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Escape from X inactivation results in expression of genes embedded within inactive chromatin, suggesting the existence of boundary elements between domains. We report that the 5' end of Jarid1c, a mouse escape gene adjacent to an inactivated gene, binds CTCF, displays high levels of histone H3 acetylation, and functions as a CTCF-dependent chromatin insulator. CpG island methylation at Jarid1c was very low during development and virtually absent at the CTCF sites, signifying that CTCF may influence DNA methylation and chromatin modifications. CTCF binding sites were also present at the 5' end of two other escape genes, mouse Eif2s3x and human EIF2S3, each adjacent to an inactivated gene, but not at genes embedded within large escape domains. Thus, CTCF was specifically bound to transition regions, suggesting a role in maintaining both X inactivation and escape domains. Furthermore, the evolution of X chromosome domains appears to be associated with repositioning of chromatin boundary elements.
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http://dx.doi.org/10.1016/j.devcel.2004.10.018 | DOI Listing |
ACS Synth Biol
September 2025
Department of Biochemistry, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 5C1, Canada.
Imbalances in the mammalian gut are associated with acute and chronic conditions, and using engineered probiotic strains to deliver synthetic constructs to treat them is a promising strategy. However, high rates of mutational escape and genetic instability limit the effectiveness of biocontainment circuits needed for safe and effective use. Here, we describe STALEMATE (equence enngd ulti lyered geneic buffring), a dual-layered failsafe biocontainment strategy that entangles genetic sequences to create pseudoessentiality and buffer against mutations.
View Article and Find Full Text PDFBlood Cancer Discov
September 2025
Memorial Sloan Kettering Cancer Center, New York, NY, United States.
Genomic antigen loss is a recurring mechanism of resistance to chimeric antigen receptor T-cell (CAR-T) and T-cell engagers (TCE) in relapsed/refractory multiple myeloma (RRMM). Yet, it remains unclear whether these events are acquired under treatment or merely selected from pre-existing, undetectable clones. By leveraging chemotherapy mutational signatures as temporal barcodes within whole genome sequencing data, we could time genomic antigen escape in 4 out of 11 RRMM patients.
View Article and Find Full Text PDFBMC Cancer
September 2025
Graduate School, Kunming Medical University, Kunming, Yunnan, 650500, People's Republic of China.
Background: The imbalance of immune checkpoint molecules leads to immune escape of tumor cells. It has been established that KRAS mutation plays a key role in regulating PD-L1 expression of lung adenocarcinoma. However, the specific mechanism by which KRAS mutation regulates PD-L1 expression still needs further been clarified.
View Article and Find Full Text PDFMicroorganisms
August 2025
Center for Surgical Infections & Biofilm, School of Biomedical Engineering, Science & Health Systems, Drexel University, Philadelphia, PA 19104, USA.
Nosocomial infections caused by ESKAPE pathogens represent a significant burden to global health. These pathogens may exhibit multidrug resistance (MDR) mechanisms, of which mechanisms such as efflux pumps and biofilm formation are gaining significant importance. Multidrug resistance mechanisms in ESKAPE pathogens have led to an increase in the effective costs in health care and a higher risk of mortality in hospitalized patients.
View Article and Find Full Text PDFNat Chem Biol
August 2025
Department of Gastroenterology and Hepatology, Chang Gung Memorial Hospital, Linkou Medical Center, Taoyuan, Taiwan.
F-Actin cytoskeleton remodeling is vital for cell migration, organ development and immune responses. The small GTPase CDC42, a key regulator of F-actin dynamics, cycles between inactive GDP- and active GTP-bound states. However, mechanisms governing CDC42 turnover and their biological significance remain unclear.
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