Recommended Readings: Maurice Swanson, Ph.D.

Friday Lecture Series

RNA-mediated Pathways to Disease

Maurice Swanson, Ph.D., associate director, Center for NeuroGenetics,

and professor of molecular genetics and microbiology,

University of Florida College of Medicine

 February 15, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

Recommended Readings

Daughters, R. S., Tuttle, D. L., Gao, W., Ikeda, Y., Moseley, M. L., Ebner, T. J., . . . Ranum, L. P. W. (2009). RNA gain-of-function in spinocerebellar ataxia type 8. PLoS Genetics, 5(8)

Ho, T. H., Savkur, R. S., Poulos, M. G., Mancini, M. A., Swanson, M. S., & Cooper, T. A. (2005). Colocalization of muscleblind with RNA foci is separable from mis-regulation of alternative splicing in myotonic dystrophy. Journal of Cell Science, 118(13), 2923-2933

Kanadia, R. N., Shin, J., Yuan, Y., Beattie, S. G., Wheeler, T. M., Thornton, C. A., & Swanson, M. S. (2006). Reversal of RNA missplicing and myotonia after muscleblind overexpression in a mouse poly(CUG) model for myotonic dystrophy. Proceedings of the National Academy of Sciences of the United States of America, 103(31), 11748-11753

Osborne, R. J., Lin, X., Welle, S., Sobczak, K., O’Rourke, J. R., Swanson, M. S., & Thornton, C. A. (2009). Transcriptional and post-transcriptional impact of toxic RNA in myotonic dystrophy. Human Molecular Genetics, 18(8), 1471-1481

Shin, J., Charizanis, K., & Swanson, M. S. (2009). Pathogenic RNAs in microsatellite expansion disease. Neuroscience Letters, 466(2), 99-102

Yuan, Y., Compton, S. A., Sobczak, K., Stenberg, M. G., Thornton, C. A., Griffith, J. D., & Swanson, M. S. (2007). Muscleblind-like 1 interacts with RNA hairpins in splicing target and pathogenic RNAs. Nucleic Acids Research, 35(16), 5474-5486

 

Recommended Readings: Howard Chang, M.D., Ph.D.

Friday Lecture Series

Genome Regulation by Long Noncoding RNA

Howard Chang, M.D., Ph.D., early career scientist,

Howard Hughes Medical Institute; professor of dermatology,

Stanford University School of Medicine, member, Stanford Cancer Center and Stanford Institute for Stem Cell Biology and Regenerative Medicine

February 10, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

 

Recommended Readings:

Hung, T., Y. Wang, M. F. Lin, A. K. Koegel, Y. Kotake, G. D. Grant, H. M. Horlings, et al. 2011. Extensive and coordinated transcription of noncoding RNAs within cell-cycle promoters. Nature genetics 43, (7): 621-629

Rinn, J. L., M. Kertesz, J. K. Wang, S. L. Squazzo, X. Xu, S. A. Brugmann, L. H. Goodnough, et al. 2007. Functional demarcation of active and silent chromatin domains in human HOX loci by noncoding RNAs. Cell 129, (7): 1311-1323

Tsai, M. -C, O. Manor, Y. Wan, N. Mosammaparast, J. K. Wang, F. Lan, Y. Shi, E. Segal, and H. Y. Chang. 2010. Long noncoding RNA as modular scaffold of histone modification complexes. Science 329, (5992): 689-693

Wang, K., and H. Chang. 2011. Molecular mechanisms of long noncoding RNAs. Molecular cell 43, (6): 904-914

Wang, K. C., Y. W. Yang, B. Liu, A. Sanyal, R. Corces-Zimmerman, Y. Chen, B. R. Lajoie, et al. 2011. A long noncoding RNA maintains active chromatin to coordinate homeotic gene expression. Nature 472, (7341): 120-126

 

Recommended Readings: Jeannie T. Lee, M.D., Ph.D.

Friday Lecture Series

Richard M. Furlaud Distinguished Lecture

X-Chromosome Inactivation as a Model for Epigenomic Regulation by Long

Noncoding RNAs

Jeannie T. Lee, M.D., Ph.D., professor of genetics and pathology,

Harvard Medical School, investigator,

Howard Hughes Medical Institute

January 27, 2012

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

Recommended Readings:

Lengner, C. J., A. A. Gimelbrant, J. A. Erwin, A. W. Cheng, M. G. Guenther, G. G. Welstead, R. Alagappan, et al. 2010. Derivation of pre-X inactivation human embryonic stem cells under physiological oxygen concentrations. Cell 141, (5): 872-883

Namekawa, S. H., B. Payer, K. D. Huynh, R. Jaenisch, and J. T. Lee. 2010. Two-step imprinted X inactivation: Repeat versus genic silencing in the mouse. Molecular and cellular biology 30, (13): 3187-3205

Sarma, K., P. Levasseur, A. Aristarkhov, and J. T. Lee. 2010. Locked nucleic acids (LNAs) reveal sequence requirements and kinetics of xist RNA localization to the X chromosome. Proceedings of the National Academy of Sciences of the United States of America 107, (51): 22196-22201

Tian, D., S. Sun, and J. T. Lee. 2010. The long noncoding RNA, jpx, is a molecular switch for X chromosome inactivation. Cell 143, (3): 390-403

Zhou, D., C. Conrad, F. Xia, J. -S Park, B. Payer, Y. Yin, G. Y. Lauwers, et al. 2009. Mst1 and Mst2 maintain hepatocyte quiescence and Suppress hepatocellular carcinoma development through inactivation of the Yap1 oncogene. Cancer Cell 16, (5): 425-438

“Democratizing science?” Play Video Games to Fold RNA

First Foldit, then Phylo, now EteRNA. Investigators at Carnegie Mellon University and Stanford University have launched “an online video game that challenges players to design new ways to fold RNA molecules,” reports The New York Times. EteRNA, which was designed for non-scientists, allows players to “design elaborate [RNA] structures including knots, lattices and switches,” the Times reports, adding that the game will go beyond simulations, in that “each week the best designs created by game players and chosen by the gaming community will be synthesized at Stanford.” Carnegie Mellon’s Adrien Treuille, who was part of the team that created Foldit, tells the Times that EteRNA “is like putting a molecular chess game in people’s hands at a massive level. … I think we are democratizing science.” Users must register for a free account on the EteRNA homepage, which greets visitors with the message “played by humans, scored by nature.”

Recommended Readings: Jennifer A. Doudna, Ph.D.; May 8, 2009

Friday Lecture Series

“Dicer and Beyond: Regulatory RNA Processing and Function”

Jennifer A. Doudna, Ph.D., professor, departments of molecular and cell biology and of chemistry; investigator, Howard Hughes Medical Institute

University of California, Berkeley

May 8, 2009

3:45 p.m.-5:00 p.m. (Refreshments, 3:15 p.m., Abby Lounge)

Caspary Auditorium

Recommended Articles:

Aggarwal, A. K., and J. A. Doudna. 2005. Protein-nucleic acid interactions: Unlocking mysteries old and new. Current opinion in structural biology. 15(1 SPEC. ISS.):65-67.

 

Fukunaga, R., and J. A. Doudna. 2009. dsRNA with 5′ overhangs contributes to endogenous and antiviral RNA silencing pathways in plants. EMBO Journal. 28(5):545-555.

 

Jinek, M., and J. A. Doudna. 2009. A three-dimensional view of the molecular machinery of RNA interference. Nature. 457(7228):405-412.

 

Ma, E., I. J. MacRae, J. F. Kirsch, and J. A. Doudna. 2008. Autoinhibition of human dicer by its internal helicase domain. Journal of Molecular Biology. 380(1):237-243.

 

MacRae, I. J., and J. A. Doudna. 2007. Ribonuclease revisited: Structural insights into ribonuclease III family enzymes. Current opinion in structural biology. 17(1):138-145.

 

MacRae, I. J., K. Zhou, and J. A. Doudna. 2007. Structural determinants of RNA recognition and cleavage by dicer. Nature Structural and Molecular Biology. 14(10):934-940.

 

MacRae, I. J., K. Zhou, F. Li, A. Repic, A. N. Brooks, W. Z. Cande, P. D. Adams, and J. A. Doudna. 2006. Structural basis for double-stranded RNA processing by dicer. Science. 311(5758):195-198.

Wistar Raises Hopes for Block on Cancer

In an article published Aug. 31 in Nature online, researchers at The Wistar Institute have elucidated an active region of telomerase, an enzyme that plays a major role in the development of most human cancers.  This discovery could open the door for discovering new drugs that shut down telomerase.  The enzyme is inactive in most normal cells.

The research provides the first full-length view of the telomerase active region and how its configuration works to replicate the ends of chromosomes.  The enzyme has a complex structure of multiple protein domains and a stretch of RNA.  Many cancer cells hijack the telomerase system to promote their uninhibited growth.  Deactivating the enzyme could likely work against cancers, with few side effects.

Extracted from BBC News, Medical News Today, and Nature