Genetic variation and recombination of RdRp and HSP 70h genes of Citrus tristeza virus isolates from orange trees showing symptoms of citrus sudden death disease

<p>Abstract</p> <p>Background</p> <p>Citrus sudden death (CSD), a disease that rapidly kills orange trees, is an emerging threat to the Brazilian citrus industry. Although the causal agent of CSD has not been definitively determined, based on the disease's distribution and symptomatology it is suspected that the agent may be a new strain of <it>Citrus tristeza virus </it>(CTV). CTV genetic variation was therefore assessed in two Brazilian orange trees displaying CSD symptoms and a third with more conventional CTV symptoms.</p> <p>Results</p> <p>A total of 286 RNA-dependent-RNA polymerase (RdRp) and 284 heat shock protein 70 homolog (HSP70h) gene fragments were determined for CTV variants infecting the three trees. It was discovered that, despite differences in symptomatology, the trees were all apparently coinfected with similar populations of divergent CTV variants. While mixed CTV infections are common, the genetic distance between the most divergent population members observed (24.1% for RdRp and 11.0% for HSP70h) was far greater than that in previously described mixed infections. Recombinants of five distinct RdRp lineages and three distinct HSP70h lineages were easily detectable but respectively accounted for only 5.9 and 11.9% of the RdRp and HSP70h gene fragments analysed and there was no evidence of an association between particular recombinant mosaics and CSD. Also, comparisons of CTV population structures indicated that the two most similar CTV populations were those of one of the trees with CSD and the tree without CSD.</p> <p>Conclusion</p> <p>We suggest that if CTV is the causal agent of CSD, it is most likely a subtle feature of population structures within mixed infections and not merely the presence (or absence) of a single CTV variant within these populations that triggers the disease.</p

A reciprocal feedback between the PDZ binding kinase and androgen receptor drives prostate cancer

We acknowledge support from the National Cancer Research Institute (National Institute of Health Research (NIHR) collaborative study: “Prostate Cancer: Mechanism of Progression and Treatment (PROMPT)” (grant G0500966/75466). This work was funded by a Cancer Research UK program grant (to DEN) and funding from the US Department of Defense (Prostate Cancer Research Program Transformative Impact Award, grant ID W81XWH-13- 2-0093; WDT, SMD and LAS), National Health and medical Research Council (grant ID 1083961; LAS) and PCFA/Cancer Australia/Movember (grant IDs 1012337 and 1043482; WDT and LAS). The research programs of WDT and LAS are supported by the Movember Foundation and the Prostate Cancer Foundation of Australia through the Movember Revolutionary Team Award. This work was also supported by the National Institutes of Health (NIH) grant R01CA174777 to SMD. FO was supported by a PhD project grant from Prostate Cancer UK (S10-10). LAS and MA were supported by a Young Investigator Award from the Prostate Cancer Foundation of the USA.Peer reviewe

Valence-bond treatment of distortions in polyacene polymers

Distortions of polyacene polymers are studied within a many-body valence-bond framework using a powerful transfer-matrix technique for the valence-bond (or Heisenberg) model of the system. The computations suggest that the ground-state geometry is either totally symmetric or possibly exhibits a slight (A2 or B2 symmetry) bond-alternation distortion. The lowest-energy (nonsymmetric, in-plane) distortions are the A2 and B2 modes, which, within our approximations, are degenerate