Telomeres are specific structures that protect chromosome ends and act as a biological clock, preventing normal cells from replicating indefinitely. Mammalian telomeres are replicated throughout S-phase in a predetermined order. However, the mechanism of this regulation is still unknown. We wished to investigate this phenomenon under physiological conditions in a changing environment, such as the immortalization process to better understand the mechanism for its control. We thus examined the timing of human telomere replication in normal and SV40 immortalized cells, which are cytogenetically very similar to cancer cells. We found that the timing of telomere replication was globally conserved under different conditions during the immortalization process. The timing of telomere replication was conserved despite changes in telomere length due to endogenous telomerase reactivation, in duplicated homologous chromosomes, and in rearranged chromosomes. Importantly, translocated telomeres, possessing their initial subtelomere, retained the replication timing of their homolog, independently of the proportion of the translocated arm, even when the remaining flanking DNA is restricted to its subtelomere, the closest chromosome-specific sequences (inferior to 500 kb). Our observations support the notion that subtelomere regions strongly influence the replication timing of the associated telomere.
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http://dx.doi.org/10.1038/srep32510 | DOI Listing |
Int J Mol Sci
January 2025
Department of Life Sciences, Ben Gurion University of the Negev, Beer-Sheva 8410501, Israel.
Phenotypic variability in isogenic bacterial populations is a remarkable feature that helps them cope with external stresses, yet it is incompletely understood. This variability can stem from gene expression noise and/or the unequal partitioning of low-copy-number freely diffusing proteins during cell division. Some high-copy-number components are transiently associated with almost immobile large assemblies (hyperstructures) and may be unequally distributed, contributing to bacterial phenotypic variability.
View Article and Find Full Text PDFPhilos Trans R Soc Lond B Biol Sci
January 2025
Institute of Ecology and Evolution, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3FL, UK.
The environments that parasites experience within hosts change dramatically over 24 h. How rhythms shape host-parasite-vector interactions is poorly understood owing to the challenges of disentangling the roles of rhythms of multiple interacting species in the context of the complex lifecycles of parasites. Using canonical circadian clock-disrupted hosts, we probe the limits of flexibility in the rhythmic replication of malaria () parasites and quantify the consequences for fitness proxies of both parasite and host.
View Article and Find Full Text PDFPhilos Trans R Soc Lond B Biol Sci
January 2025
Laboratory of Immunopathology - Instituto René Rachou, Fundação Oswaldo Cruz - Minas, Belo Horizonte 30190-002, Brazil.
The synchronization of parasites as they replicate within red blood cells of their vertebrate host remains largely unexplored. Understanding this synchronization could reveal how parasites optimize their lifecycle to maximize transmission, evade the immune response and maximize energy acquisition. Rhythmic replication fulfils some criteria of an endogenous oscillator with time of day cues potentially provided by temperature, oxygen levels, hormones and/or nutrient availability.
View Article and Find Full Text PDFPLoS Pathog
January 2025
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health; Bethesda, Maryland, United States of America.
Viral infections of the central nervous system (CNS) are a major cause of morbidity largely due to lack of prevention and inadequate treatments. While mortality from viral CNS infections is significant, nearly two thirds of the patients survive. Thus, it is important to understand how the human CNS can successfully control virus infection and recover.
View Article and Find Full Text PDFElife
January 2025
Translational Science and Therapeutics Division, Human Biology Division, Fred Hutchinson Cancer Center, Seattle, United States.
The association between late replication timing and low transcription rates in eukaryotic heterochromatin is well known, yet the specific mechanisms underlying this link remain uncertain. In , the histone deacetylase Sir2 is required for both transcriptional silencing and late replication at the repetitive ribosomal DNA (rDNA) arrays. We have previously reported that in the absence of , a de-repressed RNA PolII repositions MCM replicative helicases from their loading site at the ribosomal origin, where they abut well-positioned, high-occupancy nucleosomes, to an adjacent region with lower nucleosome occupancy.
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