152 research outputs found
PICALM Rescues Endocytic Defects Caused by the Alzheimer's Disease Risk Factor APOE4
APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). Narayan and Sienski et al. find that APOE4 disrupts early endocytosis, a process by which cells take up external material. By increasing the levels of another AD risk factor, PICALM, the authors are able to reverse these disruptions
Non-Coding RNAs : multi-tasking molecules in the cell
Articles in International JournalsIn the last years it has become increasingly clear that the mammalian
transcriptome is highly complex and includes a large number of small non-coding RNAs
(sncRNAs) and long noncoding RNAs (lncRNAs). Here we review the biogenesis
pathways of the three classes of sncRNAs, namely short interfering RNAs (siRNAs),
microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs). These ncRNAs have been
extensively studied and are involved in pathways leading to specific gene silencing and the
protection of genomes against virus and transposons, for example. Also, lncRNAs have
emerged as pivotal molecules for the transcriptional and post-transcriptional regulation of
gene expression which is supported by their tissue-specific expression patterns, subcellular
distribution, and developmental regulation. Therefore, we also focus our attention on their
role in differentiation and development. SncRNAs and lncRNAs play critical roles in
defining DNA methylation patterns, as well as chromatin remodeling thus having a
substantial effect in epigenetics. The identification of some overlaps in their biogenesis
pathways and functional roles raises the hypothesis that these molecules play concerted
functions in vivo, creating complex regulatory networks where cooperation with regulatory
proteins is necessary. We also highlighted the implications of biogenesis and gene
expression deregulation of sncRNAs and lncRNAs in human diseases like cancer
Distinct features of the piRNA pathway in somatic and germ cells: from piRNA cluster transcription to piRNA processing and amplification
The discovery, distribution, and evolution of viruses associated with drosophila melanogaster
Drosophila melanogaster is a valuable invertebrate model for viral infection and antiviral immunity, and is a focus for studies of insect-virus coevolution. Here we use a metagenomic approach to identify more than 20 previously undetected RNA viruses and a DNA virus associated with wild D. melanogaster. These viruses not only include distant relatives of known insect pathogens, but also novel groups of insect-infecting viruses. By sequencing virus-derived small RNAs we show that the viruses represent active infections of Drosophila. We find that the RNA viruses differ in the number and properties of their small RNAs, and we detect both siRNAs and a novel miRNA from the DNA virus. Analysis of small RNAs also allows us to identify putative viral sequences that lack detectable sequence similarity to known viruses. By surveying >2000 individually collected wild adult Drosophila we show that more than 30% of D. melanogaster carry a detectable virus, and more than 6% carry multiple viruses. However, despite a high prevalence of the Wolbachia endosymbiontâwhich is known to be protective against virus infections in Drosophilaâwe were unable to detect any relationship between the presence of Wolbachia and the presence of any virus. Using publicly available RNA-seq datasets we show that the community of viruses in Drosophila laboratories is very different from that seen in the wild, but that some of the newly discovered viruses are nevertheless widespread in laboratory lines and are ubiquitous in cell culture. By sequencing viruses from individual wild-collected flies we show that some viruses are shared between D. melanogaster and D. simulans. Our results provide an essential evolutionary and ecological context for host-virus interaction in Drosophila, and the newly reported viral sequences will help develop D. melanogaster further as a model for molecular and evolutionary virus research
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