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28 results on '"Aravamudhan, Pavithra"'

5. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease

Author

Bouziat, Romain, Hinterleitner, Reinhard, Brown, Judy J., Stencel-Baerenwald, Jennifer E., Ikizler, Mine, Mayassi, Toufic, Meisel, Marlies, Kim, Sangman M., Discepolo, Valentina, Pruijssers, Andrea J., Ernest, Jordan D., Iskarpatyoti, Jason A., Costes, Léa M. M., Lawrence, Ian, Palanski, Brad A., Varma, Mukund, Zurenski, Matthew A., Khomandiak, Solomiia, McAllister, Nicole, Aravamudhan, Pavithra, Boehme, Karl W., Hu, Fengling, Samsom, Janneke N., Reinecker, Hans-Christian, Kupfer, Sonia S., Guandalini, Stefano, Semrad, Carol E., Abadie, Valérie, Khosla, Chaitan, Barreiro, Luis B., Xavier, Ramnik J., Ng, Aylwin, Dermody, Terence S., and Jabri, Bana

Published
2017

6. NgR1 binding to reovirus reveals an unusual bivalent interaction and a new viral attachment protein

Author

Sutherland, Danica M., primary, Strebl, Michael, additional, Koehler, Melanie, additional, Welsh, Olivia L., additional, Yu, Xinzhe, additional, Hu, Liya, additional, dos Santos Natividade, Rita, additional, Knowlton, Jonathan J., additional, Taylor, Gwen M., additional, Moreno, Rodolfo A., additional, Wörz, Patrick, additional, Lonergan, Zachery R., additional, Aravamudhan, Pavithra, additional, Guzman-Cardozo, Camila, additional, Kour, Sukhleen, additional, Pandey, Udai Bhan, additional, Alsteens, David, additional, Wang, Zhao, additional, Prasad, B. V. Venkataram, additional, Stehle, Thilo, additional, and Dermody, Terence S., additional

Published
2023
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11. The human neuronal receptor NgR1 bridges reovirus capsid proteins to initiate infection

Author

Sutherland, Danica M., primary, Strebl, Michael, additional, Koehler, Melanie, additional, Welsh, Olivia L., additional, Yu, Xinzhe, additional, Hu, Liya, additional, dos Santos Natividade, Rita, additional, Knowlton, Jonathan J., additional, Taylor, Gwen M., additional, Moreno, Rodolfo A., additional, Wörz, Patrick, additional, Lonergan, Zachary R., additional, Aravamudhan, Pavithra, additional, Guzman-Cardozo, Camila, additional, Alsteens, David, additional, Wang, Zhao, additional, Prasad, B. V. V., additional, Stehle, Thilo, additional, and Dermody, Terence S., additional

Published
2021
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17. Reovirus-Induced Apoptosis in the Intestine Limits Establishment of Enteric Infection

Author

Brown, Judy J., primary, Short, Sarah P., additional, Stencel-Baerenwald, Jennifer, additional, Urbanek, Kelly, additional, Pruijssers, Andrea J., additional, McAllister, Nicole, additional, Ikizler, Mine, additional, Taylor, Gwen, additional, Aravamudhan, Pavithra, additional, Khomandiak, Solomiia, additional, Jabri, Bana, additional, Williams, Christopher S., additional, and Dermody, Terence S., additional

Published
2018
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25. Conformational dynamics of single pre-mRNA molecules during in vitro splicing

Author

Abelson, John, primary, Blanco, Mario, additional, Ditzler, Mark A, additional, Fuller, Franklin, additional, Aravamudhan, Pavithra, additional, Wood, Mona, additional, Villa, Tommaso, additional, Ryan, Daniel E, additional, Pleiss, Jeffrey A, additional, Maeder, Corina, additional, Guthrie, Christine, additional, and Walter, Nils G, additional

Published
2010
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26. Architecture-Function Analysis of the Kinetochore Reveals the Mechanism of Spindle Assembly Checkpoint Signaling.

Author

Aravamudhan, Pavithra

Subjects
Mechanism of mitotic checkpoint that ensures accurate chromosome segregation during cell division, Developmental of biophysical tools to probe and characterize macromolecular structures, Macromolecular protein architecture of kinetochore shapes emergent functions, Biochemical parameters provide handles to modulate checkpoint signaling, High resolution and fluorescence microscopy approaches to address biological problems, Quantitative approaches to define checkpoint signaling to predict implications in diseased conditions like cancer
Abstract

In a dividing cell, equal segregation of chromosomes between the two daughters is necessary for accurate genome inheritance. For successful segregation, chromosomes must attach to and move along microtubule tracks provided by the division machinery. A complex, multi-protein machine called the kinetochore establishes this attachment and generates force to move chromosomes. It also signals the absence of attachment by triggering a biochemical cascade called the Spindle Assembly Checkpoint (SAC), which in turn stalls the cell cycle. My thesis work provides mechanistic insights into this attachment-sensitive execution of the SAC by the kinetochore. These findings have significant implications in understanding how the checkpoint fails in conditions like cancer and Down's syndrome. Functionality of kinetochore emerges from its 'architecture', defined by the spatial arrangement of multiple copies of > 60 proteins. I first reconstructed this architecture in the presence of microtubule attachment by combining high resolution imaging with FRET microscopy in budding yeast. This allowed me to then probe this architecture for changes that directly controlled SAC signaling. Using novel methods, I discovered a specific attachment-sensitive change in kinetochore architecture that regulates SAC signaling. Attachment controls the spatial separation between two conserved kinetochore proteins, Ndc80 and Spc105, like a mechanical toggle-switch. This nanoscale separation of ~ 30 nm in turn controls a key phosphorylation event, to turn the SAC on or off. I then investigated the biochemical reaction cascade that acts downstream from the triggering phosphorylation event to produce the final SAC signal. To understand the operational characteristics of individual steps in this cascade, I perturbed key parameters that govern these reactions and measured the effects on the steady-state concentration of the reaction intermediates in vivo, using quantitative fluorescence microscopy. This revealed novel mechanisms that tune the maximal signaling capacity of unattached kinetochores in the cell. Two commonly occurring regulatory themes, substrate limitation and modulation of binding affinities through negative cooperativity, tune the maximal SAC signal output from unattached kinetochores. These regulations likely enable sensitive detection of unattached kinetochores, while ensuring rapid reversibility of the SAC cascade following microtubule attachment.

Published
2015

27. Cytidine Monophosphate N-Acetylneuraminic Acid Synthetase and Solute Carrier Family 35 Member A1 Are Required for Reovirus Binding and Infection.

Author

Urbanek, Kelly, Sutherland, Danica M., Orchard, Robert C., Wilen, Craig B., Knowlton, Jonathan J., Aravamudhan, Pavithra, Taylor, Gwen M., Virgin, Herbert W., and Dermody, Terence S.

Subjects
*CELL receptors, *CELL membranes, *SIALIC acids, *VIRAL tropism, *PROTEIN binding, *CELL death
Abstract

Engagement of cell surface receptors by viruses is a critical determinant of viral tropism and disease. The reovirus attachment protein σ1 binds sialylated glycans and proteinaceous receptors to mediate infection, but the specific requirements for different cell types are not entirely known. To identify host factors required for reovirus-induced cell death, we conducted a CRISPR-knockout screen targeting over 20,000 genes in murine microglial BV2 cells. Candidate genes required for reovirus to cause cell death were highly enriched for sialic acid synthesis and transport. Two of the top candidates identified, CMP N-acetylneuraminic acid synthetase (Cmas) and solute carrier family 35 member A1 (Slc35a1), promote sialic acid expression on the cell surface. Two reovirus strains that differ in the capacity to bind sialic acid, T3SA+ and T3SA-, were used to evaluate Cmas and Slc35a1 as potential host genes required for reovirus infection. Following CRISPR-Cas9 disruption of either gene, cell surface expression of sialic acid was diminished. These results correlated with decreased binding of strain T3SA+, which is capable of engaging sialic acid. Disruption of either gene did not alter the low-level binding of T3SA-, which does not engage sialic acid. Furthermore, infectivity of T3SA+ was diminished to levels similar to those of T3SA- in cells lacking Cmas and Slc35a1 by CRISPR ablation. However, exogenous expression of Cmas and Slc35a1 into the respective null cells restored sialic acid expression and T3SA+ binding and infectivity. These results demonstrate that Cmas and Slc35a1, which mediate cell surface expression of sialic acid, are required in murine microglial cells for efficient reovirus binding and infection. [ABSTRACT FROM AUTHOR]

Published
2021
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28. Plasticity and Epigenetic Inheritance of Centromere-specific Histone H3 (CENP-A)-containing Nucleosome Positioning in the Fission Yeast.

Author

Jianhui Yao, Xingkun Liu, Takeshi Sakuno, Wenzhu Li, Yuanxin Xi, Aravamudhan, Pavithra, Joglekar, Ajit, Wei Li, Watanabe, Yoshinori, and Xiangwei He

Subjects
*MATERIAL plasticity, *YEAST, *CHROMATIN, *CELL division, *EPIGENESIS, *CHROMOSOMES
Abstract

Nucleosomes containing the specific histone H3 variant CENP-A mark the centromere locus on each chromatin and initiate kinetochore assembly. For the common type of regional centromeres, little is known in molecular detail of centromeric chromatin organization, its propagation through cell division, and how distinct organization patterns may facilitate kinetochore assembly. Here, we show that in the fission yeast S. pombe, a relatively small number of CENP-A/Cnp1 nucleosomes are found within the centromeric core and that their positioning relative to underlying DNA varies among genetically homogenous cells. Consistent with the flexible positioning of Cnp1 nucleosomes, a large portion of the endogenous centromere is dispensable for its essential activity in mediating chromosome segregation. We present biochemical evidence that Cnp1 occupancy directly correlates with silencing of the underlying reporter genes. Furthermore, using a newly developed pedigree analysis assay, we demonstrated the epigenetic inheritance of Cnp1 positioning and quantified the rate of occasional repositioning of Cnp1 nucleosomes throughout cell generations. Together, our results reveal the plasticity and the epigenetically inheritable nature of centromeric chromatin organization. [ABSTRACT FROM AUTHOR]

Published
2013
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