iLIR@viral : a web resource for LIR motif-containing proteins in viruses

Autophagy has been shown to mediate the lysosomal degradation of pathogenic bacteria and viruses (xenophagy), and to contribute to the activation of innate and adaptative immune responses. Autophagy can serve as an antiviral defense mechanism but also as a proviral process during infection. ATG8-family proteins play a central role in the autophagy process due to their ability to interact with components of the autophagy machinery as well as selective autophagy receptors and adaptor proteins. Such interactions are usually mediated through LC3-interacting region (LIR) motifs. So far, only one viral protein has been experimentally shown to have a functional LIR motif, leaving open a vast field for investigation. Here, we have developed the iLIR@viral database (http://ilir.uk/virus/) as a freely accessible web resource listing all the putative canonical LIR motifs identified in viral proteins. Additionally, we used a curated text-mining analysis of the literature to identify novel putative LIR motif-containing protein (LICRPs) in viruses. We anticipate that iLIR@viral will assist with elucidating the full complement of LIRCPs in viruses

Selective autophagic degradation of the IKK complex in Drosophila is mediated by Kenny/IKKy to control inflammation

Implication of autophagy in the downregulation of immune signalling pathways through the degradation of their components constitutes an emerging field of investigation. Our work showed that the selective interaction of Drosophila Kenny/IKK with the autophagic machinery is required for the degradation of the IKK complex. This regulatory mechanism is essential for the downregulation of the IMD immune pathway in response to commensal microbiota to prevent inflammatio

Kenny mediates selective autophagic degradation of the IKK complex to control innate immune responses

Selective autophagy is a catabolic process with which cellular material is specifically targeted for degradation by lysosomes. The function of selective autophagic degradation of self-components in the regulation of innate immunity is still unclear. Here we show that Drosophila Kenny, the homologue of mammalian IKKγ, is a selective autophagy receptor that mediates the degradation of the IB kinase complex. Selective autophagic degradation of the IκB kinase complex prevents constitutive activation of the immune deficiency pathway in response to commensal microbiota. We show that autophagy-deficient flies have a systemic innate immune response that promotes a hyperplasia phenotype in the midgut. Remarkably, human IKKγ does not interact with mammalian Atg8-family proteins. Using a mathematical model, we suggest mechanisms by which pathogen selection might have driven the loss of LIR-motif functionality during evolution. Our results suggest that there may have been an autophagy-related switch during the evolution of the IKKγ proteins in metazoans

Assistência de enfermagem na creche pertinho da mamãe

Trabalho apresentado no 31º SEURS - Seminário de Extensão Universitária da Região Sul, realizado em Florianópolis, SC, no período de 04 a 07 de agosto de 2013 - Universidade Federal de Santa Catarina.O Projeto de Extensão "Assistência de Enfermagem no Centro de Educação Infantil Pertinho da Mamãe da UEM" teve início em abril de 2006, e conta com a participação de docentes, alunos de graduação e de pós-graduação em enfermagem. O projeto desenvolve atividades voltadas ao atendimento integral das crianças, trabalhando junto à equipe de saúde e educação da instituição, bem como junto aos pais das crianças matriculadas, com o objetivo de integrar o cuidado e a educação, de modo a melhorar a qualidade da assistência do CEI. A educação em saúde e o compartilhamento de experiências entre a equipe de enfermagem, docentes, alunos e usuários proporciona um crescimento conjunto e a integração de saberes, em direção a uma consciência articulada com a prática, contribuindo desta maneira para a construção da autonomia dos sujeitos envolvidos, por meio da qualificação da assistência em saúde e do desenvolvimento de novas pesquisas voltadas a esta realidade de atuação do enfermeiro

ESTUDOS SOBRE ARTE MARCIAL E LUTAS NA LITERATURA BRASILEIRA: REVISÃO SISTEMÁTICA

Objetivo: Analisar, utilizando um modelo de revisão sistemática da literatura nacional, a produção de artigos científicos na área de lutas. Métodos: A revisão sistemática da literatura foi realizada na base de dados Scientific Electronic Library Online (SCIELO). Foram feitas buscas apenas de artigos originais utilizando o termo artes marciais ou lutas. Na análise estatística o teste do qui-quadrado foi utilizado para comparar as proporções. Resultados: Os 18 trabalhos científicos foram publicados em nove periódicos entre os anos de 1998 e 2011. O maior número de estudos foi com Judô quando comparados as outras modalidades (Judô: 66,8%, outras 33,2% ; teste qui-quadrado com p= 0,001). Os estudos encontrados enfocaram mais o esporte (Esporte: 86,6%, Saúde: 5,8%, Educação: 5,8% e Outros: 11,7%; teste qui-quadrado com p= 0,001). Conclusão: Há necessidade de mais investigações a cerca do tema artes marciais, bem como, mais trabalhos com o sexo feminino, com idosos, crianças e adolescentes

Targeted interplay between bacterial pathogens and host autophagy

Due to the critical role played by autophagy in pathogen clearance, pathogens have developed diverse strategies to subvert autophagy. Despite previous key findings of bacteria-autophagy interplay, a systems level insight into selective targeting by the host and autophagy modulation by the pathogens is lacking. We predicted potential interactions between human autophagy proteins and effector proteins from 56 pathogenic bacterial species by identifying bacterial proteins predicted to have recognition motifs for selective autophagy receptors p62/NDP52 and LC3. Conversely, using structure-based interaction prediction methods, we identified bacterial effector proteins that could putatively modify core autophagy components. Our analysis revealed that autophagy receptors in general potentially target mostly genus specific proteins, and not those present in multiple genera. We also show that the complementarity between the predicted p62 and NDP52 targets, which has been shown for Salmonella, Listeria and Shigella, could be observed across other pathogens. Using literature evidence, we hypothesize that this complementarity potentially leave the host more susceptible to chronic infections upon the mutation of one of the autophagy receptors. To check any bias caused by our pathogenic protein selection criteria, control analysis using proteins derived from entero-toxigenic and non-toxigenic Bacillus outer membrane vesicles indicated that autophagy targets pathogenic proteins rather than non-pathogenic ones. We also observed a pathogen specific pattern as to which autophagy phase could be modulated by specific genera. We found intriguing examples of bacterial proteins which could modulate autophagy, and in turn capable of being targeted by the autophagy receptors and LC3 as a host defence mechanism. To demonstrate the validity of our predictions, we confirmed experimentally with in vitro Salmonella invasion assays the bi-directional interactions underlying the interplay between a Salmonella protease, YhjJ and autophagy. Our comparative meta-analysis points out key commonalities and differences in how pathogens could affect autophagy and how autophagy potentially recognises these pathogenic effectors

A nuclear role for Atg8-family proteins

Despite the growing evidence that the macroautophagy/autophagy-related protein LC3 is localized in the nucleus, why and how it is targeted to the nucleus are poorly understood. In our recent study, we found that transcription factor seq (sequoia) interacts via its LIR motif with Atg8a, the Drosophila homolog of LC3, to negatively regulate the transcription of autophagy genes. Atg8a was found to also interact with the nuclear acetyltransferase complex subunit YL-1 and deacetylase Sirt2. Modulation of the acetylation status of Atg8a by YL-1 and Sirt2 affects the interaction between seq and Atg8a, and controls the induction of autophagy. Our work revealed a novel nuclear role for Atg8a, which is linked with the transcriptional regulation of autophagy genes

Degradation of arouser by endosomal microautophagy is essential for adaptation to starvation in Drosophila

Hunger drives food-seeking behaviour and controls adaptation of organisms to nutrient availability and energy stores. Lipids constitute an essential source of energy in the cell that can be mobilised during fasting by autophagy. Selective degradation of proteins by autophagy is made possible essentially by the presence of LIR and KFERQ-like motifs. Using in silico screening of Drosophila proteins that contain KFERQ-like motifs, we identified and characterized the adaptor protein Arouser, which functions to regulate fat storage and mobilisation and is essential during periods of food deprivation. We show that hypomorphic arouser mutants are not satiated, are more sensitive to food deprivation, and are more aggressive, suggesting an essential role for Arouser in the coordination of metabolism and food-related behaviour. Our analysis shows that Arouser functions in the fat body through nutrient-related signalling pathways and is degraded by endosomal microautophagy. Arouser degradation occurs during feeding conditions, whereas its stabilisation during non-feeding periods is essential for resistance to starvation and survival. In summary, our data describe a novel role for endosomal microautophagy in energy homeostasis, by the degradation of the signalling regulatory protein Arouser

Regulation of expression of autophagy genes by Atg8a-interacting partners Sequoia, YL-1 and Sir2 in Drosophila

Autophagy is the degradation of cytoplasmic material through the lysosomal pathway. One of the most studied autophagy-related proteins is LC3. Despite growing evidence that LC3 is enriched in the nucleus, its nuclear role is poorly understood. Here, we show that Drosophila Atg8a protein, homologous to mammalian LC3, interacts with the transcription factor Sequoia in a LIR motif-dependent manner. We show that Sequoia depletion induces autophagy in nutrient-rich conditions through the enhanced expression of autophagy genes. We show that Atg8a interacts with YL-1, a component of a nuclear acetyltransferase complex, and that it is acetylated in nutrient-rich conditions. We also show that Atg8a interacts with the deacetylase Sir2, which deacetylates Atg8a during starvation to activate autophagy. Our results suggest a mechanism of regulation of the expression of autophagy genes by Atg8a, which is linked to its acetylation status and its interaction with Sequoia, YL-1, and Sir2