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4 results on '"Eaton, Matthew L"'

1. Developmental control of gene copy number by repression of replication initiation and fork progression.

Author

Sher N, Bell GW, Li S, Nordman J, Eng T, Eaton ML, Macalpine DM, and Orr-Weaver TL

Subjects
Animals, Cell Differentiation physiology, DNA-Binding Proteins genetics, Drosophila Proteins genetics, Drosophila melanogaster, Histones genetics, Polytene Chromosomes genetics, DNA Replication physiology, DNA-Binding Proteins metabolism, Drosophila Proteins metabolism, Gene Dosage physiology, Gene Expression Regulation, Developmental physiology, Histones metabolism, Polytene Chromosomes metabolism
Abstract

Precise DNA replication is crucial for genome maintenance, yet this process has been inherently difficult to study on a genome-wide level in untransformed differentiated metazoan cells. To determine how metazoan DNA replication can be repressed, we examined regions selectively under-replicated in Drosophila polytene salivary glands, and found they are transcriptionally silent and enriched for the repressive H3K27me3 mark. In the first genome-wide analysis of binding of the origin recognition complex (ORC) in a differentiated metazoan tissue, we find that ORC binding is dramatically reduced within these large domains, suggesting reduced initiation as one mechanism leading to under-replication. Inhibition of replication fork progression by the chromatin protein SUUR is an additional repression mechanism to reduce copy number. Although repressive histone marks are removed when SUUR is mutated and copy number restored, neither transcription nor ORC binding is reinstated. Tethering of the SUUR protein to a specific site is insufficient to block replication, however. These results establish that developmental control of DNA replication, at both the initiation and elongation stages, is a mechanism to change gene copy number during differentiation.

Published
2012
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2. Identification of Functional Elements and Regulatory Circuits by Drosophila modENCODE

Author

The modeENCODE Consortium, Roy, Sushmita, Ernst, Jason, Kharchenko, Peter V., Kheradpour, Pouya, Negre, Nicolas, Eaton, Matthew L., Landolin, Jane M., Bristow, Christopher A., Ma, Lijia, Lin, Michael F., Washietl, Stefan, Arshinoff, Bradley I., Ay, Ferhat, Meyer, Patrick E., Robine, Nicolas, Washington, Nicole L., Di Stefano, Luisa, Berezikov, Eugene, Brown, Christopher D., Candeias, Rogerio, Carlson, Joseph W., Carr, Adrian, Jungreis, Irwin, Marbach, Daniel, Sealfon, Rachel, Tolstorukov, Michael Y., Will, Sebastian, Alekseyenko, Artyom A., Artieri, Carlo, Booth, Benjamin W., Brooks, Angela N., Dai, Qi, Davis, Carrie A., Duff, Michael O., Feng, Xin, Gorchakov, Andrey A., Gu, Tingting, Henikoff, Jorja G., Kapranov, Philipp, Li, Renhua, MacAlpine, Heather K., Malone, John, Minoda, Aki, Nordman, Jared, Okamura, Katsutomo, Perry, Marc, Powell, Sara K., Riddle, Nicole C., Sakai, Akiko, Samsonova, Anastasia, Sandler, Jeremy E., Schwartz, Yuri B., Sher, Noa, Spokony, Rebecca, Sturgill, David, van Baren, Marijke, Wan, Kenneth H., Yang, Li, Yu, Charles, Feingold, Elise, Good, Peter, Guyer, Mark, Lowdon, Rebecca, Ahmad, Kami, Andrews, Justen, Berger, Bonnie, Brenner, Steven E., Brent, Michael R., Cherbas, Lucy, Elgin, Sarah C. R., Gingeras, Thomas R., Grossman, Robert, Hoskins, Roger A., Kaufman, Thomas C., Kent, William, Kuroda, Mitzi I., Orr-Weaver, Terry, Perrimon, Norbert, Pirrotta, Vincenzo, Posakony, James W., Ren, Bing, Russell, Steven, Cherbas, Peter, Graveley, Brenton R., Lewis, Suzanna, Micklem, Gos, Oliver, Brian, Park, Peter J., Celniker, Susan E., Henikoff, Steven, Karpen, Gary H., Lai, Eric C., MacAlpine, David M., Stein, Lincoln D., White, Kevin P., and Kellis, Manolis

Published
2010

3. Identification of functional elements and regulatory circuits by Drosophila modENCODE

Author

Roy, Sushmita, Ernst, Jason, Kharchenko, Peter V., Kheradpour, Pouya, Negre, Nicolas, Eaton, Matthew L., Landolin, Jane M., Bristow, Christopher A., Ma, Lijia, Lin, Michael F., Washietl, Stefan, Arshinoff, Bradley I., Ay, Ferhat, Meyer, Patrick E., Robine, Nicolas, Washington, Nicole L., Di Stefano, Luisa, Berezikov, Eugene, Brown, Christopher D., Candeias, Rogerio, Carlson, Joseph W., Carr, Adrian, Jungreis, Irwin, Marbach, Daniel, Sealfon, Rachel, Tolstorukov, Michael Y., Will, Sebastian, Alekseyenko, Artyom A., Artieri, Carlo, Booth, Benjamin W., Brooks, Angela N., Dai, Qi, Davis, Carrie A., Duff, Michael O., Feng, Xin, Gorchakov, Andrey A., Gu, Tingting, Henikoff, Jorja G., Kapranov, Philipp, Li, Renhua, MacAlpine, Heather K., Malone, John, Minoda, Aki, Nordman, Jared, Okamura, Katsutomo, Perry, Marc, Powell, Sara K., Riddle, Nicole C., Sakai, Akiko, Samsonova, Anastasia A., Sandler, Jeremy E., Schwartz, Yuri B., Sher, Noa, Spokony, Rebecca, Sturgill, David, van Baren, Marijke, Wan, Kenneth H., Yang, Li, Yu, Charles, Feingold, Elise, Good, Peter, Guyer, Mark, Lowdon, Rebecca, Ahmad, Kami, Andrews, Justen, Berger, Bonnie, Brenner, Steven E., Brent, Michael R., Cherbas, Lucy, Elgin, Sarah C.R., Gingeras, Thomas R., Grossman, Robert, Hoskins, Roger A., Kaufman, Thomas C., Kent, William, Kuroda, Mitzi I., Orr-Weaver, Terry, Perrimon, Norbert, Pirrotta, Vincenzo, Posakony, James W., Ren, Bing, Russell, Steven, Cherbas, Peter, Graveley, Brenton R., Lewis, Suzanna, Micklem, Gos, Oliver, Brian, Park, Peter J., Celniker, Susan E., Henikoff, Steven, Karpen, Gary H., Lai, Eric C., MacAlpine, David M., Stein, Lincoln D., White, Kevin P., Kellis, Manolis, Booth, Benjamin, Comstock, Charles L.G., Dobin, Alex, Drenkow, Jorg, Dudoit, Sandrine, Dumais, Jacqueline, Fagegaltier, Delphine, Ghosh, Srinka, Hansen, Kasper D., Jha, Sonali, Langton, Laura, Lin, Wei, Miller, David, Tenney, Aaron E., Wang, Huaien, Willingham, Aarron T., Zaleski, Chris, Zhang, Dayu, Acevedo, David, Bishop, Eric P., Gadel, Sarah E., Jung, Youngsook L., Kennedy, Cameron D., Lee, Ok Kyung, Linder-Basso, Daniela, Marchetti, Sarah E., Shanower, Gregory, Nègre, Nicolas, Grossman, Robert L., Auburn, Richard, Bellen, Hugo J., Chen, Jia, Domanus, Marc H., Hanley, David, Heinz, Elizabeth, Li, Zirong, Meyer, Folker, Miller, Steven W., Morrison, Carolyn A., Scheftner, Douglas A., Senderowicz, Lionel, Shah, Parantu K., Suchy, Sarah, Tian, Feng, Venken, Koen J.T., White, Robert, Wilkening, Jared, Zieba, Jennifer, Nordman, Jared T., Orr-Weaver, Terry L., DeNapoli, Leyna C., Ding, Queying, Eng, Thomas, Kashevsky, Helena, Li, Sharon, Prinz, Joseph A., Hannon, Gregory J., Hirst, Martin, Marra, Marco, Rooks, Michelle, Zhao, Yongjun, Bryson, Terri D., Perry, Marc D., Kent, William J., Lewis, Suzanna E., Barber, Galt, Chateigner, Aurelien, Clawson, Hiram, Contrino, Sergio, Guillier, Francois, Hinrichs, Angie S., Kephart, Ellen T., Lloyd, Paul, Lyne, Rachel, McKay, Sheldon, Moore, Richard A., Mungall, Chris, Rutherford, Kim M., Ruzanov, Peter, Smith, Richard, Stinson, E. O., Zha, Zheng, Artieri, Carlo G., Malone, John H., Jiang, Lichun, Mattiuzzo, Nicolas, Feingold, Elise A., Good, Peter J., Guyer, Mark S., Lowdon, Rebecca F., Stem Cell Aging Leukemia and Lymphoma (SALL), and Restoring Organ Function by Means of Regenerative Medicine (REGENERATE)

Subjects
Transcription, Genetic, Genome, Insect, Gene regulatory network, Genomics, Genes, Insect, Computational biology, Biology, Genome, Article, Epigenesis, Genetic, Histones, Nucleosome, Animals, Drosophila Proteins, Gene Regulatory Networks, Promoter Regions, Genetic, Gene, Genetics, Multidisciplinary, Binding Sites, REDfly, Computational Biology, Molecular Sequence Annotation, Chromatin, Nucleosomes, Drosophila melanogaster, Gene Expression Regulation, RNA, Small Untranslated, Drosophila Protein, Transcription Factors
Abstract

From Genome to Regulatory Networks For biologists, having a genome in hand is only the beginning—much more investigation is still needed to characterize how the genome is used to help to produce a functional organism (see the Perspective by Blaxter ). In this vein, Gerstein et al. (p. 1775 ) summarize for the Caenorhabditis elegans genome, and The modENCODE Consortium (p. 1787 ) summarize for the Drosophila melanogaster genome, full transcriptome analyses over developmental stages, genome-wide identification of transcription factor binding sites, and high-resolution maps of chromatin organization. Both studies identified regions of the nematode and fly genomes that show highly occupied targets (or HOT) regions where DNA was bound by more than 15 of the transcription factors analyzed and the expression of related genes were characterized. Overall, the studies provide insights into the organization, structure, and function of the two genomes and provide basic information needed to guide and correlate both focused and genome-wide studies.

Published
2010

4. Noncoding Transcription Is a Driving Force for Nucleosome Instability in spt16 Mutant Cells.

Author

Jianxun Feng, Haiyun Gan, Eaton, Matthew L., Hui Zhou, Shuqi Li, Belsky, Jason A., MacAlpine, David M., Zhiguo Zhang, and Qing Li

Subjects
CHROMATIN, HISTONES, GENETIC mutation, RNA polymerase II, GENETIC transcription
Abstract

FACT (facilitates chromatin transcription) consists of two essential subunits, Spt16 and Pob3, and functions as a histone chaperone. Mutation of spt16 results in a global loss of nucleosomes as well as aberrant transcription. Here, we show that the majority of nucleosome changes upon Spt16 depletion are alterations in nucleosome fuzziness and position shift. Most nucleosomal changes are suppressed by the inhibition of RNA polymerase II (Pol II) activity. Surprisingly, a small subgroup of nucleosome changes is resistant to transcriptional inhibition. Notably, Spt16 and distinct histone modifications are enriched at this subgroup of nucleosomes. We also report 1,037 Spt16-suppressed noncoding transcripts (SNTs) and found that the SNT start sites are enriched with the subgroup of nucleosomes resistant to Pol II inhibition. Finally, the nucleosomes at genes overlapping SNTs are more susceptible to changes upon Spt16 depletion than those without SNTs. Taken together, our results support a model in which Spt16 has a role in maintaining local nucleosome stability to inhibit initiation of SNT transcription, which once initiated drives additional nucleosome loss upon Spt16 depletion. [ABSTRACT FROM AUTHOR]

Published
2016
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