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Article ; Online: Accelerated transcriptional elongation during aging impairs longevity.

Tyshkovskiy, Alexander / Zhang, Sirui / Gladyshev, Vadim N

2023 Volume 33, Issue 11, Page(s) 817–818

MeSH term(s)	Longevity/genetics ; Oxidative Stress
Language	English
Publishing date	2023-05-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/s41422-023-00829-9
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Article ; Online: There is no evidence of SARS-CoV-2 laboratory origin: Response to Segreto and Deigin (DOI: 10.1002/bies.202000240).

Tyshkovskiy, Alexander / Panchin, Alexander Y

BioEssays : news and reviews in molecular, cellular and developmental biology

2021 Volume 43, Issue 5, Page(s) e2000325

Abstract: The origin of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the subject of many hypotheses. One of them, proposed by Segreto and Deigin, assumes artificial chimeric construction of SARS-CoV-2 from a backbone of RaTG13-like CoV and ... ...

Abstract	The origin of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the subject of many hypotheses. One of them, proposed by Segreto and Deigin, assumes artificial chimeric construction of SARS-CoV-2 from a backbone of RaTG13-like CoV and receptor binding domain (RBD) of a pangolin MP789-like CoV, followed by serial cell or animal passage. Here we show that this hypothesis relies on incorrect or weak assumptions, and does not agree with the results of comparative genomics analysis. The genetic divergence between SARS-CoV-2 and both its proposed ancestors is too high to have accumulated in a lab, given the timeframe of several years. Furthermore, comparative analysis of S-protein gene sequences suggests that the RBD of SARS-CoV-2 probably represents an ancestral non-recombinant variant. These and other arguments significantly weaken the hypothesis of a laboratory origin for SARS-CoV-2, while the hypothesis of a natural origin is consistent with all available genetic and experimental data.
MeSH term(s)	Animals ; COVID-19 ; Chiroptera ; Humans ; Laboratories ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus
Chemical Substances	Spike Glycoprotein, Coronavirus
Language	English
Publishing date	2021-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202000325
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Article ; Online: There is still no evidence of SARS-CoV-2 laboratory origin: Response to Segreto and Deigin (10.1002/bies.202100137).

Tyshkovskiy, Alexander / Panchin, Alexander Y

BioEssays : news and reviews in molecular, cellular and developmental biology

2021 Volume 43, Issue 12, Page(s) e2100194

Abstract: The causative agent of COVID-19 SARS-CoV-2 has led to over 4 million deaths worldwide. Understanding the origin of this coronavirus is important for the prevention of future outbreaks. The dominant point of view that the virus transferred to humans ... ...

Abstract	The causative agent of COVID-19 SARS-CoV-2 has led to over 4 million deaths worldwide. Understanding the origin of this coronavirus is important for the prevention of future outbreaks. The dominant point of view that the virus transferred to humans either directly from bats or through an intermediate mammalian host has been challenged by Segreto and Deigin, who claim that the genome of SARS-CoV-2 has certain features suggestive of its artificial creation. Following their response to our commentary, here we continue the discussion of the proposed arguments for this hypothesis. We show that neither the existence of a furin cleavage site in SARS-CoV-2, nor the presence of specific sequences within the nucleotide insertion encoding that site are evidence for intelligent design. We also explain why existing genetic data, viral diversity and past human history suggest that a natural origin of the virus is the most likely scenario. Genetic evidence suggesting otherwise is yet to be presented.
MeSH term(s)	Animals ; COVID-19 ; Chiroptera ; Humans ; Laboratories ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus
Chemical Substances	Spike Glycoprotein, Coronavirus
Language	English
Publishing date	2021-10-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202100194
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Article ; Online: AgeMeta: Quantitative Gene Expression Database of Mammalian Aging.

Tikhonov, Stanislav / Batin, Mikhail / Gladyshev, Vadim N / Dmitriev, Sergey E / Tyshkovskiy, Alexander

Biochemistry. Biokhimiia

2024 Volume 89, Issue 2, Page(s) 313–321

Abstract: AgeMeta is a database that provides systemic and quantitative description of mammalian aging at the level of gene expression. It encompasses transcriptomic changes with age across various tissues of humans, mice, and rats, based on a comprehensive meta- ... ...

Abstract	AgeMeta is a database that provides systemic and quantitative description of mammalian aging at the level of gene expression. It encompasses transcriptomic changes with age across various tissues of humans, mice, and rats, based on a comprehensive meta-analysis of 122 publicly available gene expression datasets from 26 studies. AgeMeta provides an intuitive visual interface for quantification of aging-associated transcriptomics at the level of individual genes and functional groups of genes, allowing easy comparison among various species and tissues. Additionally, all the data in the database can be downloaded and analyzed independently. Overall, this work contributes to the understanding of the complex network of biological processes underlying mammalian aging and supports future advancements in this field. AgeMeta is freely available at: https://age-meta.com/.
MeSH term(s)	Rats ; Mice ; Humans ; Animals ; Gene Expression Profiling ; Transcriptome ; Aging/genetics ; Databases, Factual ; Mammals/genetics
Language	English
Publishing date	2024-03-11
Publishing country	United States
Document type	Meta-Analysis ; Journal Article
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S000629792402010X
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Article: There is no evidence of SARS‐CoV‐2 laboratory origin: Response to Segreto and Deigin (DOI: 10.1002/bies.202000240)

Tyshkovskiy, Alexander / Panchin, Alexander Y

BioEssays. 2021 May, v. 43, no. 5

2021

Abstract: The origin of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the subject of many hypotheses. One of them, proposed by Segreto and Deigin, assumes artificial chimeric construction of SARS‐CoV‐2 from a backbone of RaTG13‐like CoV and ... ...

Abstract	The origin of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the subject of many hypotheses. One of them, proposed by Segreto and Deigin, assumes artificial chimeric construction of SARS‐CoV‐2 from a backbone of RaTG13‐like CoV and receptor binding domain (RBD) of a pangolin MP789‐like CoV, followed by serial cell or animal passage. Here we show that this hypothesis relies on incorrect or weak assumptions, and does not agree with the results of comparative genomics analysis. The genetic divergence between SARS‐CoV‐2 and both its proposed ancestors is too high to have accumulated in a lab, given the timeframe of several years. Furthermore, comparative analysis of S‐protein gene sequences suggests that the RBD of SARS‐CoV‐2 probably represents an ancestral non‐recombinant variant. These and other arguments significantly weaken the hypothesis of a laboratory origin for SARS‐CoV‐2, while the hypothesis of a natural origin is consistent with all available genetic and experimental data.
Keywords	Severe acute respiratory syndrome coronavirus 2 ; animals ; genes ; genetic variation ; genomics
Language	English
Dates of publication	2021-05
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	NAL-AP-2-clean ; JOURNAL ARTICLE
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202000325
Database	NAL-Catalogue (AGRICOLA)

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Article: There is still no evidence of SARS‐CoV‐2 laboratory origin: Response to Segreto and Deigin (10.1002/bies.202100137)

Tyshkovskiy, Alexander / Panchin, Alexander Y.

BioEssays. 2021 Dec., v. 43, no. 12

2021

Abstract: The causative agent of COVID‐19 SARS‐CoV‐2 has led to over 4 million deaths worldwide. Understanding the origin of this coronavirus is important for the prevention of future outbreaks. The dominant point of view that the virus transferred to humans ... ...

Abstract	The causative agent of COVID‐19 SARS‐CoV‐2 has led to over 4 million deaths worldwide. Understanding the origin of this coronavirus is important for the prevention of future outbreaks. The dominant point of view that the virus transferred to humans either directly from bats or through an intermediate mammalian host has been challenged by Segreto and Deigin, who claim that the genome of SARS‐CoV‐2 has certain features suggestive of its artificial creation. Following their response to our commentary, here we continue the discussion of the proposed arguments for this hypothesis. We show that neither the existence of a furin cleavage site in SARS‐CoV‐2, nor the presence of specific sequences within the nucleotide insertion encoding that site are evidence for intelligent design. We also explain why existing genetic data, viral diversity and past human history suggest that a natural origin of the virus is the most likely scenario. Genetic evidence suggesting otherwise is yet to be presented.
Keywords	COVID-19 infection ; Severe acute respiratory syndrome coronavirus 2 ; etiological agents ; genome ; humans ; viruses
Language	English
Dates of publication	2021-12
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	JOURNAL ARTICLE
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202100194
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Rilmenidine extends lifespan and healthspan in Caenorhabditis elegans via a nischarin I1-imidazoline receptor.

Bennett, Dominic F / Goyala, Anita / Statzer, Cyril / Beckett, Charles W / Tyshkovskiy, Alexander / Gladyshev, Vadim N / Ewald, Collin Y / de Magalhães, João Pedro

Aging cell

2023 Volume 22, Issue 2, Page(s) e13774

Abstract: Repurposing drugs capable of extending lifespan and health span has a huge untapped potential in translational geroscience. Here, we searched for known compounds that elicit a similar gene expression signature to caloric restriction and identified ... ...

Abstract	Repurposing drugs capable of extending lifespan and health span has a huge untapped potential in translational geroscience. Here, we searched for known compounds that elicit a similar gene expression signature to caloric restriction and identified rilmenidine, an I1-imidazoline receptor agonist and prescription medication for the treatment of hypertension. We then show that treating Caenorhabditis elegans with rilmenidine at young and older ages increases lifespan. We also demonstrate that the stress-resilience, health span, and lifespan benefits of rilmenidine treatment in C. elegans are mediated by the I1-imidazoline receptor nish-1, implicating this receptor as a potential longevity target. Consistent with the shared caloric-restriction-mimicking gene signature, supplementing rilmenidine to calorically restricted C. elegans, genetic reduction of TORC1 function, or rapamycin treatment did not further increase lifespan. The rilmenidine-induced longevity required the transcription factors FOXO/DAF-16 and NRF1,2,3/SKN-1. Furthermore, we find that autophagy, but not AMPK signaling, was needed for rilmenidine-induced longevity. Moreover, transcriptional changes similar to caloric restriction were observed in liver and kidney tissues in mice treated with rilmenidine. Together, these results reveal a geroprotective and potential caloric restriction mimetic effect by rilmenidine that warrant fresh lines of inquiry into this compound.
MeSH term(s)	Animals ; Mice ; Caenorhabditis elegans/metabolism ; Rilmenidine/pharmacology ; Imidazoline Receptors/metabolism ; Longevity ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Forkhead Transcription Factors/metabolism
Chemical Substances	Rilmenidine (P67IM25ID8) ; Imidazoline Receptors ; Caenorhabditis elegans Proteins ; Forkhead Transcription Factors
Language	English
Publishing date	2023-01-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13774
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Multi-omics characterization of partial chemical reprogramming reveals evidence of cell rejuvenation.

Mitchell, Wayne / Goeminne, Ludger J E / Tyshkovskiy, Alexander / Zhang, Sirui / Chen, Julie Y / Paulo, Joao A / Pierce, Kerry A / Choy, Angelina H / Clish, Clary B / Gygi, Steven P / Gladyshev, Vadim N

eLife

2024 Volume 12

Abstract: Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma ...

Abstract	Partial reprogramming by cyclic short-term expression of Yamanaka factors holds promise for shifting cells to younger states and consequently delaying the onset of many diseases of aging. However, the delivery of transgenes and potential risk of teratoma formation present challenges for in vivo applications. Recent advances include the use of cocktails of compounds to reprogram somatic cells, but the characteristics and mechanisms of partial cellular reprogramming by chemicals remain unclear. Here, we report a multi-omics characterization of partial chemical reprogramming in fibroblasts from young and aged mice. We measured the effects of partial chemical reprogramming on the epigenome, transcriptome, proteome, phosphoproteome, and metabolome. At the transcriptome, proteome, and phosphoproteome levels, we saw widescale changes induced by this treatment, with the most notable signature being an upregulation of mitochondrial oxidative phosphorylation. Furthermore, at the metabolome level, we observed a reduction in the accumulation of aging-related metabolites. Using both transcriptomic and epigenetic clock-based analyses, we show that partial chemical reprogramming reduces the biological age of mouse fibroblasts. We demonstrate that these changes have functional impacts, as evidenced by changes in cellular respiration and mitochondrial membrane potential. Taken together, these results illuminate the potential for chemical reprogramming reagents to rejuvenate aged biological systems and warrant further investigation into adapting these approaches for in vivo age reversal.
MeSH term(s)	Animals ; Mice ; Rejuvenation/physiology ; Proteome/metabolism ; Multiomics ; Cellular Reprogramming/genetics ; Aging/physiology ; Induced Pluripotent Stem Cells/metabolism
Chemical Substances	Proteome
Language	English
Publishing date	2024-03-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.90579
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Article ; Online: Global remodeling of the mouse DNA methylome during aging and in response to calorie restriction.

Sziráki, András / Tyshkovskiy, Alexander / Gladyshev, Vadim N

Aging cell

2018 Volume 17, Issue 3, Page(s) e12738

Abstract: Aging is characterized by numerous molecular changes, such as accumulation of molecular damage and altered gene expression, many of which are linked to DNA methylation. Here, we characterize the blood DNA methylome across 16 age groups of mice and report ...

Abstract	Aging is characterized by numerous molecular changes, such as accumulation of molecular damage and altered gene expression, many of which are linked to DNA methylation. Here, we characterize the blood DNA methylome across 16 age groups of mice and report numerous global, region- and site-specific features, as well as the associated dynamics of methylation changes. Transition of the methylome throughout lifespan was not uniform, with many sites showing accelerated changes in late life. The associated genes and promoters were enriched for aging-related pathways, pointing to a fundamental link between DNA methylation and control of the aging process. Calorie restriction both shifted the overall methylation pattern and was accompanied by its gradual age-related remodeling, the latter contributing to the lifespan-extending effect. With age, both highly and poorly methylated sites trended toward intermediate levels, and aging was accompanied by an accelerated increase in entropy, consistent with damage accumulation. However, the entropy effects differed for the sites that increased, decreased and did not change methylation with age. Many sites trailed behind, whereas some followed or even exceeded the entropy trajectory and altered the developmental DNA methylation pattern. The patterns we observed in certain genomic regions were conserved between humans and mice, suggesting common principles of functional DNA methylome remodeling and its critical role in aging. The highly resolved DNA methylome remodeling provides an excellent model for understanding systemic changes that characterize the aging process.
MeSH term(s)	Aging/genetics ; Animals ; Caloric Restriction/methods ; DNA/genetics ; DNA Methylation/genetics ; Mice
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2018-03-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12738
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Article: A torpor-like state (TLS) in mice slows blood epigenetic aging and prolongs healthspan.

Jayne, Lorna / Lavin-Peter, Aurora / Roessler, Julian / Tyshkovskiy, Alexander / Antoszewski, Mateusz / Ren, Erika / Markovski, Aleksandar / Sun, Senmiao / Yao, Hanqi / Sankaran, Vijay G / Gladyshev, Vadim N / Brooke, Robert T / Horvath, Steve / Griffith, Eric C / Hrvatin, Sinisa

bioRxiv : the preprint server for biology

2024

Abstract: Torpor and hibernation are extreme physiological adaptations of homeotherms associated with pro-longevity effects. Yet the underlying mechanisms of how torpor affects aging, and whether hypothermic and hypometabolic states can be induced to slow aging ... ...

Abstract	Torpor and hibernation are extreme physiological adaptations of homeotherms associated with pro-longevity effects. Yet the underlying mechanisms of how torpor affects aging, and whether hypothermic and hypometabolic states can be induced to slow aging and increase health span, remain unknown. We demonstrate that the activity of a spatially defined neuronal population in the avMLPA, which has previously been identified as a torpor-regulating brain region, is sufficient to induce a torpor like state (TLS) in mice. Prolonged induction of TLS slows epigenetic aging across multiple tissues and improves health span. We isolate the effects of decreased metabolic rate, long-term caloric restriction, and decreased core body temperature (T
Language	English
Publishing date	2024-03-25
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.20.585828
Database	MEDical Literature Analysis and Retrieval System OnLINE

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