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Sager NP5797 ITE CIR Driver

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Sager NP5797 ITE CIR Driver

Other eLife digest Malaria is an infectious disease caused by a microscopic parasite called Plasmodium, which is transferred between humans by mosquitos. One species of malaria parasite called Plasmodium falciparum can cause particularly severe and Sager NP5797 ITE CIR forms of the disease.

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Currently, the most widely used treatment for P. However, resistance to artemisinin has started to spread throughout Southeast Asia.

Artemisinin resistance is caused by mutations in a parasite gene called kelch13, and researchers have identified over 20 different mutations in P. The diversity of mutations involved, and the Sager NP5797 ITE CIR that the same mutation can arise independently in different locations, make it difficult to track the spread of resistance using conventional molecular marker approaches. Here, Amato, Miotto et al.


Amato, Miotto et al. However the kelch13 mutations seen in Africa remained at low levels in the parasite population, and appeared to be under much less pressure for evolutionary selection than those found in Southeast Asia.

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These Sager NP5797 ITE CIR demonstrate that the emergence and spread of resistance to antimalarial drugs does not depend solely on the mutational process, but also on other factors that influence whether the mutations will spread in the population. Understanding how this is affected by different patterns of drug treatments and other environmental conditions will be important in developing more effective strategies for combating malaria.

However the increasing prevalence of artemisinin resistant P. One of the main contemporary challenges in global health is to prevent artemisinin resistance from becoming established in Africa, where the consequences for childhood mortality could be disastrous Dondorp Sager NP5797 ITE CIR Ringwald, Understanding the epidemiological and evolutionary driving forces behind artemisinin resistance is essential to develop effective strategies to stop it spreading. Parasites with KBPD mutations tend to grow more slowly in the early part of the erythrocytic cycle, and have an enhanced unfolded protein response, both of which might act to protect against oxidative damage caused by artemisinin Dogovski et al.

It has also recently been shown that the PI3K protein is the target of artemisinin action, and that kelch13 binds to PI3K to mark it for degradation; by affecting this binding, KBPD mutations result in high levels of PI3K which counteract the effect of artemisinin Mbengue et al. A striking characteristic of the current distribution of artemisinin resistance is that it is caused by multiple independent KPBD mutations emerging in different locations, i.

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More than 20 KPBD SNPs have been associated with delayed parasite clearance during artemisinin treatment Sager NP5797 ITE CIR there are several documented instances of the same allele arising independently in different locations Ashley et al. These are classic features of a soft selective sweep which, according to evolutionary theory, is most likely to arise in populations where the selected alleles are already present as standing genetic variations or have been repeatedly introduced by de novo mutations Hermisson and Pennings, ; Pennings and Hermisson, ; Messer and Petrov, There is ongoing debate among evolutionary biologists about how commonly soft selective sweeps occur in nature Jensen, ; Garud et al.

There are not yet any Sager NP5797 ITE CIR DNA-based methods to detect chromosome rearrangements - in particular, recent high-throughput screens for sequence change e.

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Davies et al, ; Sjoblom et al, were unable to detect rearrangements, since the screens rely on being able to amplify sequencing targets by PCR, and translocation breaks will not be amplified. Array comparative genomic hybridisation array-CGH can in principle identify the breakpoints of Sager NP5797 ITE CIR translocations as changes in genomic copy number, but cannot detect balanced translocations.

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The distinction between balanced and unbalanced translocations has been considered an important issue Dutrillaux, ; Mitelman, Balanced translocations are more likely to have effects at their breakpoints, Sager NP5797 ITE CIR unbalanced translocations result in gain or loss of material—in particular, loss of tumour suppressor genes—so that the breakpoints themselves may not be important. While the familiar gene-fusing translocations in haemopoietic disease are usually balanced, translocations in common epithelial cancers are said to be mostly, though not exclusively, unbalanced Dutrillaux, ; Davidson et al, ; Abdel-Rahman et al, ; Roschke et al, Introduced in the context of constitutional chromosome abnormalities Fiegler et al, b ; Gribble et alit is a logical extension of reverse chromosome painting, which we previously applied to three breast cancer cell lines Morris et al, In both approaches, individual chromosomes are purified using a fluorescence-activated cell sorter and the DNA amplified and hybridized to normal genomic DNA—to normal metaphase chromosomes in reverse painting and to DNA microarrays in array painting.

Array painting gives a resolution only limited by the arrays used. It can be used to map all translocation breakpoints, including those of balanced translocations, and it identifies which chromosome fragments are joined, which is important in the context of looking for fusion genes. We report here a comprehensive analysis by array painting of the chromosome translocations of three breast cancer cell lines.


Results We determined the complete karyotypes of 3 breast cancer cell lines Table 1. In total breakpoints were identified and mapped to at least 1Mb resolution by array Sager NP5797 ITE CIR The DNA of almost all chromosomes was also hybridized to normal metaphase chromosome spreads: Figure 1 and Supplementary Figures 1 and 2 show flow karyotypes of the cell lines.

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