, Adam, additional, Reynolds, Sheila M., additional, Riesterer, Jessica L., additional, Rodig, Scott, additional, Roland, Joseph T., additional, Rosenfield, Sonia, additional, Rotem, Asaf, additional, Roy, Sudipta, additional, Rozenblatt-Rosen, Orit, additional, Rudin, Charles M., additional, Ryser, Marc D., additional, Santi-Vicini, Maria, additional, Sato, Kazuhito, additional, Schrag, Deborah, additional, Schultz, Nikolaus, additional, Sears, Cynthia L., additional, Sears, Rosalie C., additional, Sen, Subrata, additional, Sen, Triparna, additional, Shalek, Alex, additional, Sheng, Jeff, additional, Sheng, Quanhu, additional, Shoghi, Kooresh I., additional, Shrubsole, Martha J., additional, Shyr, Yu, additional, Sibley, Alexander B., additional, Siex, Kiara, additional, Simmons, Alan J., additional, Singer, Dinah S., additional, Sivagnanam, Shamilene, additional, Slyper, Michal, additional, Sokolov, Artem, additional, Song, Sheng-Kwei, additional, Southard-Smith, Austin, additional, Spira, Avrum, additional, Stein, Janet, additional, Storm, Phillip, additional, Stover, Elizabeth, additional, Strand, Siri H., additional, Su, Timothy, additional, Sudar, Damir, additional, Sullivan, Ryan, additional, Surrey, Lea, additional, Suvà, Mario, additional, Terekhanova, Nadezhda V., additional, Ternes, Luke, additional, Thammavong, Lisa, additional, Thibault, Guillaume, additional, Thomas, George V., additional, Thorsson, Vésteinn, additional, Todres, Ellen, additional, Tran, Linh, additional, Tyler, Madison, additional, Uzun, Yasin, additional, Vachani, Anil, additional, Van Allen, Eliezer, additional, Vandekar, Simon, additional, Veis, Deborah J., additional, Vigneau, Sébastien, additional, Vossough, Arastoo, additional, Waanders, Angela, additional, Wagle, Nikhil, additional, Wang, Liang-Bo, additional, Wendl, Michael C., additional, West, Robert, additional, Wu, Chi-yun, additional, Wu, Hao, additional, Wu, Hung-Yi, additional, Wyczalkowski, Matthew A., additional, Xie, Yubin, additional, Yang, Xiaolu, additional, Yapp, Clarence, additional, Yu, Wenbao, additional, Yuan, Yinyin, additional, Zhang, Dadong, additional, Zhang, Kun, additional, Zhang, Mianlei, additional, Zhang, Nancy, additional, Zhang, Yantian, additional, Zhao, Yanyan, additional, Zhou, Daniel Cui, additional, Zhou, Zilu, additional, Zhu, Houxiang, additional, Zhu, Qin, additional, Zhu, Xiangzhu, additional, Zhu, Yuankun, additional, and Zhuang, Xiaowei, additional

Published
2020
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28. Loss-of-Function Mutations in PTPN11 Cause Metachondromatosis, but Not Ollier Disease or Maffucci Syndrome

Author

Wilkie, AOM, Bowen, ME, Boyden, ED, Holm, IA, Campos-Xavier, B, Bonafe, L, Superti-Furga, A, Ikegawa, S, Cormier-Daire, V, Bovee, JV, Pansuriya, TC, de Sousa, SB, Savarirayan, R, Andreucci, E, Vikkula, M, Garavelli, L, Pottinger, C, Ogino, T, Sakai, A, Regazzoni, BM, Wuyts, W, Sangiorgi, L, Pedrini, E, Zhu, M, Kozakewich, HP, Kasser, JR, Seidman, JG, Kurek, KC, Warman, ML, Wilkie, AOM, Bowen, ME, Boyden, ED, Holm, IA, Campos-Xavier, B, Bonafe, L, Superti-Furga, A, Ikegawa, S, Cormier-Daire, V, Bovee, JV, Pansuriya, TC, de Sousa, SB, Savarirayan, R, Andreucci, E, Vikkula, M, Garavelli, L, Pottinger, C, Ogino, T, Sakai, A, Regazzoni, BM, Wuyts, W, Sangiorgi, L, Pedrini, E, Zhu, M, Kozakewich, HP, Kasser, JR, Seidman, JG, Kurek, KC, and Warman, ML

Abstract

Metachondromatosis (MC) is a rare, autosomal dominant, incompletely penetrant combined exostosis and enchondromatosis tumor syndrome. MC is clinically distinct from other multiple exostosis or multiple enchondromatosis syndromes and is unlinked to EXT1 and EXT2, the genes responsible for autosomal dominant multiple osteochondromas (MO). To identify a gene for MC, we performed linkage analysis with high-density SNP arrays in a single family, used a targeted array to capture exons and promoter sequences from the linked interval in 16 participants from 11 MC families, and sequenced the captured DNA using high-throughput parallel sequencing technologies. DNA capture and parallel sequencing identified heterozygous putative loss-of-function mutations in PTPN11 in 4 of the 11 families. Sanger sequence analysis of PTPN11 coding regions in a total of 17 MC families identified mutations in 10 of them (5 frameshift, 2 nonsense, and 3 splice-site mutations). Copy number analysis of sequencing reads from a second targeted capture that included the entire PTPN11 gene identified an additional family with a 15 kb deletion spanning exon 7 of PTPN11. Microdissected MC lesions from two patients with PTPN11 mutations demonstrated loss-of-heterozygosity for the wild-type allele. We next sequenced PTPN11 in DNA samples from 54 patients with the multiple enchondromatosis disorders Ollier disease or Maffucci syndrome, but found no coding sequence PTPN11 mutations. We conclude that heterozygous loss-of-function mutations in PTPN11 are a frequent cause of MC, that lesions in patients with MC appear to arise following a "second hit," that MC may be locus heterogeneous since 1 familial and 5 sporadically occurring cases lacked obvious disease-causing PTPN11 mutations, and that PTPN11 mutations are not a common cause of Ollier disease or Maffucci syndrome.

Published
2011

32. Simultaneous acquisition of single-cell mRNA and neuroanatomy

Author

Kim, Michael Tae Woo, Macosko, Evan Z, Chen, Fei, Sabatini, Bernardo, Cohen, Adam, and Boyden, Ed

Subjects
Neurosciences, Bioinformatics
Abstract

The accurate characterization of neurons and their connectivity is crucial for understanding higher neural functions in both daily life as well as disease. However, the characterization of synapses and their connectivity has been limited to bulk observations or more granular but slower methods. Furthermore, no technology exists to link synaptic or neuroanatomical information with single cell gene expression, used to infer neuronal identity. We introduce a novel technology called Synapse-seq, which enables the labeling of subcellular targets with an RNA cell barcode via synthetic viral constructs. In particular, this dissertation concentrates on the presynaptic Synapse-seq, where we label the presynaptic terminals of virally infected neurons with distinct RNA cell barcodes. The barcodes associated with these labeled presynapses are then examined through spatial transcriptomics (Slide-seq) or bulk sequencing of ~1mm resolution dissections. Furthermore, we sequence the barcodes associated with the labeled cells using single-nuclei RNA sequencing (snRNA-seq). This enables us to establish connections between spatial projections and the transcriptomic cellular identity at regional, pseudo-cellular, and cellular levels. We validated presynaptic Synapse-seq by applying this technology to the primary visual cortex (VISP) of mice, achieving unmatched resolution, specificity, and throughput. This groundbreaking approach emerges as a potent tool for exploring synaptic biology and connectomics in mammalian models.

Published
2024

33. Recurrent Dominant Mutations Affecting Two Adjacent Residues in the Motor Domain of the Monomeric Kinesin KIF22 Result in Skeletal Dysplasia and Joint Laxity

Author

Sebastian Kalamajski, H. Rosemarie Davidson, A. Belinda Campos-Xavier, Eugênia Ribeiro Valadares, Goranka Tanackovich, Andrea Superti-Furga, Christine Hall, Daniel H. Cohn, Massimiliano Rossi, Generoso Andria, R. Curtis Rogers, Shiro Ikegawa, Diana Ballhausen, André Mégarbané, Michael D. Briggs, Sheila Unger, David L. Rimoin, Claire L. Hartley, Rainer König, Richard H Scott, Luisa Bonafé, Ralph S. Lachman, Eric D. Boyden, John F. Bateman, Pierre-Simon Jouk, Geert Mortier, Philippe Suarez, Trevor L. Cameron, Matthew L. Warman, Hirotake Sawada, Gen Nishimura, Boyden, Ed, Campos Xavier, Ab, Kalamajski, S, Cameron, Tl, Suarez, P, Tanackovic, G, Andria, Generoso, Ballhausen, D, Briggs, Md, Hartley, C, Cohn, Dh, Davidson, Hr, Hall, C, Ikegawa, S, Jouk, P, König, R, Megarbané, A, Nishimura, G, Lachman, R, Mortier, G, Rimoin, Dl, Rogers, Rc, Rossi, M, Sawada, H, Scott, R, Unger, S, Valadares, Er, Bateman, Jf, Warman, Ml, Superti Furga, A, Bonafé, L., and Tanackovich, G

Subjects
Male, Joint Dislocations, Gene Expression, Kinesins, Joint laxity, Motor domain, Mice, 0302 clinical medicine, Missense mutation, Exome, Genetics(clinical), Growth Plate, Child, Cells, Cultured, Genetics (clinical), Genes, Dominant, Genetics, 0303 health sciences, Chemistry, Joint Laxity, Monomeric Kinesin KIF22, Phenotype, Cell biology, DNA-Binding Proteins, Kinesin, Erratum, Joint Instability, Skeletal Dysplasia, Mutation, Missense, Biology, Osteochondrodysplasias, 03 medical and health sciences, Skeletal disorder, Report, medicine, Animals, Humans, Abnormalities, Multiple, Amino Acid Sequence, Genetic Association Studies, 030304 developmental biology, Spondyloepimetaphyseal dysplasia, Base Sequence, Tibia, Sequence Analysis, DNA, medicine.disease, Protein Structure, Tertiary, Dysplasia, Human medicine, 030217 neurology & neurosurgery
Abstract

Spondyloepimetaphyseal dysplasia with joint laxity, leptodactylic type (lepto-SEMDJL, aka SEMDJL, Hall type), is an autosomal dominant skeletal disorder that, in spite of being relatively common among skeletal dysplasias, has eluded molecular elucidation so far. We used whole-exome sequencing of five unrelated individuals with lepto-SEMDJL to identify mutations in KIF22 as the cause of this skeletal condition. Missense mutations affecting one of two adjacent amino acids in the motor domain of KIF22 were present in 20 familial cases from eight families and in 12 other sporadic cases. The skeletal and connective tissue phenotype produced by these specific mutations point to functions of KIF22 beyond those previously ascribed functions involving chromosome segregation. Although we have found Kif22 to be strongly upregulated at the growth plate, the precise pathogenetic mechanisms remain to be elucidated.

Published
2011
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34. Intracellular Protein Scaffolds Enable Simultaneous Measurement of Multiple Biological Signals From Spectrally Identical Fluorescent Sensors

Author

Johnson, Shannon L., Denkin, Steven, and Boyden, Ed

Subjects
spatially multiplexed imaging, genetically encoded sensors, fluorescent sensors, live cell imaging, protein scaffold, calcium imaging, cAMP, PKA, mammalian cells, neuron
Abstract

Biological signals interact in complex ways within cells, and can exhibit great cell-to-cell heterogeneity as a function of cell history and state. Therefore, there is increasing desire to use multiple fluorescent sensors to simultaneously image multiple biological signals at the same time in individual cells. For decades the limited number of sensors recorded simultaneously has been due to spectral overlap. To circumvent this limitation of spectrally multiplexing sensors, molecular tools for spatially multiplexing have been engineered. Three biological signals were simultaneously measured with spectrally-overlapping sensors using these novel molecular tools. This initial demonstration of the spatial multiplexing strategy opens the door for the simultaneous imaging of dozens of signals within a physiological cascade as more peptide sequences for clustering are designed., Bioengineering & Nanotechnology

Published
2020

35. Analysis of Voluntary Behavior to Interrogate Neural Function

Author

Roberson, David, Born, Richard, Rogulja, Dragana, and Boyden, Ed

Subjects
Biology, Neuroscience, Engineering, Biomedical
Abstract

Mice and rats are critical to our understanding of human biology. They share most of our genome, are susceptible to most of the same diseases and usually benefit from clinical therapeutics, if only at very high doses. Equally important has been the development of new rodent research tools that allow us to manipulate their genome, to induce new likenesses and illuminate our similarities. However, there remain substantial obstacles to modeling clinically relevant human somatosensory experiences, such as chronic pain, in rodents. Conventional rodent pain assays require robust stimuli to generate brief behavioral readouts and they are able to detect the effects of analgesics only at levels well beyond clinically effective human doses. New technologies are needed that are sensitive to low intensity nociceptive stimuli and are able to detect the effects of analgesic drugs at clinically relevant doses. It is possible to tell when someone is in pain simply by his or her body language; but rodents and other prey animals do not as readily show behaviors that betray the presence of pain or injury. We propose that ancestral selection pressures have favored propagation of prey that mask outward signs of injury or disease from the predator, and that behavioral indicators of ongoing pain or itch in rodents should therefore be most evident when the appearance of predation risk is minimized and/or from a viewpoint not naturally seen by predators. Based on this hypothesis, we developed new devices and techniques for observation and analysis of voluntary rodent behavior, with careful consideration of their ecological position as nocturnal prey animals. Here, we demonstrate the capability of one of these new technologies to detect the prolonged effects of low intensity nociceptive stimuli in freely behaving mice and rats and to show that clinically relevant analgesic doses can extinguish pain related behaviors in rodents. Applying the same hypothesis to the study of pruriception (itch), we built another device that optimizes quantification of rodent scratching behavior. We demonstrate its utility by using it to reveal new insights into the cellular basis of pain and itch sensation and advance novel therapeutics for human injury and disease., Medical Sciences, Neurobiology; pain; itch; rodent behavior; device development

Published
2016

36. Imaging and Molecular Annotation of Xenographs and Tumours (IMAXT): High throughput data and analysis infrastructure.

Author

González-Solares EA, Dariush A, González-Fernández C, Küpcü Yoldaş A, Molaeinezhad A, Al Sa'd M, Smith L, Whitmarsh T, Millar N, Chornay N, Falciatori I, Fatemi A, Goodwin D, Kuett L, Mulvey CM, Páez Ribes M, Qosaj F, Roth A, Vázquez-García I, Watson SS, Windhager J, Aparicio S, Bodenmiller B, Boyden E, Caldas C, Harris O, Shah SP, Tavaré S, Bressan D, Hannon GJ, and Walton NA

Abstract

With the aim of producing a 3D representation of tumors, imaging and molecular annotation of xenografts and tumors (IMAXT) uses a large variety of modalities in order to acquire tumor samples and produce a map of every cell in the tumor and its host environment. With the large volume and variety of data produced in the project, we developed automatic data workflows and analysis pipelines. We introduce a research methodology where scientists connect to a cloud environment to perform analysis close to where data are located, instead of bringing data to their local computers. Here, we present the data and analysis infrastructure, discuss the unique computational challenges and describe the analysis chains developed and deployed to generate molecularly annotated tumor models. Registration is achieved by use of a novel technique involving spherical fiducial marks that are visible in all imaging modalities used within IMAXT. The automatic pipelines are highly optimized and allow to obtain processed datasets several times quicker than current solutions narrowing the gap between data acquisition and scientific exploitation., Competing Interests: S.P.S. is a founder and shareholder of Canexia Health Inc. No other author has competing interests to declare., (© The Author(s) 2023.)

Published
2023
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37. Loss-of-function mutations in PTPN11 cause metachondromatosis, but not Ollier disease or Maffucci syndrome.

Author

Bowen ME, Boyden ED, Holm IA, Campos-Xavier B, Bonafé L, Superti-Furga A, Ikegawa S, Cormier-Daire V, Bovée JV, Pansuriya TC, de Sousa SB, Savarirayan R, Andreucci E, Vikkula M, Garavelli L, Pottinger C, Ogino T, Sakai A, Regazzoni BM, Wuyts W, Sangiorgi L, Pedrini E, Zhu M, Kozakewich HP, Kasser JR, Seidman JG, Kurek KC, and Warman ML

Subjects
Chromosomes, Human genetics, DNA Copy Number Variations, Enchondromatosis pathology, Exons, Gene Deletion, Genetic Linkage, High-Throughput Nucleotide Sequencing, Humans, Loss of Heterozygosity, Mutation, Pedigree, Polymorphism, Single Nucleotide, Protein Tyrosine Phosphatase, Non-Receptor Type 11 metabolism, Sequence Analysis, DNA, Enchondromatosis genetics, Exostoses, Multiple Hereditary genetics, Protein Tyrosine Phosphatase, Non-Receptor Type 11 genetics
Abstract

Metachondromatosis (MC) is a rare, autosomal dominant, incompletely penetrant combined exostosis and enchondromatosis tumor syndrome. MC is clinically distinct from other multiple exostosis or multiple enchondromatosis syndromes and is unlinked to EXT1 and EXT2, the genes responsible for autosomal dominant multiple osteochondromas (MO). To identify a gene for MC, we performed linkage analysis with high-density SNP arrays in a single family, used a targeted array to capture exons and promoter sequences from the linked interval in 16 participants from 11 MC families, and sequenced the captured DNA using high-throughput parallel sequencing technologies. DNA capture and parallel sequencing identified heterozygous putative loss-of-function mutations in PTPN11 in 4 of the 11 families. Sanger sequence analysis of PTPN11 coding regions in a total of 17 MC families identified mutations in 10 of them (5 frameshift, 2 nonsense, and 3 splice-site mutations). Copy number analysis of sequencing reads from a second targeted capture that included the entire PTPN11 gene identified an additional family with a 15 kb deletion spanning exon 7 of PTPN11. Microdissected MC lesions from two patients with PTPN11 mutations demonstrated loss-of-heterozygosity for the wild-type allele. We next sequenced PTPN11 in DNA samples from 54 patients with the multiple enchondromatosis disorders Ollier disease or Maffucci syndrome, but found no coding sequence PTPN11 mutations. We conclude that heterozygous loss-of-function mutations in PTPN11 are a frequent cause of MC, that lesions in patients with MC appear to arise following a "second hit," that MC may be locus heterogeneous since 1 familial and 5 sporadically occurring cases lacked obvious disease-causing PTPN11 mutations, and that PTPN11 mutations are not a common cause of Ollier disease or Maffucci syndrome., Competing Interests: The authors have declared that no competing interests exist.

Published
2011
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38. Lethal skeletal dysplasia in mice and humans lacking the golgin GMAP-210.

Author

Smits P, Bolton AD, Funari V, Hong M, Boyden ED, Lu L, Manning DK, Dwyer ND, Moran JL, Prysak M, Merriman B, Nelson SF, Bonafé L, Superti-Furga A, Ikegawa S, Krakow D, Cohn DH, Kirchhausen T, Warman ML, and Beier DR

Subjects
Animals, Cell Differentiation, Cell Proliferation, Cytoskeletal Proteins, Endoplasmic Reticulum ultrastructure, Genes, Recessive, Glycosylation, Golgi Apparatus ultrastructure, Humans, Mice, Mice, Mutant Strains, Nuclear Proteins deficiency, Phenotype, Polymorphism, Single Nucleotide, Protein Processing, Post-Translational physiology, Sequence Analysis, DNA, Chondrocytes cytology, Codon, Nonsense, Nuclear Proteins genetics, Osteochondrodysplasias genetics
Abstract

Background: Establishing the genetic basis of phenotypes such as skeletal dysplasia in model organisms can provide insights into biologic processes and their role in human disease., Methods: We screened mutagenized mice and observed a neonatal lethal skeletal dysplasia with an autosomal recessive pattern of inheritance. Through genetic mapping and positional cloning, we identified the causative mutation., Results: Affected mice had a nonsense mutation in the thyroid hormone receptor interactor 11 gene (Trip11), which encodes the Golgi microtubule-associated protein 210 (GMAP-210); the affected mice lacked this protein. Golgi architecture was disturbed in multiple tissues, including cartilage. Skeletal development was severely impaired, with chondrocytes showing swelling and stress in the endoplasmic reticulum, abnormal cellular differentiation, and increased cell death. Golgi-mediated glycosylation events were altered in fibroblasts and chondrocytes lacking GMAP-210, and these chondrocytes had intracellular accumulation of perlecan, an extracellular matrix protein, but not of type II collagen or aggrecan, two other extracellular matrix proteins. The similarities between the skeletal and cellular phenotypes in these mice and those in patients with achondrogenesis type 1A, a neonatal lethal form of skeletal dysplasia in humans, suggested that achondrogenesis type 1A may be caused by GMAP-210 deficiency. Sequence analysis revealed loss-of-function mutations in the 10 unrelated patients with achondrogenesis type 1A whom we studied., Conclusions: GMAP-210 is required for the efficient glycosylation and cellular transport of multiple proteins. The identification of a mutation affecting GMAP-210 in mice, and then in humans, as the cause of a lethal skeletal dysplasia underscores the value of screening for abnormal phenotypes in model organisms and identifying the causative mutations., (2010 Massachusetts Medical Society)

Published
2010
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39. Anthrax lethal toxin triggers the formation of a membrane-associated inflammasome complex in murine macrophages.

Author

Nour AM, Yeung YG, Santambrogio L, Boyden ED, Stanley ER, and Brojatsch J

Subjects
Animals, Antigens, Bacterial immunology, Apoptosis Regulatory Proteins immunology, Bacterial Toxins immunology, Blotting, Western, Caspase 1 immunology, Caspases immunology, Caspases metabolism, Caspases, Initiator, Cell Line, Cell Membrane immunology, Cell Membrane metabolism, Humans, Immunoprecipitation, Inflammation immunology, Inflammation metabolism, Macrophages immunology, Macrophages microbiology, Mice, Microscopy, Fluorescence, Phosphopyruvate Hydratase immunology, Phosphopyruvate Hydratase metabolism, Transfection, Antigens, Bacterial metabolism, Apoptosis physiology, Apoptosis Regulatory Proteins metabolism, Bacterial Toxins metabolism, Caspase 1 metabolism, Macrophages metabolism
Abstract

Multiple microbial components trigger the formation of an inflammasome complex that contains pathogen-specific nucleotide oligomerization and binding domain (NOD)-like receptors (NLRs), caspase-1, and in some cases the scaffolding protein ASC. The NLR protein Nalp1b has been linked to anthrax lethal toxin (LT)-mediated cytolysis of murine macrophages. Here we demonstrate that in unstimulated J774A.1 macrophages, caspase-1 and Nalp1b are membrane associated and part of approximately 200- and approximately 800-kDa complexes, respectively. LT treatment of these cells resulted in caspase-1 recruitment to the Nalp1b-containing complex, concurrent with processing of cytosolic caspase-1 substrates. We further demonstrated that Nalp1b and caspase-1 are able to interact with each other. Intriguingly, both caspase-1 and Nalp1b were membrane associated, while the caspase-1 substrate interleukin-18 was cytosolic. Caspase-1-associated inflammasome components included, besides Nalp1b, proinflammatory caspase-11 and the caspase-1 substrate alpha-enolase. Asc was not part of the Nalp1b inflammasome in LT-treated macrophages. Taken together, our findings suggest that LT triggers the formation of a membrane-associated inflammasome complex in murine macrophages, resulting in cleavage of cytosolic caspase-1 substrates and cell death.

Published
2009
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40. Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin.

Author

Boyden ED and Dietrich WF

Subjects
Alleles, Animals, Apoptosis Regulatory Proteins antagonists & inhibitors, Base Sequence, Caspase 1 metabolism, Cell Survival, Disease Susceptibility, Exons genetics, Macrophages metabolism, Macrophages pathology, Mice, Mice, Transgenic, Molecular Sequence Data, Polymorphism, Genetic, RNA, Messenger genetics, RNA, Messenger metabolism, Antigens, Bacterial toxicity, Apoptosis Regulatory Proteins metabolism, Bacterial Toxins toxicity, Macrophages drug effects
Abstract

The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections. EF and LF can be transported by PA into the cytosol of many cell types. In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections. Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis. This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7,8). Here we show that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.

Published
2006
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