"In vivo" toxicity of a truncated version of the Drosophila Rst-IrreC protein is dependent on the presence of a glutamine-rich region in its intracellular domain

The roughest-irregular chiasm C ( rst-irreC) gene of Drosophila melanogaster encodes a transmembrane glycoprotein containing five immunoglobulin-like domains in its extracellular portion and an intracytoplasmic tail rich in serine and threonine as well some conserved motifs suggesting signal transduction activity. In the compound eye, loss-of-function rst-irreC mutants lack the characteristic wave of programmed cell death happening in early pupa and which is essential for the elimination of the surplus interommatidial cells. Here we report an investigation on the role played by the Rst-irreC molecule in triggering programmed cell death. "In vivo" transient expression assays showed that deletion of the last 80 amino acids of the carboxyl terminus produces a form of the protein that is highly toxic to larvae. This toxicity is suppressed if an additional 47 amino acid long, glutamine-rich region ("opa-like domain"), is also removed from the protein. The results suggest the possibility that the opa-like domain and the carboxyl terminus act in concert to modulate rst-irreC function in apoptosis, and we discuss this implication in the context of the general mechanisms causing glutamine-rich neurodegenerative diseases in humans

Ubiquitous overexpression of a transgene encoding the extracellular portion of the Drosophila Roughest-Irregular Chiasm C protein induces early embryonic lethality

The cell adhesion molecule Rst-irreC is a transmembrane glycoprotein of the immunoglobulin superfamily involved in several important developmental processes in Drosophila, including axonal pathfinding in the optic lobe and programmed cell death and pigment cell differentiation in the pupal retina. As an initial step towards the "in vivo" functional analysis of this protein we have generated transgenic fly stocks carrying a truncated cDNA construct encoding only the extracellular domain of Rst-IrreC under the transcriptional control of the heat shock inducible promoter hsp70. We show that heat-shocking embryos bearing the transgene during the first 8hs of development lead to a 3-4 fold reduction in their viability compared to wild type controls. The embryonic lethality can already be produced by applying the heat pulse in the first 3hs of embryonic development, does not seem to be suppressed in the absence of wildtype product and is progressively reduced as the heat treatment is applied later in embryogenesis. These results are compatible with the hypothesis of the lethal phenotype being primarily due to heterophilic interactions between Rst-IrreC extracellular domain and an yet unknown ligand.

Ocorrência do Campylobacter pylori em pacientes com gastrite e úlcera péptica / Occurrence of Campylobacter pylori in patients with gastritis and peptic ulcer

Biopsias endoscópicas do antro e da borda da lesäo péptica (úlcera gástrica e úlcera duodenal)foram obtidas de 56 pacientes para estudo histológico e microbiológico, no sentido de se determinar a ocorrência do C. pylori. Trinta e nove pacientes apresentaram evidências de gastrite antral e em 37 (94,8%) deles o bacilo foi detectado, enquanto que nos 17 com histologia normal a cultura foi positiva em somente dois (p<0,01). Nos pacientes com úlcera duodenal e úlcera gástrica a positividade para o C. pylori, no fragmento da borda da lesäo, foi de 100% e 88,8%, respectivamente. Os achados sobre a microbiologia do C. pylori näo diferiram daqueles previamente descritos em estudos similares. A microscopia eletrónica o bacilo foi encontrado próximo ou aderido às superfícies celulares sem haver sinais e localizaçäo intraepitelial. Este estudo confirma a associaçäo do C. pylori com a gastrite e a úlcera gastroduodenal, descrita na literatura