7 results on '"Margarita V. Meer"'
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2. Local fitness landscape of the green fluorescent protein.
- Author
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Karen S. Sarkisyan, Dmitry Bolotin, Margarita V. Meer, Dinara R. Usmanova, Alexander S. Mishin, George V. Sharonov, Dmitry N. Ivankov, Nina G. Bozhanova, Mikhail S. Baranov, Onuralp Soylemez, Natalya S. Bogatyreva, Peter K. Vlasov, Evgeny S. Egorov, Maria D. Logacheva, Alexey S. Kondrashov, Dmitry M. Chudakov, Ekaterina V. Putintseva, Ilgar Z. Mamedov, Dan S. Tawfik, Konstantin A. Lukyanov, and Fyodor A. Kondrashov
- Published
- 2016
- Full Text
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3. A whole lifespan mouse multi-tissue DNA methylation clock
- Author
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Margarita V Meer, Dmitriy I Podolskiy, Alexander Tyshkovskiy, and Vadim N Gladyshev
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aging ,DNA methylation ,biological age ,clock ,lifespan ,Medicine ,Science ,Biology (General) ,QH301-705.5 - Abstract
Age predictors based on DNA methylation levels at a small set of CpG sites, DNAm clocks, have been developed for humans and extended to several other species. Three currently available versions of mouse DNAm clocks were either created for individual tissues or tuned toward young ages. Here, we constructed a robust multi-tissue age predictor based on 435 CpG sites, which covers the entire mouse lifespan and remains unbiased with respect to any particular age group. It can successfully detect the effects of certain lifespan-modulating interventions on DNAm age as well as the rejuvenation effect related to the transition from fibroblasts to iPSCs. We have carried out comparative analyses of available mouse DNAm clocks, which revealed their broad applicability, but also certain limitations to the use of tissue-specific and multi-tissue age predictors. Together, these tools should help address diverse questions in aging research.
- Published
- 2018
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4. Loss of epigenetic information as a cause of mammalian aging
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Jae-Hyun Yang, Motoshi Hayano, Patrick T. Griffin, João A. Amorim, Michael S. Bonkowski, John K. Apostolides, Elias L. Salfati, Marco Blanchette, Elizabeth M. Munding, Mital Bhakta, Yap Ching Chew, Wei Guo, Xiaojing Yang, Sun Maybury-Lewis, Xiao Tian, Jaime M. Ross, Giuseppe Coppotelli, Margarita V. Meer, Ryan Rogers-Hammond, Daniel L. Vera, Yuancheng Ryan Lu, Jeffrey W. Pippin, Michael L. Creswell, Zhixun Dou, Caiyue Xu, Sarah J. Mitchell, Abhirup Das, Brendan L. O’Connell, Sachin Thakur, Alice E. Kane, Qiao Su, Yasuaki Mohri, Emi K. Nishimura, Laura Schaevitz, Neha Garg, Ana-Maria Balta, Meghan A. Rego, Meredith Gregory-Ksander, Tatjana C. Jakobs, Lei Zhong, Hiroko Wakimoto, Jihad El Andari, Dirk Grimm, Raul Mostoslavsky, Amy J. Wagers, Kazuo Tsubota, Stephen J. Bonasera, Carlos M. Palmeira, Jonathan G. Seidman, Christine E. Seidman, Norman S. Wolf, Jill A. Kreiling, John M. Sedivy, George F. Murphy, Richard E. Green, Benjamin A. Garcia, Shelley L. Berger, Philipp Oberdoerffer, Stuart J. Shankland, Vadim N. Gladyshev, Bruce R. Ksander, Andreas R. Pfenning, Luis A. Rajman, and David A. Sinclair
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General Biochemistry, Genetics and Molecular Biology - Published
- 2023
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5. TIME-Seq Enables Scalable and Inexpensive Epigenetic Age Predictions
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Patrick T Griffin, Alice E Kane, Alexandre Trapp, Jien Li, Matthew Arnold, Jesse R Poganik, Maeve S McNamara, Margarita V Meer, Noah Hoffman, João Amorim, Xiao Tian, Michael R MacArthur, Sarah J Mitchell, Amber L Mueller, Colleen Carmody, Daniel L Vera, Csaba Kerepesi, Nicole Noren Hooten, James R Mitchell, Michele K Evans, Vadim N Gladyshev, and David A Sinclair
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Computer science ,Scalability ,DNA methylation ,Epigenetics ,Computational biology ,Biomarker Analysis - Abstract
Epigenetic “clocks” based on DNA methylation (DNAme) have emerged as the most robust and widely employed aging biomarkers, but conventional methods for applying them are expensive and laborious. Here, we developTagmentation-based Indexing forMethylationSequencing (TIME-Seq), a highly multiplexed and scalable method for low-cost epigenetic clocks. Using TIME-Seq, we applied multi-tissue and tissue-specific epigenetic clocks to over 1,600 mouse DNA samples. We also discovered a novel approach for age prediction from shallow sequencing (e.g., 10,000 reads) by adaptingscAgefor bulk measurements. In benchmarking experiments, TIME-Seq performed favorably against prevailing methods and could quantify the effects of interventions thought to accelerate, slow, and reverse aging in mice. Finally, we built and validated a highly accurate human blood clock from 1,056 demographically representative individuals. Our methods increase the scalability and reduce the cost of epigenetic age predictions by more than 100-fold, enabling accurate aging biomarkers to be applied in more large-scale animal and human studies.
- Published
- 2021
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6. Recent Origin of the Methacrylate Redox System in Geobacter sulfurreducens AM-1 through Horizontal Gene Transfer.
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Oksana V Arkhipova, Margarita V Meer, Galina V Mikoulinskaia, Marina V Zakharova, Alexander S Galushko, Vasilii K Akimenko, and Fyodor A Kondrashov
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Medicine ,Science - Abstract
The origin and evolution of novel biochemical functions remains one of the key questions in molecular evolution. We study recently emerged methacrylate reductase function that is thought to have emerged in the last century and reported in Geobacter sulfurreducens strain AM-1. We report the sequence and study the evolution of the operon coding for the flavin-containing methacrylate reductase (Mrd) and tetraheme cytochrome с (Mcc) in the genome of G. sulfurreducens AM-1. Different types of signal peptides in functionally interlinked proteins Mrd and Mcc suggest a possible complex mechanism of biogenesis for chromoproteids of the methacrylate redox system. The homologs of the Mrd and Mcc sequence found in δ-Proteobacteria and Deferribacteres are also organized into an operon and their phylogenetic distribution suggested that these two genes tend to be horizontally transferred together. Specifically, the mrd and mcc genes from G. sulfurreducens AM-1 are not monophyletic with any of the homologs found in other Geobacter genomes. The acquisition of methacrylate reductase function by G. sulfurreducens AM-1 appears linked to a horizontal gene transfer event. However, the new function of the products of mrd and mcc may have evolved either prior or subsequent to their acquisition by G. sulfurreducens AM-1.
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- 2015
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7. Loss of Epigenetic Information as a Cause of Mammalian Aging
- Author
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Brendan O'Connell, Xiaojing Yang, Jaime M. Ross, Yuancheng Lu, Jonathan G. Seidman, Mital Bhakta, Amy J. Wagers, João A. Amorim, Qiao Su, Bruce R. Ksander, Jae-Hyun Yang, Jill A. Kreiling, Elias L. Salfati, Stuart J. Shankland, Richard E. Green, Christine E. Seidman, Ana-Maria Balta, Andreas R. Pfenning, George F. Murphy, Michael Bonkowski, Benjamin A. Garcia, Luis A. Rajman, Patrick Griffin, Marco Blanchette, Yasuaki Mohri, Meghan A. Rego, Sarah J. Mitchell, Meredith S Gregory-Ksander, Kazuo Tsubota, Sachin Thakur, Raul Mostoslavsky, Caiyue Xu, Hiroko Wakimoto, John M. Sedivy, Norman S. Wolf, Philipp Oberdoerffer, Yap Ching Chew, John K. Apostolides, Alice E. Kane, Michael L. Creswell, Laura Schaevitz, Motoshi Hayano, Zhixun Dou, Margarita V. Meer, Giuseppe Coppotelli, Elizabeth M. Munding, Xiao Tian, Carlos M. Palmeira, Wei Guo, Shelley L. Berger, Tatjana C. Jakobs, Daniel L. Vera, Emi K. Nishimura, Lei Zhong, David A. Sinclair, Abhirup Das, Jeffrey W. Pippin, Vadim N. Gladyshev, Stephen J. Bonasera, and Neha Garg
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Senescence ,History ,Polymers and Plastics ,DNA damage ,Epigenome ,Biology ,Industrial and Manufacturing Engineering ,Chromatin ,Cell biology ,KLF4 ,Ectopic expression ,sense organs ,Epigenetics ,Business and International Management ,Reprogramming - Abstract
All living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. In yeast, epigenetic changes result in a loss of cell identity and sterility, both hallmarks of yeast aging. In mammals, epigenetic information is also lost over time, but what causes it to be lost and whether it is a cause or a consequence of aging is not known. Using a transgenic mouse system called "ICE" (for Inducible Changes to the Epigenome), we show that the process of repairing non-mutagenic DNA breaks accelerates age-related physiological, cognitive, and molecular changes, including the erosion of the epigenetic landscape, a loss of cellular identity, cellular senescence and advancement of the epigenetic clock. Epigenetic reprogramming through ectopic expression of Oct4, Sox2 and Klf4 (OSK) restores patterns of youthful gene expression. These data support a model in which a loss of epigenetic information is a cause of aging in mammals.
- Published
- 2021
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