Stem emissions of monoterpenes, acetaldehyde, and methanol from Scots pine (Pinus sylvestris L.) affected by tree water relations and cambial growth

Abstract Tree stems are an overlooked source of volatile organic compounds (VOCs). Their contribution to ecosystem processes and total VOC fluxes is not well studied, and assessing it requires better understanding of stem emission dynamics and their driving processes. To gain more mechanistic insight into stem emission patterns, we measured monoterpene, methanol, and acetaldehyde emissions from the stems of mature Scots pines (Pinus sylvestris L.) in a boreal forest over three summers. We analysed the effects of temperature, soil water content, tree water status, transpiration, and growth on the VOC emissions, and used generalized linear models to test their relative importance in explaining the emissions. We show that Scots pine stems are considerable sources of monoterpenes, methanol, and acetaldehyde, and their emissions are strongly regulated by temperature. However, even small changes in water availability affected the emission potentials: increased soil water content increased the monoterpene emissions within a day, whereas acetaldehyde and methanol emissions responded within two to four days. This lag corresponded to their transport time in the xylem sap from the roots to the stem. Moreover, the emissions of monoterpenes, methanol, and acetaldehyde were influenced by the cambial growth rate of the stem with six- to ten-day lags. This article is protected by copyright. All rights reserved.Peer reviewe

Chk2 deficiency in Myc-overexpressing lymphoma cells elicits a synergistic lethal response in combination with PARP inhibition

Myc is a transcription factor frequently found deregulated in human cancer. The Myc-mediated cellular transformation process is associated with fast proliferative cells and inherent genomic instability, giving rise to malignant, invasive neoplasms with poor prognosis for survival. Transcription-independent functions of Myc include stimulation of replication. Excessive Myc expression stimulates a replication-associated DNA damage response that signals via the phosphoinositide-3-kinase (PI3K)-related protein kinases (PIKKs) ATM and ATR. These, in turn, activate the DNA damage transducers Chk1 and Chk2. Here, we show that Myc can stimulate Chek2 transcript indirectly in vitro as well as in B cells of λ-Myc transgenic mice or in the intestine of ApcMin mice. However, Chk2 is dispensable for Myc's ability to transform cells in vitro and for the survival of established lymphoma cells from λ-Myc transgenic mice. Chk2 deficiency induces polyploidy and slow growth, but the cells are viable and protected against DNA damage. Furthermore, inhibition of both Chk1/Chk2 with AZD7762 induces cell death and significantly delays disease progression of transplanted lymphoma cells in vivo. DNA damage recruits PARP family members to sites of DNA breaks that, in turn, facilitate the induction of DNA repair. Strikingly, combining Chk2 and PARP inhibition elicits a synergistic lethal response in the context of Myc overexpression. Our data indicates that only certain types of chemotherapy would give rise to a synergistic lethal response in combination with specific Chk2 inhibitors, which will be important if Chk2 inhibitors enter the clinic

TMPRSS2-ERG Expression Predicts Prostate Cancer Survival and Associates with Stromal Biomarkers

The TMPRSS2-ERG gene fusion is found in approximately half of all prostate cancers. The functional and prognostic significance of TMPRSS2-ERG is, however, not fully understood. Based on a historical watchful waiting cohort, an association between TMPRSS2-ERG, evaluated as positive immune staining, and shorter survival of prostate cancer patients was identified. Expression of ERG was also associated with clinical markers such as advanced tumor stage, high Gleason score, presence of metastasis and prognostic tumor cell markers such as high Ki67, pEGFR and pAkt. Novel associations between TMPRSS2-ERG and alterations in the tumor stroma, for example, increased vascular density, hyaluronan and PDGFR beta and decreased Caveolin-1, all known to be associated with an aggressive disease, were found. The present study suggests that the TMPRSS2-ERG fusion gene is associated with a more aggressive prostate cancer phenotype, supported by changes in the tumor stroma