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The genes identified in this signature organize the response of T-cells, the response of natural killer lymphocytes, or the complex factor of HLA-DRB1 antigens.
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In the quest to understand the mysterious multisystem inflammatory syndrome in children (MIS-C) associated with SARS-CoV-2, researchers have uncovered an epigenetic signature named EPIMISC. This signature, identified in a cohort study comparing healthy children, children with COVID-19 without MIS-C, and children with MIS-C, sheds light on the altered immune response and viral activity control implicated in MIS-C development.
The study, led by the Josep Carreras Leukemia Research Institute and the Bellvitge Biomedical Research Institute in Barcelona, suggests potential applications for early diagnosis and management of MIS-C, emphasizing the role of immune system hyperreactivity in severe outcomes…
A new mouse study by researchers at Northwestern Medicine offers hope as it demonstrates an epigenetics drug currently being used for blood cancers and rare sarcomas may halt the growth of bladder cancer by activating the immune system.
Tom Accart Lescarcelle's insight:
In this recent study, researchers at Northwestern Medicine have discovered that an epigenetic drug, tazemetostat, initially developed for blood cancers and rare sarcomas, shows promise in halting the growth of bladder cancer in mice. Unlike traditional tumor inhibition, this drug activates the immune system, marking a paradigm shift in treating one of the most common solid tumors. Lead author Joshua Meeks highlights the drug's unique mechanism and its potential to enhance survival in advanced bladder cancer. The study underscores the role of epigenetic therapy in bladder cancer, with tazemetostat now undergoing clinical trials for late-stage bladder cancer patients, offering a new avenue for effective treatment.
Epigenetic processes allow plasticity in gene regulation in response to significant environmental events. Accumulating evidence suggests that effective psychotherapy is accompanied by epigenetic changes, rendering DNA methylation a potential biomarker of therapy success.
Tom Accart Lescarcelle's insight:
Epigenetic processes enable plasticity in gene regulation in response to significant environmental events.
The study investigated the relationship between methylation at the glucocorticoid receptor gene (NR3C1) and the success of evidence-based psychotherapy in treating Posttraumatic Stress Disorder (PTSD). A sample of 153 conflict survivors underwent Narrative Exposure Therapy (NET), with diagnostic interviews and saliva sampling conducted at pretreatment and 4 and 10 months post-treatment.
The research explored associations between PTSD symptom development and methylation changes at 38 CpG sites spanning NR3C1 using repeated measures correlation. Notably, DNA methylation at CpG site cg25535999 exhibited a negative association with PTSD symptoms, and treatment responders showed a significant cg25535999 methylation increase post NET. Lower methylation at cg25535999 pretreatment predicted higher symptom improvement, highlighting the distinctive epigenetic profile dynamics at NR3C1 cg25535999 in therapy responders compared to non-responders.
The findings underscore the central role of glucocorticoid signaling in trauma-focused therapy.
Ageing has always been inevitable but fasting, epigenetic reprogramming and parabiosis are just some of the scientific techniques that seem to help people stay young. Might the Peter Pan dream become real?
00:00 - Can science turn back the clock? 01:01 - Centenarians 02:51 - What is ageing? 04:51 - Dietary restriction 06:00 - Roundworms 07:55 - Epigenetics 09:43 - Blood and guts 11:40 - Senolytics 12:38 - Metformin 13:51 - Anti-ageing treatments are coming
DNA methylation has been found in most invertebrate lineages except for Diptera, Placozoa and the majority of Nematoda.In contrast to the mammalian methylation toolkit that consists of one DNMT1 and several DNMT3s, some of which are catalytically inactive accessory isoforms, invertebrates have diff...
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This article delves into the complex world of DNA methylation in insects, shedding light on the unique properties of this epigenetic modification in honey bees and other invertebrates. Unlike heavily methylated mammalian genomes, invertebrate genomes exhibit sparse methylation in a 'mosaic' pattern, often associated with active transcription. The insect DNA methyltransferases (DNMTs), akin to mammalian counterparts, present distinctive combinations, such as honey bees having two DNMT1s and one DNMT3. The study underscores the lineage-specific nature of DNA methylation in insects and emphasizes the need for future research to unravel the intricate relationship between insect DNMTs, genetic variation, DNA methylation patterns, other epigenetic modifications, and the transcriptome, ultimately deciphering the role of DNA methylation in shaping insect phenotypes.
DNA methylation regulates the expression of PKMzeta, a gene implicated in long-term memory formation. Reduced levels of PKMzeta in the brain are associated with Alzheimer's disease and other memory deficit disorders.
Tom Accart Lescarcelle's insight:
The article "The Mechanism That Regulates Activity of Memory Gene" uncovers the role of DNA methylation in controlling the expression of PKMzeta, a gene crucial for long-term memory formation. Reduced levels of PKMzeta are associated with Alzheimer's disease and memory disorders.
The study, utilizing epigenetics, reveals that hypermethylation inhibits the gene, resulting in lower PKMzeta protein levels.
The researchers, led by Deborah Schechtman from the University of São Paulo, highlight the broader implications of DNA methylation in the central nervous system, suggesting its relevance to various pathologies.
The findings open avenues for understanding memory-related disorders and potential therapeutic interventions.
In Caenorhabditis elegans, RNAi-initiated gene silencing can persist for multiple generations. A study shows that this heritable silencing requires parallel contributions of both a nuclear transcriptional silencing pathway and perinuclear condensate-localized poly(UG)-tailed transcripts to produce...
Scientists like Prof Sinclair have evidence of speeding up, slowing, and even reversing aging. Thanks to LastPass for sponsoring this video. Click here to start using LastPass: https://ve42.co/VeLP
What causes aging? According to Professor David Sinclair, it is a loss of information in our epigenome, the system of proteins like histones and chemical markers like methylation that turn on and off genes. Epigenetics allow different cell types to perform their specific functions - they are what differentiate a brain cell from a skin cell. Our DNA is constantly getting broken, by cosmic rays, UV radiation, free radicals, x-rays and regular cell division etc. When our cells repair that damage, the epigenome is not perfectly reset. And hence over time, noise accumulates in our epigenome. Our cells no longer perform their functions well.
To counter this decline, we can activate the body's own defenses against aging by stressing the body. Eat less, eat less protein, engage in intense exercise, experience uncomfortable cold. When the body senses existential threats it triggers longevity genes, which attempt to maintain the body to ensure its survival until good times return. This may be the evolutionary legacy of early bacteria, which established these two modes of living (repair and protect vs grow and reproduce). Scientists are uncovering ways to mimic stresses on the body without the discomfort of fasting. Molecules like NMN also trigger sirtuins to monitor and repair the epigenome. This may slow aging.
Reversing aging requires an epigenetic reset, which may be possible using Yamanaka factors. These four factors can revert an adult cell into a pluripotent stem cell. Prof. Sinclair used three of the four factors to reverse aging in the retinal cells of old mice. He found they could see again after the treatment.
Special thanks to: Professor David Sinclair, check out his book "Lifespan: Why We Age & Why We Don't Have To" Assistant Professor David Gold Noemie Sierra (for polyp images) Genepool Productions for telomere animations from Immortal: https://ve42.co/immortal Epigenetics animations (DNA, histones, methylation etc) courtesy of: http://wehi.tv Animation: Etsuko Uno Art and Technical Direction: Drew Berry Sound Design: Francois Tetaz & Emma Bortignon Scientific Consultation: Marnie Blewitt Courtesy of Walter and Eliza Hall Institute of Medical Research
Filming, editing and animation by Jonny Hyman and Derek Muller
Here, the authors use single-cell multiomics and profiling of mitochondrial mutations as endogenous barcodes to show that human adaptive NK cells induced by CMV persist as clonal expansions that inherit clone-specific epigenetic profiles.
"Project Blueprint" involves eating the same two meals every day, a regimented exercise routine and a structured sleep schedule. But can it really slow or reverse the ageing process?
Tom Accart Lescarcelle's insight:
Discover now how this controversial American millionaire managed to reverse his aging thanks to epigenetics!
Author summary A complicated biochemical choreography is responsible for both the behavior of cells that make up organisms and, at a larger scale, the behavior of cooperating groups like honey bee colonies.
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In this research endeavor, the scientists embarked on unraveling the intricate biochemical processes dictating cellular behavior within organisms and the collective dynamics observed in groups, such as honey bee colonies.
The focus was on understanding how specialized roles emerge, both at the cellular level and within cooperative entities like bee colonies. The challenge lay in identifying transitions from continuous variation to distinct roles, a task tackled through a novel statistical physics-inspired method applied to gene expression data.
The researchers successfully employed this method to pinpoint a known transition in honey bees, distinguishing individuals within the nest from those venturing out for food.
Substance use disorder (SUD) is an extremely difficult disorder to overcome, and many individuals with SUD return to regular use after repeated attempts to quit.
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A recent research led by Dr. Christopher Cowan at the Medical University of South Carolina reveals a potential breakthrough in addressing substance use disorder (SUD), focusing on opioid addiction.
The study identifies an epigenetic enzyme, histone deacetylase 5 (HDAC5), as a key player in limiting heroin-associated memories and drug-seeking behavior after a period of abstinence in rats. HDAC5, known for its role in gene expression regulation, has previously been linked to cocaine use. By manipulating HDAC5 levels, researchers observed a significant impact on heroin-seeking behavior, suggesting a crucial role in modulating drug-associated memories. Understanding these molecular mechanisms opens avenues for targeted therapies to treat SUD, providing hope for more effective interventions in addiction recovery.
Joint analysis of the spatial patterns of gene expression and chromatin state provide insights into how genes are regulated.
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Gene expression and features of the DNA–protein complex chromatin were mapped together at high spatial resolution in tissue sections of the mouse or human brain.
This spatially resolved technology enables the examination of the spatio-temporal dynamics and regulation of gene expression in complex mammalian tissues !
B cells play a pivotal role in the pathogenesis of autoimmune diseases. Although previous studies have shown many genetic polymorphisms associated with B-cell activation in patients with various autoimmune disorders, progress in epigenetic research has revealed new mechanisms leading to B-cell...
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B cells assume a pivotal role in the pathogenesis of autoimmune diseases. Previous studies have identified numerous genetic polymorphisms linked to B-cell activation across various autoimmune disorders.
Recent advancements in epigenetic research unveil additional mechanisms driving B-cell hyperactivation. Epigenetic processes, encompassing histone modifications, DNA methylation, and noncoding RNAs, intricately regulate B-cell responses, and their perturbation can significantly contribute to autoimmune disease pathogenesis.
Patients afflicted with autoimmune diseases exhibit epigenetic alterations initiating and perpetuating autoimmune inflammation. Clinical and animal model studies consistently demonstrate the promising potential of epigenetic therapies for these patients.
This review comprehensively outlines current insights into epigenetic mechanisms, emphasizing their roles in regulating functional B-cell subsets.
Additionally, it delves into the discussion of epigenetic dysregulation in B cells and underscores its substantial contribution to autoimmune disease development. Drawing on clinical and preclinical evidence, the review explores novel epigenetic biomarkers and potential therapeutic avenues for individuals grappling with autoimmune disorders.
Article Figures and data Abstract Data availability Article and author information Metrics Reproduction involves the investment of resources into offspring. Although variation in reproductive effort often affects the number of offspring, adjustments of propagule size are also found in numerous species, including the Western honey bee, Apis mellifera. However, the proximate causes of these adjustments are insufficiently understood, especially in oviparous species with complex social organization in which adaptive evolution is shaped by kin selection. Here, we show in a series of experiments that queens predictably and reversibly increase egg size in small colonies and decrease egg size in large colonies, while their ovary size changes in the opposite direction. Additional results suggest that these effects cannot solely explained by egg laying rate and are due to the queens' perception of colony size. Egg size plasticity is associated with quantitative changes of 290 ovarian proteins, most of which relate to energy metabolism, protein transport, and cytoskeleton. Based on functional and network analyses, we further study the small GTPase Rho1 as a candidate regulator of egg size. Spatio-temporal expression analysis via RNAscope® and qPCR supports an important role of Rho1 in egg size determination, and subsequent RNAi-mediated gene knock-down confirmed that Rho1 has a major effect on egg size in honey bees. These results elucidate how the social environment of the honey bee colony may be translated into a specific cellular process to adjust maternal investment into eggs. It remains to be studied how widespread this mechanism is and whether it has consequences for population dynamics and epigenetic influences on offspring phenotype in honey bees and other species. The LC−MS/MS data and search results were deposited in ProteomeXchange Consortium (http://proteomecentral.proteomexchange.org) via the iProX partner repository with the dataset identifier IPX0002748002.All other data are provided as supplementary files. The following data sets were generated Bin Han Shufa Xu (2022) Honeybee queen ovary proteomics ProteomeXchange: IPX0002748002. https://www.iprox.cn/page/PSV023.html;?url=1653983195786jrAZ Author details Bin Han Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China Competing interests The authors declare that no competing interests exist. "This ORCID iD identifies the author of this article:" 0000-0001-6974-8699 Qiaohong Wei Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China Competing interests The authors declare that no competing interests exist. Esmaeil Amiri Delta Research and Extension Center, Mississippi State University, Stoneville, United States Competing interests The authors declare that no competing interests exist. Han Hu Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China Competing interests The authors declare that no competing interests exist. Lifeng Meng Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China Competing interests The authors declare that no competing interests exist. Micheline K Strand Biological and Biotechnology Sciences Branch, United States Army Research Office, Research Triangle Park, United States Competing interests The authors declare that no competing interests exist. David R Tarpy Department of Applied Ecology, North Carolina State University, Raleigh, United States Competing interests The authors declare that no competing interests exist. "This ORCID iD identifies the author of this article:" 0000-0001-8601-6094 Shufa Xu Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China Competing interests The authors declare that no competing interests exist. Jianke Li Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing, China For correspondence apislijk@126.com Competing interests The authors declare that no competing interests exist. "This ORCID iD identifies the author of this article:" 0000-0002-9344-0886 Olav Rueppell Department of Biological Sciences, University of Alberta, Edmonton, Canada For correspondence olav@ualberta.ca Competing interests The authors declare that no competing interests exist. "This ORCID iD identifies the author of this article:" 0000-0001-5370-4229 Bin Han Bin Han Esmaeil Amiri Shufa Xu Jianke Li Olav Rueppell Olav Rueppell Olav Rueppell Olav Rueppell The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. Rosalyn Gloag, University of Sydney, Australia Received: May 23, 2022 Accepted: November 7, 2022 Accepted Manuscript published: November 8, 2022 (version 1) This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication. 174 Page views 55 Downloads 0 Citations Article citation count generated by polling the highest count across the following sources: Crossref, PubMed Central, Scopus. A two-part list of links to download the article, or parts of the article, in various formats. Downloads (link to download the article as PDF) Article PDF Open citations (links to open the citations from this article in various online reference manager services) Mendeley Cite this article (links to download the citations from this article in formats compatible with various reference manager tools) Bin Han Qiaohong Wei Esmaeil Amiri Han Hu Lifeng Meng Micheline K Strand David R Tarpy Shufa Xu Jianke Li Olav Rueppell (2022) The molecular basis of socially induced egg size plasticity in honey bees eLife 11:e80499. https://doi.org/10.7554/eLife.80499 Download BibTeX Download .RIS Of interest Further reading
Tom Accart Lescarcelle's insight:
This study provides valuable insights into the control of egg size plasticity, a key form of maternal investment. It presents convincing evidence from both experimental manipulations and molecular investigations of egg plasticity in honey bee queens. It will be of interest to evolutionary biologists, particularly those working on life-history trade-offs and reproductive strategies.
In the early stages, every stem cell is presented with a decisive selection. For example, during the development of skin, the embryonic epidermis starts off with a single layer of epidermal progenitor cells.
Tom Accart Lescarcelle's insight:
We have here some groundbreaking insights into cancer development by uncovering the role of the transcription factor SOX9 as a pioneer factor : responsible for guiding stem cells in skin development, SOX9 can activate silent genes by prying open sealed pockets of genetic material.
While crucial for normal tissue development, misregulation of SOX9 has been linked to lethal cancers like lung, skin, head and neck, and bone cancer.
The study sheds light on how cancer hijacks stem cells' decision-making, providing potential therapeutic targets and understanding of SOX9-activated genes…
There's a causal mechanism happening during hibernation which would result in faster ageing occurring at the DNA level during active periods and a plateau or slower ageing during the hibernating months.
Tom Accart Lescarcelle's insight:
This article explores the intriguing connection between hibernation and epigenetic aging in yellow-bellied marmots. Dr. Julien Martin's research reveals a distinctive hibernation cycle involving metabolic slowdown and periodic boosts, impacting DNA methylation—a marker of epigenetic aging. The study supports the hibernation-ageing hypothesis, suggesting a plateau or even reversal of epigenetic aging during hibernation. This discovery raises questions about the ecological implications of climate change on hibernating species and emphasizes the need to understand the significance of hibernation in the overall life history of these animals.
Autism is characterized by impairments in social communication and interaction and restricted and repetitive behaviors. In this video, I discuss the neuroscience of autism along with potential factors and mechanisms involved in the development of autism.
TRANSCRIPT:
Autism, also known as autism spectrum disorder, is characterized by symptoms that include impairments in social communication and interaction and restricted and repetitive behaviors. Although the neuroscience of autism is still poorly understood, autism is considered to be a complex developmental disorder that involves atypical brain organization starting early in development.
Individuals with autism often experience a period of unusually rapid brain growth in infancy and early childhood. This accelerated brain growth is linked to an atypical pattern of connectivity between brain regions. A number of studies report that alterations in brain circuitry involved with social interaction and attention can be detected well before the symptoms of autism begin to appear. At this point, however, it’s unclear how brain overgrowth and atypical connectivity might be linked to the occurrence of autism symptoms.
Research suggests that the risk of autism is strongly influenced by genetics, yet studies consistently report that environmental factors also play a large role. Although a number of potential environmental factors have been identified, the risk factors for autism are far from definitive, and it remains unclear which factors are responsible for causing an increase in autism risk, and which are associated in a non-causal way. The risk factors that are most strongly linked to autism are associated with the prenatal or perinatal period. Thus, it’s possible they might be responsible for disruptions to typical neural development, leading to symptoms of autism months or years later. How these risk factors might interfere with neural development is still uncertain, but hypotheses have suggested potential mechanisms such as epigenetic effects, inflammation, oxidative stress, or damage caused by oxygen deficiency. More work needs to be done, however, to fully elucidate the genetic and environmental risk factors for autism, as well as the mechanisms for the development of autism symptoms.
REFERENCES:
Lord C, Brugha TS, Charman T, Cusack J, Dumas G, Frazier T, Jones EJH, Jones RM, Pickles A, State MW, Taylor JL, Veenstra-VanderWeele J. Autism spectrum disorder. Nat Rev Dis Primers. 2020 Jan 16;6(1):5. doi: 10.1038/s41572-019-0138-4. PMID: 31949163.
Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet. 2018 Aug 11;392(10146):508-520. doi: 10.1016/S0140-6736(18)31129-2. Epub 2018 Aug 2. PMID: 30078460; PMCID: PMC7398158.
Modabbernia A, Velthorst E, Reichenberg A. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Mol Autism. 2017 Mar 17;8:13. doi: 10.1186/s13229-017-0121-4. PMID: 28331572; PMCID: PMC5356236.
Muhle RA, Reed HE, Stratigos KA, Veenstra-VanderWeele J. The Emerging Clinical Neuroscience of Autism Spectrum Disorder: A Review. JAMA Psychiatry. 2018 May 1;75(5):514-523. doi: 10.1001/jamapsychiatry.2017.4685. PMID: 29590280.
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Surprisingly again, epigenetic effects could play a role in the development of autism according to this source
Statins designed to lower cholesterol have long been noted to work in mysterious ways to improve other aspects of cardiovascular health. A Stanford Medicine-led study uncovers how they do it.
This very interesting YouTube video features Nessa Carey, a distinguished British biologist with decades of research in molecular biology and biotechnology. The discussion centers around the often misunderstood field of epigenetics, shedding light on how DNA expression evolves throughout our lives. The exploration extends to gene editing and CRISPR, providing insights into their current state, potential applications in disease healing and ecological problem-solving, as well as the regulatory challenges they present. The conversation delves into the profound implications of gene editing for both humanity and the planet, offering a comprehensive overview of the cutting-edge developments in these scientific realms.
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