Role of mixed-species stands in attenuating the vulnerability of boreal forests to climate change and insect epidemics

We investigated whether stand species mixture can attenuate the vulnerability of eastern Canada’s boreal forests to climate change and insect epidemics. For this, we focused on two dominant boreal species, black spruce [Picea mariana (Mill.) BSP] and trembling aspen (Populus tremuloides Michx.), in stands dominated by black spruce or trembling aspen (“pure stands”), and mixed stands (M) composed of both species within a 36 km2 study area in the Nord-du-Québec region. For each species in each stand composition type, we tested climate-growth relations and assessed the impacts on growth by recorded insect epidemics of a black spruce defoliator, the spruce budworm (SBW) [Choristoneura fumiferana (Clem.)], and a trembling aspen defoliator, the forest tent caterpillar (FTC; Malacosoma disstria Hübn.). We implemented linear models in a Bayesian framework to explain baseline and long-term trends in tree growth for each species according to stand composition type and to differentiate the influences of climate and insect epidemics on tree growth. Overall, we found climate vulnerability was lower for black spruce in mixed stands than in pure stands, while trembling aspen was less sensitive to climate than spruce, and aspen did not present differences in responses based on stand mixture. We did not find any reduction of vulnerability for mixed stands to insect epidemics in the host species, but the non-host species in mixed stands could respond positively to epidemics affecting the host species, thus contributing to stabilize ecosystem-scale growth over time. Our findings partially support boreal forest management strategies including stand species mixture to foster forests that are resilient to climate change and insect epidemics

Ferredoxin containing bacteriocins suggest a novel mechanism of iron uptake in <i>Pectobacterium spp</i>

In order to kill competing strains of the same or closely related bacterial species, many bacteria produce potent narrow-spectrum protein antibiotics known as bacteriocins. Two sequenced strains of the phytopathogenic bacterium &lt;i&gt;Pectobacterium carotovorum&lt;/i&gt; carry genes encoding putative bacteriocins which have seemingly evolved through a recombination event to encode proteins containing an N-terminal domain with extensive similarity to a [2Fe-2S] plant ferredoxin and a C-terminal colicin M-like catalytic domain. In this work, we show that these genes encode active bacteriocins, pectocin M1 and M2, which target strains of &lt;i&gt;Pectobacterium carotovorum&lt;/i&gt; and &lt;i&gt;Pectobacterium atrosepticum&lt;/i&gt; with increased potency under iron limiting conditions. The activity of pectocin M1 and M2 can be inhibited by the addition of spinach ferredoxin, indicating that the ferredoxin domain of these proteins acts as a receptor binding domain. This effect is not observed with the mammalian ferredoxin protein adrenodoxin, indicating that &lt;i&gt;Pectobacterium spp.&lt;/i&gt; carries a specific receptor for plant ferredoxins and that these plant pathogens may acquire iron from the host through the uptake of ferredoxin. In further support of this hypothesis we show that the growth of strains of &lt;i&gt;Pectobacterium carotovorum&lt;/i&gt; and &lt;i&gt;atrosepticum&lt;/i&gt; that are not sensitive to the cytotoxic effects of pectocin M1 is enhanced in the presence of pectocin M1 and M2 under iron limiting conditions. A similar growth enhancement under iron limiting conditions is observed with spinach ferrodoxin, but not with adrenodoxin. Our data indicate that pectocin M1 and M2 have evolved to parasitise an existing iron uptake pathway by using a ferredoxin-containing receptor binding domain as a Trojan horse to gain entry into susceptible cells

Acute WNT signalling activation perturbs differentiation within the adult stomach and rapidly leads to tumour formation

A role for WNT signalling in gastric carcinogenesis has been suggested due to two major observations. First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stomach polyps and second, in gastric cancer, WNT activation confers a poor prognosis. However, the functional significance of deregulated WNT signalling in gastric homoeostasis and cancer is still unclear. In this study we have addressed this by investigating the immediate effects of WNT signalling activation within the stomach epithelium. We have specifically activated the WNT signalling pathway within the mouse adult gastric epithelium via deletion of either glycogen synthase kinase 3 (GSK3) or APC or via expression of a constitutively active β-catenin protein. WNT pathway deregulation dramatically affects stomach homoeostasis at very short latencies. In the corpus, there is rapid loss of parietal cells with fundic gland polyp (FGP) formation and adenomatous change, which are similar to those observed in familial adenomatous polyposis. In the antrum, adenomas occur from 4 days post-WNT activation. Taken together, these data show a pivotal role for WNT signalling in gastric homoeostasis, FGP formation and adenomagenesis. Loss of the parietal cell population and corresponding FGP formation, an early event in gastric carcinogenesis, as well as antral adenoma formation are immediate effects of nuclear β-catenin translocation and WNT target gene expression. Furthermore, our inducible murine model will permit a better understanding of the molecular changes required to drive tumourigenesis in the stomach

Phosphate Starvation Triggers Production and Secretion of an Extracellular Lipoprotein in Caulobacter crescentus

Life in oligotrophic environments necessitates quick adaptive responses to a sudden lack of nutrients. Secretion of specific degradative enzymes into the extracellular medium is a means to mobilize the required nutrient from nearby sources. The aquatic bacterium Caulobacter crescentus must often face changes in its environment such as phosphate limitation. Evidence reported in this paper indicates that under phosphate starvation, C. crescentus produces a membrane surface-anchored lipoprotein named ElpS subsequently released into the extracellular medium. A complete set of 12 genes encoding a type II secretion system (T2SS) is located adjacent to the elpS locus in the C. crescentus genome. Deletion of this T2SS impairs release of ElpS in the environment, which surprisingly remains present at the cell surface, indicating that the T2SS is not involved in the translocation of ElpS to the outer membrane but rather in its release. Accordingly, treatment with protease inhibitors prevents release of ElpS in the extracellular medium suggesting that ElpS secretion relies on a T2SS-secreted protease. Finally, secretion of ElpS is associated with an increase in alkaline phosphatase activity in culture supernatants, suggesting a role of the secreted protein in inorganic phosphate mobilization. In conlusion, we have shown that upon phosphate starvation, C. crescentus produces an outer membrane bound lipoprotein, ElpS, which is further cleaved and released in the extracellular medium in a T2SS-dependent manner. Our data suggest that ElpS is associated with an alkaline phosphatase activity, thereby allowing the bacterium to gather inorganic phosphates from a poor environment

Full Sequence and Comparative Analysis of the Plasmid pAPEC-1 of Avian Pathogenic E. coli χ7122 (O78∶K80∶H9)

(APEC), are very diverse. They cause a complex of diseases in Human, animals, and birds. Even though large plasmids are often associated with the virulence of ExPEC, their characterization is still in its infancy., are also present in the sequence of pAPEC-1. The comparison of the pAPEC-1 sequence with the two available plasmid sequences reveals more gene loss and reorganization than previously appreciated. The presence of pAPEC-1-associated genes is assessed in human ExPEC by PCR. Many patterns of association between genes are found.The pathotype typical of pAPEC-1 was present in some human strains, which indicates a horizontal transfer between strains and the zoonotic risk of APEC strains. ColV plasmids could have common virulence genes that could be acquired by transposition, without sharing genes of plasmid function

Dissection of the Transformation of Primary Human Hematopoietic Cells by the Oncogene NUP98-HOXA9

NUP98-HOXA9 is the prototype of a group of oncoproteins associated with acute myeloid leukemia. It consists of an N-terminal portion of NUP98 fused to the homeodomain of HOXA9 and is believed to act as an aberrant transcription factor that binds DNA through the homeodomain. Here we show that NUP98-HOXA9 can regulate transcription without binding to DNA. In order to determine the relative contributions of the NUP98 and HOXA9 portions to the transforming ability of NUP98-HOXA9, the effects of NUP98-HOXA9 on primary human CD34+ cells were dissected and compared to those of wild-type HOXA9. In contrast to previous findings in mouse cells, HOXA9 had only mild effects on the differentiation and proliferation of primary human hematopoietic cells. The ability of NUP98-HOXA9 to disrupt the differentiation of primary human CD34+ cells was found to depend primarily on the NUP98 portion, whereas induction of long-term proliferation required both the NUP98 moiety and an intact homeodomain. Using oligonucleotide microarrays in primary human CD34+ cells, a group of genes was identified whose dysregulation by NUP98-HOXA9 is attributable primarily to the NUP98 portion. These include RAP1A, HEY1, and PTGS2 (COX-2). Their functions may reflect the contribution of the NUP98 moiety of NUP98-HOXA9 to leukemic transformation. Taken together, these results suggest that the effects of NUP98-HOXA9 on gene transcription and cell transformation are mediated by at least two distinct mechanisms: one that involves promoter binding through the homeodomain with direct transcriptional activation, and another that depends predominantly on the NUP98 moiety and does not involve direct DNA binding

Climate, soil organic layer, and nitrogen jointly drive forest development after fire in the North American boreal zone

Previous empirical work has shown that feedbacks between fire severity, soil organic layer thickness, tree recruitment, and forest growth are important factors controlling carbon accumulation after fire disturbance. However, current boreal forest models inadequately simulate this feedback. We address this deficiency by updating the ED2 model to include a dynamic feedback between soil organic layer thickness, tree recruitment, and forest growth. The model is validated against observations spanning monthly to centennial time scales and ranging from Alaska to Quebec. We then quantify differences in forest development after fire disturbance resulting from changes in soil organic layer accumulation, temperature, nitrogen availability, and atmospheric CO2. First, we find that ED2 accurately reproduces observations when a dynamic soil organic layer is included. Second, simulations indicate that the presence of a thick soil organic layer after a mild fire disturbance decreases decomposition and productivity. The combination of the biological and physical effects increases or decreases total ecosystem carbon depending on local conditions. Third, with a 48C temperature increase, some forests transition from undergoing succession to needleleaf forests to recruiting multiple cohorts of broadleaf trees, decreasing total ecosystem carbon by �40% after 300 years. However, the presence of a thick soil organic layer due to a persistently mild fire regime can prevent this transition and mediate carbon losses even under warmer temperatures. Fourth, nitrogen availability regulates successional dynamics; broadleaf species are less competitive with needleleaf trees under low nitrogen regimes. Fifth, the boreal forest shows additional short-term capacity for carbon sequestration as atmospheric CO2 increases

Effects of temperature and of heat shock on the expression and action of the colicin A lysis protein.

At low temperature, the synthesis of the colicin A lysis protein in Escherichia coli was slowed down, and consequently its functioning was retarded. The rates were restored when the bacteria were shifted for 10 min to 42 degrees C, except in an rpoH mutant, suggesting that one or more proteins regulated by sigma 32 is necessary for expression of colicin A lysis protein