C. elegans RNA-dependent RNA polymerases rrf-1 and ego-1 silence Drosophila transgenes by differing mechanisms

Drosophila possesses the core gene silencing machinery but, like all insects, lacks the canonical RNA-dependent RNA polymerases (RdRps) that in C. elegans either trigger or enhance two major small RNA-dependent gene silencing pathways. Introduction of two different nematode RdRps into Drosophila showed them to be functional, resulting in differing silencing activities. While RRF-1 enhanced transitive dsRNA-dependent silencing, EGO-1 triggered dsRNA-independent silencing, specifically of transgenes. The strain w; da-Gal4; UAST-ego-1, constitutively expressing ego-1, is capable of silencing transgene including dsRNA hairpin upon a single cross, which created a powerful tool for research in Drosophila. In C. elegans, EGO-1 is involved in transcriptional gene silencing (TGS) of chromosome regions that are unpaired during meiosis. There was no opportunity for meiotic interactions involving EGO-1 in Drosophila that would explain the observed transgene silencing. Transgene DNA is, however, unpaired during the pairing of chromosomes in embryonic mitosis that is an unusual characteristic of Diptera, suggesting that in Drosophila, EGO-1 triggers transcriptional silencing of unpaired DNA during embryonic mitosis. © 2012 Springer Basel.

Desafios Para A Implementação Do Processo De Projeto Colaborativo: Análise Do Fator Humano

The ineffectiveness of current design processes has been well studied and has resulted in widespread calls for the evolution and development of new management processes. Perhaps one problem is that with the advent of BIM we are moving from one stage to another without necessarily having resolved all the issues. CAD design technology, if well handled, could have significantly raised the level of quality and efficiency of current processes, but in practice this was not fully realized. Therefore, technology alone can´t solve all the problems and the advent of BIM could result in a similar bottleneck. For a precise definition of the problem to be solved we should start by understanding what are the main current bottlenecks that have yet to be overcome by either new technologies or management processes, and the impact of human behavior related issues despite the advent of new technologies. The fragmented and dispersed nature of the AEC sector and the huge number of small organizations that comprise it would probably be a major limiting factor. Several authors have addressed this issue and more recently IDDS has been defined as the highest level of achievement. However, what is written on IDDS shows an extremely ideal situation on a state to be achieved; it shows a holistic utopian proposition with the intent to create the research agenda to move towards that state. Key to IDDS is the framing of a new management model which should address the problems associated with key aspects: technology, processes, policies and people. One of the primary areas to be further studied is the process of collaborative work and understanding, together with the development of proposals to overcome the many cultural barriers that currently exist and impede the advance of new management methods. The purpose of this paper is to define and delimit problems to be solved so that it is possible to implement a new management model for a collaborative design process.

Geminin and Brahma act antagonistically to regulate EGFR–Ras–MAPK signaling in Drosophila

Geminin was identified in Xenopus as a dual function protein involved in the regulation of DNA replication and neural differentiation. In Xenopus, Geminin acts to antagonize the Brahma (Brm) chromatin-remodeling protein, Brg1, during neural differentiation. Here, we investigate the interaction of Geminin with the Brm complex during Drosophila development. We demonstrate that Drosophila Geminin (Gem) interacts antagonistically with the Brm–BAP complex during wing development. Moreover, we show in vivo during wing development and biochemically that Brm acts to promote EGFR–Ras–MAPK signaling, as indicated by its effects on pERK levels, while Gem opposes this. Furthermore, gem and brm alleles modulate the wing phenotype of a Raf gain-of-function mutant and the eye phenotype of a EGFR gain-of-function mutant. Western analysis revealed that Gem over-expression in a background compromised for Brm function reduces Mek (MAPKK/Sor) protein levels, consistent with the decrease in ERK activation observed. Taken together, our results show that Gem and Brm act antagonistically to modulate the EGFR–Ras–MAPK signaling pathway, by affecting Mek levels during Drosophila development.

Um Jardim na Mata dos Medos : ou da análise inventiva do pictoresco

This text discusses the project for a garden by Gonçalo Ribeiro-Telles that argues for a different possibility of creating a garden as landscape continuum and exploring picturesque as an apparatus to expand the experience of the place

Differential interaction between the C2B domain of synaptotagmin-I and the Drosophila stonedA and stonedB proteins

The stoned locus in Drosophila encodes two proteins StonedA (STNA) and StonedB (STNB), both of which have been suggested to act as adaptins in mediating synaptic vesicle recycling. A combination of immunological, genetic and biochemical studies have shown an interaction of STNA and STNB with the C2B domain of Synaptotagmin-I (SYT-1), an integral synaptic vesicle protein that mediates Ca2+-dependent exocytosis, as well as endocytosis. The C2B domain of SYT-1 contains an AP-2 binding site that controls the size of recycled vesicles, and a C-terminal tryptophan-containing motif that acts as an internalization signal. Investigation of SYT-1 mutations in Drosophila has shown that altering the Ca2+ binding region of the C2B domain, results in a reduction in the rate of vesicle recycling, implicating this region in SYT-I endocytosis. In this poster, we report the molecular dissection of the interactions between the STNA and STNB proteins and the C2B domain of SYT-1. Deletion of the AP-2 binding site decreased the binding of both STNA and STNB. However, C-terminal deletions of the C2B domain significantly increased STNB binding. In contrast, the same C-terminal deletions reduced the affinity of the C2B domain for STNA. The possible interactions of both STNB and STNA with the Ca2+ binding region of SYT-1 will be also investigated.