The role of glandular and non-glandular trichomes in the negative interactions between strawberry cultivars and spider mite

In tropical countries, spider mite (Tetranychus urticae Koch) is a major pest of strawberries. This pest is mainly controlled by the application of pesticides. Use of pest-resistant cultivars is a healthy and environment-friendly alternative to pesticide use. This paper describes the role of glandular and non-glandular trichomes in the interaction between strawberry cultivars and spider mite. The methodology used in this study was based on two bioassays. First, the thumbtack bioassay of Weston and Snyder was used to differentiate strawberry cultivars in terms of the distance travelled by the mites. Second, different types of trichomes present on the abaxial surface of the strawberry leaves were identified and counted. The results of this study showed a significantly negative correlation between the distance travelled by the spider mites and the density of glandular trichomes on the strawberry plant. The cultivars Camino Real and Dover had the highest densities of glandular trichomes and the shortest distance travelled by the mites. In contrast, the cultivars Ventana and Toyonoka had the lowest density of glandular trichomes and the longest distance travelled by the spider mites. The high density of glandular trichomes might have been responsible for the spider mite non-preference to the Camino Real and Dover strawberry cultivars, whereas the non-glandular trichomes minimally contributed to this non-preference. The results of this study affirm the role of glandular trichomes in negative interactions between strawberry and spider mites.     

International comparisons of the incidence and mortality of sinonasal cancer

Background: This paper reviews international patterns in sinonasal cancer incidence and mortality in light of changes in exposure to known risk factors. Sinonasal tumours are relatively rare, but they have the second highest occupational attributable fraction of all types of cancer, with a well-established link for workers exposed to wood dust. Methods: Data for a variety of countries, mainly in Europe, North America and the Asia-Pacific region, were obtained from publicly accessible sources and supplemented with information requested from selected cancer registries. Rates were directly age-standardised to the World Health Organization Standard Population. Results: The average annual incidence of sinonasal cancer was typically between 5 and 10 per million in males and between 2 and 5 per million in females between 2004 and 2008. Denmark reported the highest rates, with incidence continuing to increase, in contrast to trends in other countries which either remained relatively stable, or were decreasing slightly. There were significant recent decreases in sinonasal cancer mortality rates within two-thirds of the included countries. Conclusions: Our observations are generally consistent with efforts to limit exposure to wood dust and other potentially causal substances in the workplace, as well as a reduction in the prevalence of smoking in many developed countries. Of concern is that occupational and behavioural risks related to sinonasal cancer are likely to increase among people in less developed countries into the future. However the incentive to intervene in these countries is limited by the lack of accurate and reliable cancer data.     

The Deoxyhypusine Synthase Mutant dys1-1 Reveals the Association of eIF5A and Asc1 with Cell Wall Integrity

The putative eukaryotic translation initiation factor 5A (eIF5A) is a highly conserved protein among archaea and eukaryotes that has recently been implicated in the elongation step of translation. eIF5A undergoes an essential and conserved posttranslational modification at a specific lysine to generate the residue hypusine. The enzymes deoxyhypusine synthase (Dys1) and deoxyhypusine hydroxylase (Lia1) catalyze this two-step modification process. Although several Saccharomyces cerevisiae eIF5A mutants have importantly contributed to the study of eIF5A function, no conditional mutant of Dys1 has been described so far. In this study, we generated and characterized the dys1-1 mutant, which showed a strong depletion of mutated Dys1 protein, resulting in more than 2-fold decrease in hypusine levels relative to the wild type. The dys1-1 mutant demonstrated a defect in total protein synthesis, a defect in polysome profile indicative of a translation elongation defect and a reduced association of eIF5A with polysomes. The growth phenotype of dys1-1 mutant is severe, growing only in the presence of 1 M sorbitol, an osmotic stabilizer. Although this phenotype is characteristic of Pkc1 cell wall integrity mutants, the sorbitol requirement from dys1-1 is not associated with cell lysis. We observed that the dys1-1 genetically interacts with the sole yeast protein kinase C (Pkc1) and Asc1, a component of the 40S ribosomal subunit. The dys1-1 mutant was synthetically lethal in combination with asc1Δ and overexpression of TIF51A (eIF5A) or DYS1 is toxic for an asc1Δ strain. Moreover, eIF5A is more associated with translating ribosomes in the absence of Asc1 in the cell. Finally, analysis of the sensitivity to cell wall-perturbing compounds revealed a more similar behavior of the dys1-1 and asc1Δ mutants in comparison with the pkc1Δ mutant. These data suggest a correlated role for eIF5A and Asc1 in coordinating the translational control of a subset of mRNAs associated with cell integrity.     

Paleobiology, palaeopathology and necrophobic practices in early Iron Age burials (IX-VII century BC) in Capo Colonna, Trani, Apulia, southern Italy--the state of health of a small sample from Iron Age

In this palaeobiological and palaeopathological study of skeletal remains, we attempt to define the physical characteristics, living conditions and the state of health of a small sample from two early Iron Age (IX-VIII century BC) graves at Capo Colonna, Trani (Bari, Apulia, southern Italy). In the thoraco-lumbar segment (T11-L1) of the vertebral column of an adult male 35 years old, we found wedge-shaped deformation of the anterior part of T12 with kyphosis of the affected tract. Digital radiography and volumetric reconstruction by 3D CT indicated that the alteration did not result from an infectious process (Pott's disease). Instead, it was a traumatic lesion probably caused by falling from a height. The archaeological investigation revealed extraordinary arrangements of the bodies in the graves: they were buried with a boulder placed on the coffin. This practice has been seen in similar graves in the Balkan area, particularly in Greece, from the Neolithic to the Early Middle Ages. The most likely explanation is a funeral ritual characterized by necrophobia, the purpose of which was to prevent the deceased from returning to terrorize the living.     

Postpartum glycemic homeostasis in early lactating rats is accompanied by transient and specific increase of soleus insulin response through IRS2/AKT pathway

It is known that at the moment of delivery immediate lost of conceptus (main site of glucose disposal in late pregnancy) is not able to disturb glucose homeostasis in early lactating mothers. However, the mechanism by which this adaptation takes place in early lactation is still unknown. Most studies concerning insulin sensitivity in lactating rats were carried out at 11-13 days postpartum and did not describe functional changes in insulin response in early lactation. Here we show that lactation hypersensitivity to insulin is observed as early as 3 days after delivery (L3). We show that the oxidative soleus muscle displays a transient increased maximal insulin-induced glucose uptake and CO2 production, which is temporally limited to L3. Response of soleus muscle was accompanied by an increase in glucose transporter 4 (GLUT4) content at L3. This adaptive response was not detected in the glycolytic plantaris muscle, which displayed lower content of GLUT4. We also found that soleus muscle from early lactating rats have higher insulin receptor expression and tyrosine phosphorylation. Downstream steps of insulin signaling pathway; e.g., insulin receptor substrate 2 tyrosine phosphorylation and its association with phosphatidylinositol 3-kinase were also upregulated in soleus muscle. In parallel, protein tyrosine phosphatase 1B expression, a negative regulator of insulin signal, was reduced. Importantly, all of these molecular alterations were time limited to L3 and were not observed in plantaris muscle. These results suggest that improved insulin action in oxidative, but not in glycolytic muscle might contribute to achievement of glucose homeostasis postpartum.     

Testing for Linkage and Association Across the Dihydrolipoyl Dehydrogenase Gene Region with Alzheimer’s Disease in Three Sample Populations

Prior case-control studies from our laboratory of a population enriched with individuals of Ashkenazi Jewish descent suggested that association exists between Alzheimer's disease (AD) and the chromosomal region near the DLD gene, which encodes the mitochondrial dihydrolipoamide dehydrogenase enzyme. In support of this finding, we found that linkage analysis restricted to autopsy-proven patients in the National Institute of Mental Health-National Cell Repository for Alzheimer's Disease (NIMH-NCRAD) Genetics Initiative pedigree data resulted in point-wise significant evidence for linkage (minimum p-value = 0.024) for a marker position close to the DLD locus. We now report case-control replication studies in two independent Caucasian series from the US and Italy, as well as a linkage analysis from the NIMH-NCRAD Genetics Initiative Database. Pair-wise analysis of the SNPs in the case-control series indicated there was strong linkage disequilibrium across the DLD locus in these populations, as previously reported. These findings suggest that testing for association of complex diseases with DLD locus should have considerable statistical power. Analysis of multi-locus genotypes or haplotypes based upon three SNP loci combined with results from our previous report provided trends toward significant evidence of association of DLD with AD, although neither of the present studies' association showed significance at the 0.05 level. Combining linkage and association findings for all AD patients (males and females) results in a p-value that is more significant than any of the individual findings' p-values. Finally, minimum sample size calculations using parameters from the DLD locus suggest that sample sizes on the order of 1,000 total cases and controls are needed to detect association for a wide range of genetic model parameters.     

Genetic analysis of polynucleotide phosphorylase structure and functions

Polynucleotide phosphorylase (PNPase) is a phosphate-dependent 3' to 5' exonuclease widely diffused among bacteria and eukaryotes. The enzyme, a homotrimer, can also be found associated with the endonuclease RNase E and other proteins in a heteromultimeric complex, the RNA degradosome. PNPase negatively controls its own gene (pnp) expression by destabilizing pnp mRNA. A current model of autoregulation maintains that PNPase and a short duplex at the 5'-end of pnp mRNA are the only determinants of mRNA stability. During the cold acclimation phase autoregulation is transiently relieved and cellular pnp mRNA abundance increases significantly. Although PNPase has been extensively studied and widely employed in molecular biology for about 50 years, several aspects of structure-function relationships of such a complex protein are still elusive. In this work, we performed a systematic PCR mutagenesis of discrete pnp regions and screened the mutants for diverse phenotypic traits affected by PNPase. Overall our results support previous proposals that both first and second core domains are involved in the catalysis of the phosphorolytic reaction, and that both phosphorolytic activity and RNA binding are required for autogenous regulation and growth in the cold, and give new insights on PNPase structure-function relationships by implicating the alpha-helical domain in PNPase enzymatic activity.     

Involvement of a 1-Cys Peroxiredoxin in Bacterial Virulence

The killing of bacterial pathogens by macrophages occurs via the oxidative burst and bacteria have evolved to overcome this challenge and survive, using several virulence and defense strategies, including antioxidant mechanisms. We show here that the 1-Cys peroxiredoxin LsfA from the opportunistic pathogen Pseudomonas aeruginosa is endowed with thiol-dependent peroxidase activity that protects the bacteria from H₂O₂ and that this protein is implicated in pathogenicity. LsfA belongs to the poorly studied Prx6 subfamily of peroxiredoxins. The function of these peroxiredoxins has not been characterized in bacteria, and their contribution to host-pathogen interactions remains unknown. Infection of macrophages with the lsfA mutant strains resulted in higher levels of the cytokine TNF-α production due to the activation of the NF-kB and MAPK pathways, that are partially inhibited by the wild-type P. aeruginosa strain. A redox fluorescent probe was more oxidized in the lsfA mutant-infected macrophages than it was in the macrophages infected with the wild-type strain, suggesting that the oxidative burst was overstimulated in the absence of LsfA. Although no differences in the phagocytosis rates were observed when macrophages were infected with wild-type and mutant bacteria in a gentamicin exclusion assay, a higher number of wild-type bacterial cells was found in the supernatant. This difference was not observed when macrophages were pre-treated with a NADPH oxidase inhibitor, confirming the role of LsfA in the bacterial resistance to ROS generated via NADPH oxidase. In an acute pneumonia model, mice infected with the mutant strains presented higher cytokine release in the lungs and increased activated neutrophil recruitment, with reduced bacterial burden and improved survival rates compared to mice infected with the wild-type bacteria. LsfA is the first bacterial 1-Cys Prx shown to modulate host immune responses and its characterization will allow a better understanding of the role of redox signaling in host-pathogen interactions.