Origin of replication

Summary

The origin of replication (also called the replication origin) is a particular sequence in a genome at which replication is initiated. Propagation of the genetic material between generations requires timely and accurate duplication of DNA by semiconservative replication prior to cell division to ensure each daughter cell receives the full complement of chromosomes. This can either involve the replication of DNA in living organisms such as prokaryotes and eukaryotes, or that of DNA or RNA in viruses, such as double-stranded RNA viruses. Synthesis of daughter strands starts at discrete sites, termed replication origins, and proceeds in a bidirectional manner until all genomic DNA is replicated. Despite the fundamental nature of these events, organisms have evolved surprisingly divergent strategies that control replication onset. Although the specific replication origin organization structure and recognition varies from species to species, some common charact

Official source

https://en.wikipedia.org/wiki/Origin_of_replication

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Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer

Shan Jiang, Anguraj Sadanandam

Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible Kras(G12D) driven mouse model of PDAC has established a critical role for sustained Kras(G12D) expression in tumor maintenance, providing a model to determine the potential for and the underlying mechanisms of Kras(G12D)-independent PDAC recurrence. Here, we show that some tumors undergo spontaneous relapse and are devoid of Kras(G12D) expression and downstream canonical MAPK signaling and instead acquire amplification and overexpression of the transcriptional coactivator Yap1. Functional studies established the role of Yap1 and the transcriptional factor Tead2 in driving Kras(G12D)-independent tumor maintenance. The Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and DNA replication program. Our studies, along with corroborating evidence from human PDAC models, portend a novel mechanism of escape from oncogenic Kras addiction in PDAC.

Cell Press2014

Telomeres, the ends of linear eukaryotic chromosomes, shorten due to incomplete DNA replication and nucleolytic degradation. Cells counteract this shortening by employing a specialized reverse transcriptase called telomerase, which uses deoxyribonucleoside triphosphates (dNTPs) to extend telomeres. Intracellular dNTP levels are tightly regulated, and perturbation of these levels is known to affect DNA synthesis. We examined whether altering the levels of the dNTP pools or changing the relative ratios of the four dNTPs in Saccharomyces cerevisiae would affect the length of the telomeres. Lowering dNTP levels leads to a modest shortening of telomeres, while increasing dNTP pools has no significant effect on telomere length. Strikingly, altering the ratio of the four dNTPs dramatically affects telomere length homeostasis, both positively and negatively. Specifically, we find that intracellular deoxyguanosine triphosphate (dGTP) levels positively correlate with both telomere length and telomerase nucleotide addition processivity in vivo. Our findings are consistent with in vitro data showing dGTP-dependent stimulation of telomerase activity in multiple organisms and suggest that telomerase activity is modulated in vivo by dGTP levels.

Genetics Soc Am2013

Preexisting Heterogeneity of Inducible Nitric Oxide Synthase Expression Drives Differential Growth of Mycobacterium tuberculosis in Macrophages

John McKinney, Ophélie Rutschmann, Chiara Toniolo

Mycobacterium tuberculosis infection is initiated by the inhalation and implantation of bacteria in the lung alveoli, where they are phagocytosed by macrophages. Even a single bacterium may be sufficient to initiate infection. Thereafter, the clinical outcome is highly variable between individuals, ranging from sterilization to active disease, for reasons that are not well understood. Here, we show that the rate of intracellular bacterial growth varies markedly between individual macrophages, and this heterogeneity is driven by cell-to-cell variation of inducible nitric oxide synthase (iNOS) activity. At the single-cell level, iNOS expression fluctuates over time, independent of infection or activation with gamma interferon. We conclude that chance encounters between individual bacteria and host cells randomly expressing different levels of an antibacterial gene can determine the outcome of single-cell infections, which may explain why some exposed individuals clear the bacteria while others develop progressive disease. IMPORTANCE In this report, we demonstrate that fluctuations in the expression of antimicrobial genes can define how single host cells control bacterial infections. We show that preexisting cell-to-cell variation in the expression of a single gene, that for inducible nitric oxide synthase, is sufficient to explain why some macrophages kill intracellular M. tuberculosis while others fail to control bacterial replication, possibly leading to disease progression. We introduce the concept that chance encounters between heterogeneous bacteria and host cells can determine the outcome of a host-pathogen interaction. This concept is particularly relevant for all the infectious diseases in which the number of interacting pathogens and host cells is small at some point during the infection.

AMER SOC MICROBIOLOGY2022

Preexisting Heterogeneity of Inducible Nitric Oxide Synthase Expression Drives Differential Growth of Mycobacterium tuberculosis in Macrophages

John McKinney, Ophélie Rutschmann, Chiara Toniolo

AMER SOC MICROBIOLOGY2022