Do Novel Weapons that Degrade Mycorrhizal Mutualisms Explain Invasive Species Success?

Invasive plants often dominate novel habitats where they did not co-evolve with local species. Several hypotheses suggest mechanisms that explain increased exotic plant success, including \u27novel weapons\u27 and \u27degraded mutualisms\u27. Japanese knotweed (Fallopia japonica) and European buckthorn (Rhamnus cathartica) are widespread plant invaders in North America that can dominate ecosystems. The goal of this study is to test whether these impacts are more consistent with novel weapons or degraded mutualism hypotheses. I examine tree seedling recruitment, (germination and initial survival) growth, (biomass) and mycorrhizal invasion (AMF content) as a function of F. japonica and R. cathartica root exudates. Given that species co-evolved with these invasive species may have compensatory mechanisms for the allelochemicals, I use arbuscular (AMF) and ectomycorrhizal (ECM) tree congeners that both co-occur and do not co-occur with the invasive species. My results suggest that novel weapons both attack the seedlings directly and indirectly degrade their mutualisms. Novel weapons imposed the greatest impact on Ulmus tree seedling germination as the root exudates significantly reduced germination in the Ulmus species that evolved in the absence of the invasive plants. However, the Ulmus species during later life stages (seedling survivorship and growth), appeared more dependent on mycorrhizal fungi, and R. cathartica degraded the AMF of Ulmus congeners. These results suggest that both novel weapons and degraded mutualisms help explain the success of these widespread invaders, and that the impacts depend on life stage. Hence, successful species invasion may bring a suite of weapons rather than a single magic bullet

Expression of a protein involved in bone resorption, Dkk1, is activated by HTLV-1 bZIP factor through its activation domain

<p>Abstract</p> <p>Background</p> <p>Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia, a malignancy characterized by uncontrolled proliferation of virally-infected CD4+ T-cells. Hypercalcemia and bone lesions due to osteoclast-mediated bone resorption are frequently associated with more aggressive forms of the disease. The HTLV-1 provirus contains a unique antisense gene that expresses HTLV-1 basic leucine zipper (bZIP) factor (HBZ). HBZ is localized to the nucleus where it regulates levels of transcription by binding to certain cellular transcriptional regulators. Among its protein targets, HBZ forms a stable complex with the homologous cellular coactivators, p300 and CBP, which is modulated through two N-terminal LXXLL motifs in the viral protein and the conserved KIX domain in the coactivators.</p> <p>Results</p> <p>To determine the effects of these interactions on transcription, we performed a preliminary microarray analysis, comparing levels of gene expression in cells with wild-type HBZ versus cells with HBZ mutated in its LXXLL motifs. <it>DKK1</it>, which encodes the secreted Wnt signaling inhibitor, Dickkopf-1 (Dkk1), was confirmed to be transcriptionally activated by HBZ, but not its mutant. Dkk1 plays a major role in the development of bone lesions caused by multiple myeloma. In parallel with the initial findings, activation of Dkk1 expression by HBZ was abrogated by siRNA-mediated knockdown of p300/CBP or by a truncated form of p300 containing the KIX domain. Among HTLV-1-infected T-cell lines tested, the detection of Dkk1 mRNA partially correlated with a threshold level of HBZ mRNA. In addition, an uninfected and an HTLV-1-infected T-cell line transfected with an HBZ expression vector exhibited <it>de novo </it>and increased DKK1 transcription, respectively. In contrast to HBZ, The HTLV-1 Tax protein repressed Dkk1 expression.</p> <p>Conclusions</p> <p>These data indicate that HBZ activates Dkk1 expression through its interaction with p300/CBP. However, this effect is limited in HTLV-1-infected T-cell lines, which in part, may be due to suppression of Dkk1 expression by Tax. Consequently, the ability of HBZ to regulate expression of Dkk1 and possibly other cellular genes may only be significant during late stages of ATL, when Tax expression is repressed.</p

Diagnostic and therapeutical role of vitamin D in chronic hepatitis C virus infection.

Although initially identified as a calcium homeostatic hormone, vitamin D is now known to have pleiotropic functions, dealing with both innate and adaptative immunity. Calcitriol mediates its biological effects by binding to the vitamin D receptor (VDR), which is expressed not only by intestine, bone and kidney but also on cell membranes of T lymphocytes, B lymphocytes, dendritic cells and macrophages. Vitamin D plays a role on the degree of liver damage in patients with chronic hepatitis C (CHC): low vitamin D levels have been associated with high hepatic necroinflammatory activity and progression of liver fibrosis. Vitamin D, in CHC patients, could also affect the response to antiviral therapy: in fact, recent studies have shown a relationship between low responsiveness to IFNbased therapy and low vitamin D serum levels. Further studies are required to better assess if vitamin D could work as a reliable noninvasive marker of liver fibrosis and whether vitamin D supplementation could be given to all CHC patients together with standard antiviral treatment, in order to improve the rate of sustained virological response (SVR)