All articles tagged with #chromatin
Researchers engineered an RNA-guided CRISPR-Cas12a2 nuclease to recognize cancer-specific transcripts and trigger transcript-activated chromatin shredding, leading to DNA damage responses and selective death of cancer cells in experimental systems, offering a potential precision approach to targeting undruggable mutations such as p53.
Scientists increased SIRT6 in mice and found that it preserved youthful chromatin in the liver and, when boosted in elderly animals, reversed many age-related chromatin changes toward a younger state within a month, suggesting some aging effects may be reversible rather than fixed—though these findings are not yet transferable to humans.
Bar-Ilan researchers showed that increasing SIRT6 levels specifically in the liver of 24‑month‑old male mice reversed about 80% of age-related chromatin accessibility changes within one month, with downstream inflammatory and metabolic gene programs moving toward a youthful pattern. The intervention used a hepatocyte-targeted viral vector and yielded tissue- and mechanism-specific reversal, not a universal rejuvenation. While scientifically significant for chromatin dynamics and aging biology, translating this to humans would require substantial further work, safety testing, and validation; the broader implications for human longevity are modest and long-term, not an immediate anti-aging breakthrough.
Scientists have found more than 200 metabolic enzymes directly attached to human DNA in the nucleus, suggesting a small, tissue- and cancer-specific 'mini-metabolism' that may influence gene regulation, DNA repair, and tumor response to therapy. The enzymes’ nuclear roles appear to differ by cancer type (e.g., oxidative phosphorylation enzymes common in breast but not lung cancer) and some, like IMPDH2, show location-dependent functions, prompting potential new biomarkers and drug targets while many details remain to be clarified.
New research suggests that the physical looping of DNA played a crucial role in the evolution of complex animals by enabling sophisticated gene regulation, which allowed cells to differentiate and form diverse tissues, marking a significant step from unicellular ancestors to multicellular organisms like cnidarians and ctenophores.
Researchers discovered that herpes simplex virus-1 (HSV-1) deliberately reshapes the human genome to facilitate its replication, but blocking the enzyme topoisomerase I can prevent this process, offering a potential new treatment strategy.
A study has revealed that MSL2, a component of the MSL complex, plays a crucial role in ensuring biallelic gene expression in mammals. Using hybrid mouse cell line models, researchers found that MSL2 regulates the expression of haploinsufficient genes, which require both copies of the gene to produce a functional amount of protein. The loss of MSL2 resulted in allele-specific changes in gene expression, with some genes transitioning from biallelic to monoallelic expression. The chromatin landscape also underwent significant changes, with alterations in histone modifications and promoter-enhancer interactions. These findings shed light on the mechanisms underlying gene dosage regulation and provide insights into the role of MSL2 in maintaining balanced gene expression in mammals.
Researchers have discovered that acetyl-methyllysine, a reversible lysine post-translational modification, marks chromatin at active transcription start sites. This modification plays a crucial role in regulating RNA synthesis and gene expression. The study provides insights into the molecular mechanisms of epigenetic control and highlights the importance of acetyl-methyllysine in chromatin structure and protein interactions. The data from various experiments have been made available in public databases for further analysis.
A recent study has found that RNA polymerase II, an enzyme responsible for transcribing DNA into RNA, remains associated with active genes during DNA replication. This discovery challenges the conventional understanding that RNA polymerase II dissociates from chromatin during replication. The findings suggest that RNA polymerase II may play a role in maintaining transcriptional memory and contribute to the regulation of gene expression.
A new study from UTHealth Houston found that the virus that causes COVID-19 can alter the genomic structure of cells, which may explain the immunological symptoms that someone experiences from an infection. The changes to the genomic structure of cells could play a role in long COVID. The study focuses on the way the virus affects chromatin, or the mixture of DNA and proteins that form the chromosomes found in cells. Researchers believe that if they can understand how those changes are occurring, they may be able to develop a treatment to prevent them or alleviate COVID-19 symptoms.