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10. Chi3l1 /YKL-40 is controlled by the astrocyte circadian clock and regulates neuroinflammation and Alzheimer’s disease pathogenesis

Author

Lananna, Brian V., primary, McKee, Celia A., additional, King, Melvin W., additional, Del-Aguila, Jorge L., additional, Dimitry, Julie M., additional, Farias, Fabiana H. G., additional, Nadarajah, Collin J., additional, Xiong, David D., additional, Guo, Chun, additional, Cammack, Alexander J., additional, Elias, Jack A., additional, Zhang, Jinsong, additional, Cruchaga, Carlos, additional, and Musiek, Erik S., additional

Published
2020
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12. Rethinking the 10‐pack‐year rule for favorable human papillomavirus–associated oropharynx carcinoma: A multi‐institution analysis

Author

Broughman, James R., primary, Xiong, David D., additional, Moeller, Benjamin J., additional, Contrera, Kevin J., additional, Prendes, Brandon L., additional, Lamarre, Eric D., additional, Ku, Jamie A., additional, Burkey, Brian B., additional, Woody, Neil M., additional, Joshi, Nikhil P., additional, Adelstein, David J., additional, Geiger, Jessica L., additional, Frenkel, Catherine H., additional, Milas, Zvonimir L., additional, Brickman, Daniel S., additional, Sumrall, Ashley L., additional, Carrizosa, Daniel R., additional, Greskovich, John F., additional, Koyfman, Shlomo A., additional, and Ward, Matthew C., additional

Published
2020
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14. Cell-Autonomous Regulation of Astrocyte Activation by the Circadian Clock Protein BMAL1

Author

Lananna, Brian V., primary, Nadarajah, Collin J., additional, Izumo, Mariko, additional, Cedeño, Michelle R., additional, Xiong, David D., additional, Dimitry, Julie, additional, Tso, Chak Foon, additional, McKee, Celia A., additional, Griffin, Percy, additional, Sheehan, Patrick W., additional, Haspel, Jeffery A., additional, Barres, Ben A., additional, Liddelow, Shane A., additional, Takahashi, Joseph S., additional, Karatsoreos, Ilia N., additional, and Musiek, Erik S., additional

Published
2018
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15. Chi3l1/YKL-40 is controlled by the astrocyte circadian clock and regulates neuroinflammation and Alzheimer's disease pathogenesis.

Author

Lananna, Brian V., McKee, Celia A., King, Melvin W., Del-Aguila, Jorge L., Dimitry, Julie M., Farias, Fabiana H. G., Nadarajah, Collin J., Xiong, David D., Guo, Chun, Cammack, Alexander J., Elias, Jack A., Zhang, Jinsong, Cruchaga, Carlos, and Musiek, Erik S.

Subjects
AMYLOID plaque, CIRCADIAN rhythms, ALZHEIMER'S disease, MOLECULAR clock, INFLAMMATION, CEREBROSPINAL fluid, GENETIC code, MICROGLIA
Abstract

Targeting astrocytes in AD: Astrocytes and microglia play a dual role in Alzheimer's disease (AD), increasing neuroinflammation and limiting plaque growth through phagocytic activity. The astrocytic protein YKL-40 is increased in the cerebrospinal fluid (CSF) of patients with AD; however, its role in AD pathophysiology is unclear. Here, Lananna et al. used mouse model and in vitro systems to show that Chi3l1, the gene coding for YKL-40, plays a detrimental role in AD. Its deletion reduced amyloid plaque formation and promoted Aβ phagocytosis. A polymorphism in CHI3L1 resulting in reduced protein expression was associated with slower AD progression in patients. The results suggest that YKL-40 could be targeted for reducing AD progression in patients. Regulation of glial activation and neuroinflammation are critical factors in the pathogenesis of Alzheimer's disease (AD). YKL-40, a primarily astrocytic protein encoded by the gene Chi3l1, is a widely studied cerebrospinal fluid biomarker that increases with aging and early in AD. However, the function of Chi3l1/YKL-40 in AD is unknown. In a cohort of patients with AD, we observed that a variant in the human CHI3L1 gene, which results in decreased CSF YKL-40 expression, was associated with slower AD progression. At baseline, Chi3l1 deletion in mice had no effect on astrocyte activation while modestly promoting microglial activation. In a mouse APP/PS1 model of AD, Chi3l1 deletion decreased amyloid plaque burden and increased periplaque expression of the microglial lysosomal marker CD68, suggesting that Chi3l1 may suppress glial phagocytic activation and promote amyloid accumulation. Accordingly, Chi3l1 knockdown increased phagocytosis of zymosan particles and of β-amyloid peptide in both astrocytes and microglia in vitro. We further observed that expression of Chi3l1 is regulated by the circadian clock, as deletion of the core clock proteins BMAL1 or CLOCK/NPAS2 strongly suppresses basal Chi3l1 expression, whereas deletion of the negative clock regulators PER1/PER2 increased Chi3l1 expression. Basal Chi3l1 mRNA was nonrhythmic because of a long mRNA half-life in astrocytes. However, inflammatory induction of Chi3l1 was gated by the clock. Our findings reveal Chi3l1/YKL-40 as a modulator of glial phagocytic activation and AD pathogenesis in both mice and humans and suggest that the astrocyte circadian clock regulates inflammatory Chi3l1 induction. [ABSTRACT FROM AUTHOR]

Published
2020
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17. Retrotransposons Are the Major Contributors to the Expansion of theDrosophila ananassaeMuller F Element

Author

Leung, Wilson, primary, Shaffer, Christopher D, additional, Chen, Elizabeth J, additional, Quisenberry, Thomas J, additional, Ko, Kevin, additional, Braverman, John M, additional, Giarla, Thomas C, additional, Mortimer, Nathan T, additional, Reed, Laura K, additional, Smith, Sheryl T, additional, Robic, Srebrenka, additional, McCartha, Shannon R, additional, Perry, Danielle R, additional, Prescod, Lindsay M, additional, Sheppard, Zenyth A, additional, Saville, Ken J, additional, McClish, Allison, additional, Morlock, Emily A, additional, Sochor, Victoria R, additional, Stanton, Brittney, additional, Veysey-White, Isaac C, additional, Revie, Dennis, additional, Jimenez, Luis A, additional, Palomino, Jennifer J, additional, Patao, Melissa D, additional, Patao, Shane M, additional, Himelblau, Edward T, additional, Campbell, Jaclyn D, additional, Hertz, Alexandra L, additional, McEvilly, Maddison F, additional, Wagner, Allison R, additional, Youngblom, James, additional, Bedi, Baljit, additional, Bettincourt, Jeffery, additional, Duso, Erin, additional, Her, Maiye, additional, Hilton, William, additional, House, Samantha, additional, Karimi, Masud, additional, Kumimoto, Kevin, additional, Lee, Rebekah, additional, Lopez, Darryl, additional, Odisho, George, additional, Prasad, Ricky, additional, Robbins, Holly Lyn, additional, Sandhu, Tanveer, additional, Selfridge, Tracy, additional, Tsukashima, Kara, additional, Yosif, Hani, additional, Kokan, Nighat P, additional, Britt, Latia, additional, Zoellner, Alycia, additional, Spana, Eric P, additional, Chlebina, Ben T, additional, Chong, Insun, additional, Friedman, Harrison, additional, Mammo, Danny A, additional, Ng, Chun L, additional, Nikam, Vinayak S, additional, Schwartz, Nicholas U, additional, Xu, Thomas Q, additional, Burg, Martin G, additional, Batten, Spencer M, additional, Corbeill, Lindsay M, additional, Enoch, Erica, additional, Ensign, Jesse J, additional, Franks, Mary E, additional, Haiker, Breanna, additional, Ingles, Judith A, additional, Kirkland, Lyndsay D, additional, Lorenz-Guertin, Joshua M, additional, Matthews, Jordan, additional, Mittig, Cody M, additional, Monsma, Nicholaus, additional, Olson, Katherine J, additional, Perez-Aragon, Guillermo, additional, Ramic, Alen, additional, Ramirez, Jordan R, additional, Scheiber, Christopher, additional, Schneider, Patrick A, additional, Schultz, Devon E, additional, Simon, Matthew, additional, Spencer, Eric, additional, Wernette, Adam C, additional, Wykle, Maxine E, additional, Zavala-Arellano, Elizabeth, additional, McDonald, Mitchell J, additional, Ostby, Kristine, additional, Wendland, Peter, additional, DiAngelo, Justin R, additional, Ceasrine, Alexis M, additional, Cox, Amanda H, additional, Docherty, James E B, additional, Gingras, Robert M, additional, Grieb, Stephanie M, additional, Pavia, Michael J, additional, Personius, Casey L, additional, Polak, Grzegorz L, additional, Beach, Dale L, additional, Cerritos, Heaven L, additional, Horansky, Edward A, additional, Sharif, Karim A, additional, Moran, Ryan, additional, Parrish, Susan, additional, Bickford, Kirsten, additional, Bland, Jennifer, additional, Broussard, Juliana, additional, Campbell, Kerry, additional, Deibel, Katelynn E, additional, Forka, Richard, additional, Lemke, Monika C, additional, Nelson, Marlee B, additional, O'Keeffe, Catherine, additional, Ramey, S Mariel, additional, Schmidt, Luke, additional, Villegas, Paola, additional, Jones, Christopher J, additional, Christ, Stephanie L, additional, Mamari, Sami, additional, Rinaldi, Adam S, additional, Stity, Ghazal, additional, Hark, Amy T, additional, Scheuerman, Mark, additional, Silver Key, S Catherine, additional, McRae, Briana D, additional, Haberman, Adam S, additional, Asinof, Sam, additional, Carrington, Harriette, additional, Drumm, Kelly, additional, Embry, Terrance, additional, McGuire, Richard, additional, Miller-Foreman, Drew, additional, Rosen, Stella, additional, Safa, Nadia, additional, Schultz, Darrin, additional, Segal, Matt, additional, Shevin, Yakov, additional, Svoronos, Petros, additional, Vuong, Tam, additional, Skuse, Gary, additional, Paetkau, Don W, additional, Bridgman, Rachael K, additional, Brown, Charlotte M, additional, Carroll, Alicia R, additional, Gifford, Francesca M, additional, Gillespie, Julie Beth, additional, Herman, Susan E, additional, Holtcamp, Krystal L, additional, Host, Misha A, additional, Hussey, Gabrielle, additional, Kramer, Danielle M, additional, Lawrence, Joan Q, additional, Martin, Madeline M, additional, Niemiec, Ellen N, additional, O'Reilly, Ashleigh P, additional, Pahl, Olivia A, additional, Quintana, Guadalupe, additional, Rettie, Elizabeth A S, additional, Richardson, Torie L, additional, Rodriguez, Arianne E, additional, Rodriguez, Mona O, additional, Schiraldi, Laura, additional, Smith, Joanna J, additional, Sugrue, Kelsey F, additional, Suriano, Lindsey J, additional, Takach, Kaitlyn E, additional, Vasquez, Arielle M, additional, Velez, Ximena, additional, Villafuerte, Elizabeth J, additional, Vives, Laura T, additional, Zellmer, Victoria R, additional, Hauke, Jeanette, additional, Hauser, Charles R, additional, Barker, Karolyn, additional, Cannon, Laurie, additional, Parsamian, Perouza, additional, Parsons, Samantha, additional, Wichman, Zachariah, additional, Bazinet, Christopher W, additional, Johnson, Diana E, additional, Bangura, Abubakarr, additional, Black, Jordan A, additional, Chevee, Victoria, additional, Einsteen, Sarah A, additional, Hilton, Sarah K, additional, Kollmer, Max, additional, Nadendla, Rahul, additional, Stamm, Joyce, additional, Fafara-Thompson, Antoinette E, additional, Gygi, Amber M, additional, Ogawa, Emmy E, additional, Van Camp, Matt, additional, Kocsisova, Zuzana, additional, Leatherman, Judith L, additional, Modahl, Cassie M, additional, Rubin, Michael R, additional, Apiz-Saab, Susana S, additional, Arias-Mejias, Suzette M, additional, Carrion-Ortiz, Carlos F, additional, Claudio-Vazquez, Patricia N, additional, Espada-Green, Debbie M, additional, Feliciano-Camacho, Marium, additional, Gonzalez-Bonilla, Karina M, additional, Taboas-Arroyo, Mariela, additional, Vargas-Franco, Dorianmarie, additional, Montañez-Gonzalez, Raquel, additional, Perez-Otero, Joseph, additional, Rivera-Burgos, Myrielis, additional, Rivera-Rosario, Francisco J, additional, Eisler, Heather L, additional, Alexander, Jackie, additional, Begley, Samatha K, additional, Gabbard, Deana, additional, Allen, Robert J, additional, Aung, Wint Yan, additional, Barshop, William D, additional, Boozalis, Amanda, additional, Chu, Vanessa P, additional, Davis, Jeremy S, additional, Duggal, Ryan N, additional, Franklin, Robert, additional, Gavinski, Katherine, additional, Gebreyesus, Heran, additional, Gong, Henry Z, additional, Greenstein, Rachel A, additional, Guo, Averill D, additional, Hanson, Casey, additional, Homa, Kaitlin E, additional, Hsu, Simon C, additional, Huang, Yi, additional, Huo, Lucy, additional, Jacobs, Sarah, additional, Jia, Sasha, additional, Jung, Kyle L, additional, Wai-Chee Kong, Sarah, additional, Kroll, Matthew R, additional, Lee, Brandon M, additional, Lee, Paul F, additional, Levine, Kevin M, additional, Li, Amy S, additional, Liu, Chengyu, additional, Liu, Max Mian, additional, Lousararian, Adam P, additional, Lowery, Peter B, additional, Mallya, Allyson P, additional, Marcus, Joseph E, additional, Ng, Patrick C, additional, Nguyen, Hien P, additional, Patel, Ruchik, additional, Precht, Hashini, additional, Rastogi, Suchita, additional, Sarezky, Jonathan M, additional, Schefkind, Adam, additional, Schultz, Michael B, additional, Shen, Delia, additional, Skorupa, Tara, additional, Spies, Nicholas C, additional, Stancu, Gabriel, additional, Vivian Tsang, Hiu Man, additional, Turski, Alice L, additional, Venkat, Rohit, additional, Waldman, Leah E, additional, Wang, Kaidi, additional, Wang, Tracy, additional, Wei, Jeffrey W, additional, Wu, Dennis Y, additional, Xiong, David D, additional, Yu, Jack, additional, Zhou, Karen, additional, McNeil, Gerard P, additional, Fernandez, Robert W, additional, Menzies, Patrick Gomez, additional, Gu, Tingting, additional, Buhler, Jeremy, additional, Mardis, Elaine R, additional, and Elgin, Sarah C R, additional

Published
2017
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20. Retrotransposons Are the Major Contributors to the Expansion of the Drosophila ananassae Muller F Element.

Author

Leung W, Shaffer CD, Chen EJ, Quisenberry TJ, Ko K, Braverman JM, Giarla TC, Mortimer NT, Reed LK, Smith ST, Robic S, McCartha SR, Perry DR, Prescod LM, Sheppard ZA, Saville KJ, McClish A, Morlock EA, Sochor VR, Stanton B, Veysey-White IC, Revie D, Jimenez LA, Palomino JJ, Patao MD, Patao SM, Himelblau ET, Campbell JD, Hertz AL, McEvilly MF, Wagner AR, Youngblom J, Bedi B, Bettincourt J, Duso E, Her M, Hilton W, House S, Karimi M, Kumimoto K, Lee R, Lopez D, Odisho G, Prasad R, Robbins HL, Sandhu T, Selfridge T, Tsukashima K, Yosif H, Kokan NP, Britt L, Zoellner A, Spana EP, Chlebina BT, Chong I, Friedman H, Mammo DA, Ng CL, Nikam VS, Schwartz NU, Xu TQ, Burg MG, Batten SM, Corbeill LM, Enoch E, Ensign JJ, Franks ME, Haiker B, Ingles JA, Kirkland LD, Lorenz-Guertin JM, Matthews J, Mittig CM, Monsma N, Olson KJ, Perez-Aragon G, Ramic A, Ramirez JR, Scheiber C, Schneider PA, Schultz DE, Simon M, Spencer E, Wernette AC, Wykle ME, Zavala-Arellano E, McDonald MJ, Ostby K, Wendland P, DiAngelo JR, Ceasrine AM, Cox AH, Docherty JEB, Gingras RM, Grieb SM, Pavia MJ, Personius CL, Polak GL, Beach DL, Cerritos HL, Horansky EA, Sharif KA, Moran R, Parrish S, Bickford K, Bland J, Broussard J, Campbell K, Deibel KE, Forka R, Lemke MC, Nelson MB, O'Keeffe C, Ramey SM, Schmidt L, Villegas P, Jones CJ, Christ SL, Mamari S, Rinaldi AS, Stity G, Hark AT, Scheuerman M, Silver Key SC, McRae BD, Haberman AS, Asinof S, Carrington H, Drumm K, Embry T, McGuire R, Miller-Foreman D, Rosen S, Safa N, Schultz D, Segal M, Shevin Y, Svoronos P, Vuong T, Skuse G, Paetkau DW, Bridgman RK, Brown CM, Carroll AR, Gifford FM, Gillespie JB, Herman SE, Holtcamp KL, Host MA, Hussey G, Kramer DM, Lawrence JQ, Martin MM, Niemiec EN, O'Reilly AP, Pahl OA, Quintana G, Rettie EAS, Richardson TL, Rodriguez AE, Rodriguez MO, Schiraldi L, Smith JJ, Sugrue KF, Suriano LJ, Takach KE, Vasquez AM, Velez X, Villafuerte EJ, Vives LT, Zellmer VR, Hauke J, Hauser CR, Barker K, Cannon L, Parsamian P, Parsons S, Wichman Z, Bazinet CW, Johnson DE, Bangura A, Black JA, Chevee V, Einsteen SA, Hilton SK, Kollmer M, Nadendla R, Stamm J, Fafara-Thompson AE, Gygi AM, Ogawa EE, Van Camp M, Kocsisova Z, Leatherman JL, Modahl CM, Rubin MR, Apiz-Saab SS, Arias-Mejias SM, Carrion-Ortiz CF, Claudio-Vazquez PN, Espada-Green DM, Feliciano-Camacho M, Gonzalez-Bonilla KM, Taboas-Arroyo M, Vargas-Franco D, Montañez-Gonzalez R, Perez-Otero J, Rivera-Burgos M, Rivera-Rosario FJ, Eisler HL, Alexander J, Begley SK, Gabbard D, Allen RJ, Aung WY, Barshop WD, Boozalis A, Chu VP, Davis JS, Duggal RN, Franklin R, Gavinski K, Gebreyesus H, Gong HZ, Greenstein RA, Guo AD, Hanson C, Homa KE, Hsu SC, Huang Y, Huo L, Jacobs S, Jia S, Jung KL, Wai-Chee Kong S, Kroll MR, Lee BM, Lee PF, Levine KM, Li AS, Liu C, Liu MM, Lousararian AP, Lowery PB, Mallya AP, Marcus JE, Ng PC, Nguyen HP, Patel R, Precht H, Rastogi S, Sarezky JM, Schefkind A, Schultz MB, Shen D, Skorupa T, Spies NC, Stancu G, Vivian Tsang HM, Turski AL, Venkat R, Waldman LE, Wang K, Wang T, Wei JW, Wu DY, Xiong DD, Yu J, Zhou K, McNeil GP, Fernandez RW, Menzies PG, Gu T, Buhler J, Mardis ER, and Elgin SCR

Subjects
Animals, Base Composition genetics, Base Sequence, Codon genetics, Female, Gene Expression Profiling, Genes, Insect, Histones metabolism, Protein Processing, Post-Translational genetics, Wolbachia genetics, Chromosomes genetics, Drosophila genetics, Retroelements genetics
Abstract

The discordance between genome size and the complexity of eukaryotes can partly be attributed to differences in repeat density. The Muller F element (∼5.2 Mb) is the smallest chromosome in Drosophila melanogaster , but it is substantially larger (>18.7 Mb) in D. ananassae To identify the major contributors to the expansion of the F element and to assess their impact, we improved the genome sequence and annotated the genes in a 1.4-Mb region of the D. ananassae F element, and a 1.7-Mb region from the D element for comparison. We find that transposons (particularly LTR and LINE retrotransposons) are major contributors to this expansion (78.6%), while Wolbachia sequences integrated into the D. ananassae genome are minor contributors (0.02%). Both D. melanogaster and D. ananassae F-element genes exhibit distinct characteristics compared to D-element genes ( e.g. , larger coding spans, larger introns, more coding exons, and lower codon bias), but these differences are exaggerated in D. ananassae Compared to D. melanogaster , the codon bias observed in D. ananassae F-element genes can primarily be attributed to mutational biases instead of selection. The 5' ends of F-element genes in both species are enriched in dimethylation of lysine 4 on histone 3 (H3K4me2), while the coding spans are enriched in H3K9me2. Despite differences in repeat density and gene characteristics, D. ananassae F-element genes show a similar range of expression levels compared to genes in euchromatic domains. This study improves our understanding of how transposons can affect genome size and how genes can function within highly repetitive domains., (Copyright © 2017 Leung et al.)

Published
2017
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