Workplace Attachment Style as Moderator of the Relationship Between Political Skills and Organizational Citizenship Behaviors.

A number of studies have demonstrated the role played by political skills on organizational citizenship behaviors (OCBs). Other research has also shown how the work environment can affect OCBs. However, no research has yet addressed the role that workplace attachment style plays in influencing employee OCBs. The present study aims to investigate the moderating role of workplace attachment style on the relationship between political skills and Organizational Citizenship Behaviors (OCBs) using a cross-sectional design. The research was carried out with the participation of 185 French office workers. Research hypotheses were tested by means of three moderation models. The results show that political skills are positively related to OCB, and that secure and preoccupied workplace attachment styles moderate the relationship between political skills and OCB. These results therefore underline the importance of appropriate organizational environmental management in promoting OCBs.

Drosophila 4EHP is essential for the larval-pupal transition and required in the prothoracic gland for ecdysone biosynthesis.

Maternal expression of the translational regulator 4EHP (eIF4E-Homologous Protein) has an established role in generating protein gradients essential for specifying the Drosophila embryonic pattern. We generated a null mutation of 4EHP, which revealed for the first time that it is essential for viability and for completion of development. In fact, 4EHP null larvae, and larvae ubiquitously expressing RNAi targeting 4EHP, are developmentally delayed, fail to grow and eventually die. In addition, we found that expressing RNAi that targets 4EHP specifically in the prothoracic gland disrupted ecdysone biosynthesis, causing a block of the transition from the larval to pupal stages. This phenotype can be rescued by dietary administration of ecdysone. Consistent with this, 4EHP is highly expressed in the prothoracic gland and it is required for wild type expression levels of steroidogenic enzymes. Taken together, these results uncover a novel essential function for 4EHP in regulating ecdysone biosynthesis.

EcR-B1 and Usp nuclear hormone receptors regulate expression of the VM32E eggshell gene during Drosophila oogenesis.

Ecdysone signaling plays key roles in Drosophila oogenesis, as its activity is required at multiple steps during egg chamber maturation. Recently, its involvement has been reported on eggshell production by controlling chorion gene transcription and amplification. Here, we present evidence that ecdysone signaling also controls the expression of the eggshell gene VM32E, whose product is a component of vitelline membrane and endochorion layers. Specifically blocking the function of the different Ecdysone receptor (EcR) isoforms we demonstrate that EcR-B1 is responsible for ecdysone-mediated VM32E transcriptional regulation. Moreover, we show that the EcR partner Ultraspiracle (Usp) is also necessary for VM32E expression. By analyzing the activity of specific VM32E regulatory regions in usp(2) clones we identify the promoter region mediating ecdysone-dependent VM32E expression. By in vitro binding assay and site-directed mutagenesis we demonstrate that this region contains a Usp binding site necessary for VM32E regulation. Our results further support the crucial role of ecdysone signaling in controlling transcription of eggshell structural genes and suggest that the heterodimeric complex EcR-B1/Usp mediates the ecdysone-dependent VM32E transcriptional activation in the main body follicle cells.

Cell survival and polarity of Drosophila follicle cells require the activity of ecdysone receptor B1 isoform.

Proper assembly and maintenance of epithelia are critical for normal development and homeostasis. Here, using the Drosophila ovary as a model, we identify a role for the B1 isoform of the ecdysone receptor (EcR-B1) in this process. We performed a reverse genetic analysis of EcR-B1 function during oogenesis and demonstrate that silencing of this receptor isoform causes loss of integrity and multilayering of the follicular epithelium. We show that multilayered follicle cells lack proper cell polarity with altered distribution of apical and basolateral cell polarity markers including atypical-protein kinase C (aPKC), Discs-large (Dlg), and Scribble (Scrib) and aberrant accumulation of adherens junctions and F-actin cytoskeleton. We find that the EcR-B1 isoform is required for proper follicle cell polarity both during early stages of oogenesis, when follicle cells undergo the mitotic cell cycle, and at midoogenesis when these cells stop dividing and undergo several endocycles. In addition, we show that the EcR-B1 isoform is required during early oogenesis for follicle cell survival and that disruption of its function causes apoptotic cell death induced by caspase.

Building up the Drosophila eggshell: first of all the eggshell genes must be transcribed.

The Drosophila eggshell provides a model system for studying the assembly of extracellular matrix. Eggshell formation is a complex process that requires time-coordinated synthesis, cleavage, and transport of various proteins and finally cross-linking mediated by particular functional domains. It has been suggested that the eggshell can act as a storage site for spatial cues involved in embryonic pattern formation. Its structural components are synthesized in the somatic follicle cells in a precise temporally and spatially regulated manner. This review will summarize our knowledge of eggshell gene expression. We will discuss the amplification of the chorion gene clusters and the data acquired on the expression patterns and the regulatory elements controlling transcription of eggshell genes. We will then focus on the findings that correlate follicular epithelium patterning and eggshell gene expression, and discuss the interesting perspectives of an involvement in eggshell assembly of embryonic patterning cues.

Egfr signaling modulates VM32E gene expression during Drosophila oogenesis.

Drosophila vitelline membrane gene VM32E is expressed in the follicle cells of the stage 10 egg chamber and shows a peculiar temporal and spatial expression pattern compared to the other members of the same gene family. Previous work has led us to demonstrate that Decapentaplegic (Dpp) signaling represses the expression of the VM32E gene in the centripetal follicle cells. In this paper, we describe another level of complexity of the VM32E gene expression regulation. Through clonal analyses, we show that the expression of the VM32E gene in the main body follicle cells is modulated by the epidermal growth factor receptor (Egfr) activity. In follicle cell clones expressing a constitutively active form of the Egfr, the VM32E gene is downregulated, while the loss of the Egfr activity upregulates VM32E expression. In addition, we show that the ectopic expression of the Egfr-induced ETS transcription factor PointedP2 (PntP2) affects the expression of the VM32E gene. From these results and our previously published data, it appears that the proper patterning of follicle cells, defined by Dpp and Egfr signaling pathways, controls the VM32E gene expression pattern. This may suggest that a fine tuning of the expression of specific eggshell structural genes could be part of the complex process that leads to a proper eggshell assembly.

Notch signaling links interactions between the C/EBP homolog slow border cells and the GILZ homolog bunched during cell migration.

In the follicle cell (FC) epithelium that surrounds the Drosophila egg, a complex set of cell signals specifies two cell fates that pattern the eggshell: the anterior centripetal FC that produce the operculum and the posterior columnar FC that produce the main body eggshell structure. We have previously shown that the long-range morphogen DPP represses the expression of the bunched (bun) gene in the anterior-most centripetal FC. bun, which encodes a homolog of vertebrate TSC-22/GILZ, in turn represses anterior gene expression and antagonizes Notch signaling to restrict centripetal FC fates in posterior cells. From a screen for novel targets of bun repression we have identified the C/EBP homolog slow border cells (slbo). At stage 10A, slbo expression overlaps bun in anterior FC; by stage 10B they repress each other's expression to establish a sharp slbo/bun expression boundary. The precise position of the slbo/bun expression boundary is sensitive to Notch signaling, which is required for both slbo activation and bun repression. As centripetal migration proceeds from stages 10B-14, slbo represses its own expression and both slbo loss-of-function mutations and overexpression approaches reveal that slbo is required to coordinate centripetal migration with nurse cell dumping. We propose that in anterior FC exposed to a Dpp morphogen gradient, high and low levels of slbo and bun, respectively, are established by modulation of Notch signaling to direct threshold cell fates. Interactions among Notch, slbo and bun resemble a conserved signaling cassette that regulates mammalian adipocyte differentiation.

Dpp signaling down-regulates the expression of VM32E eggshell gene during Drosophila oogenesis.

Among the members of the Drosophila melanogaster vitelline membrane protein gene family, VM32E has the unique feature of being a component of both the vitelline and the endochorion layers. The VM32E gene is expressed at stage 10 of egg chamber development in the main body follicle cells, and it is repressed in the anterior and posterior follicle cells. Here, we show that this spatial restriction of VM32E gene expression is conserved in the D. pseudoobscura orthologous gene, suggestive of a conserved function of VM32E protein. The VM32E gene is not expressed in the centripetal migrating follicle cells, where the Decapentaplegic (Dpp) pathway is active in patterning the anterior eggshell structures. By analyzing the native VM32E gene and the activity of specific VM32E regulatory regions, in genetic backgrounds altering the Dpp pathway, we show that VM32E gene is negatively regulated by the Dpp signaling. Therefore, it appears that the Dpp signaling pathway executes its control on eggshell morphogenesis also by controlling the expression of eggshell structural genes.