Antennal detection of sex pheromone by female Pandemis limitata (Robinson) (Lepidoptera: Tortricidae) and its impact on their calling behaviour

Previous observations lead us to believe that female Pandemis limitata (Robinson) (0 to 24 h old) are as attractive as their pheromone gland extract to males in clean air, but are more attractive in an environment permeated with their major pheromone component(Z)-11-tetradecenyl acetate. Therefore, in this study, we tested the hypothesis that females can detect and/or respond to their pheromone components. Using electroantennographic detection, we found female P. limitata able to perceive both of their known pheromone components, (Z)-11-tetradecenyl acetate and (Z)-9-tetradecenyl acetate. Female antennal response was found to be 46.3% weaker than that of males, under identical conditions, with male antennae producing significantly higher deflections to the higher pheromone doses tested and to the plant volatile,(E)-2-hexanal. Observations of females in clean air versus (Z)-11-tetradecenyl acetate-permeated air showed no significant differences with respect to onset time, frequency or duration of calling. Females moved significantly less often in a (Z)-11-tetradecenyl acetate-permeated portion of a flight tunnel than in the corresponding clean-air portion

The Role of Protein Kinase A Regulation of the E6 PDZ-Binding Domain during the Differentiation-Dependent Life Cycle of Human Papillomavirus Type 18

Human papillomavirus (HPV) E6 proteins of high-risk alpha types target a select group of PSD95/DLG1/ZO1 (PDZ) domain-containing proteins by using a C-terminal PDZ-binding motif (PBM), an interaction that can be negatively regulated by phosphorylation of the E6 PBM by protein kinase A (PKA). Here, we have mutated the canonical PKA recognition motif that partially overlaps with the E6 PBM in the HPV18 genome (E6153PKA) and compared the effect of this mutation on the HPVl8 life cycle in primary keratinocytes with the wild-type genome and with a second mutant genome that lacks the E6 PBM (E6ΔPDZ). Loss of PKA recognition of E6 was associated with increased growth of the genome-containing cells relative to cells carrying the wild-type genome, and upon stratification, a more hyperplastic phenotype, with an increase in the number of S-phase competent cells in the upper suprabasal layers, while the opposite was seen with the E6ΔPDZ genome. Moreover, the growth of wild-type genome-containing cells was sensitive to changes in PKA activity, and these changes were associated with increased phosphorylation of the E6 PBM. In marked contrast to E6ΔPDZ genomes, the E6153PKA mutation exhibited no deleterious effects on viral genome amplification or expression of late proteins. Our data suggest that the E6 PBM function is differentially regulated by phosphorylation in the HPV18 life cycle. We speculate that perturbation of protein kinase signaling pathways could lead to changes in E6 PBM function, which in turn could have a bearing on tumor promotion and progression

Romanticising the Past: Core Socialist Values and the China Dream as Legitimisation Strategy

This article examines “core socialist values” as a part of the China Dream discourse, in the context of the Chinese Communist Party (CCP)’s search for alternative sources of legitimacy. Using the “visualising our values” poster collection and the “China Dream Child” campaign as case studies, this article argues that such narratives form a crucial part of the CCP’s continuing legitimisation strategy, where the party emphasises its role in providing moral authority and guidance for the general public. In order to lay such claims, the narratives focus on romanticising and homogenising both the imperial and the socialist past, while projecting a strong sense of optimism for the future, based on similar hopes of continuity and homogeneity

E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer

Human papillomaviruses (HPV) are a major cause of malignancy worldwide, contributing to ~5% of all human cancers including almost all cases of cervical cancer and a growing number of ano-genital and oral cancers. HPV-induced malignancy is primarily driven by the viral oncogenes, E6 and E7, which manipulate host cellular pathways to increase cell proliferation and enhance cell survival, ultimately predisposing infected cells to malignant transformation. Consequently, a more detailed understanding of viral-host interactions in HPV-associated disease offers the potential to identify novel therapeutic targets. Here, we identify that the c-Jun N-terminal kinase (JNK) signalling pathway is activated in cervical disease and in cervical cancer. The HPV E6 oncogene induces JNK1/2 phosphorylation in a manner that requires the E6 PDZ binding motif. We show that blockade of JNK1/2 signalling using small molecule inhibitors, or knockdown of the canonical JNK substrate c-Jun, reduces cell proliferation and induces apoptosis in cervical cancer cells. We further demonstrate that this phenotype is at least partially driven by JNK-dependent activation of EGFR signalling via increased expression of EGFR and the EGFR ligands EGF and HB-EGF. JNK/c-Jun signalling promoted the invasive potential of cervical cancer cells and was required for the expression of the epithelial to mesenchymal transition (EMT)-associated transcription factor Slug and the mesenchymal marker Vimentin. Furthermore, JNK/c-Jun signalling is required for the constitutive expression of HPV E6 and E7, which are essential for cervical cancer cell growth and survival. Together, these data demonstrate a positive feedback loop between the EGFR signalling pathway and HPV E6/E7 expression, identifying a regulatory mechanism in which HPV drives EGFR signalling to promote proliferation, survival and EMT. Thus, our study has identified a novel therapeutic target that may be beneficial for the treatment of cervical cancer