Ulysses spacecraft in situ detections of cometary dust trails.

The Ulysses spacecraft was launched in 1990 and, after a Jupiter swing-by in 1992, became the first interplanetary spacecraft orbiting the Sun on a highly inclined trajectory with an inclination of [Formula: see text]. The spacecraft was equipped with an impact ionization dust detector which provided 17 years of in situ dust measurements in interplanetary space from 1990 to 2007. Cometary meteoroid streams (also referred to as trails) exist along the orbits of comets, forming fine structures of the interplanetary dust cloud. We use the Interplanetary Meteoroid Environment for eXploration (IMEX) dust streams in space model (Soja RH et al. 2015 Characteristics of the dust trail of 67P/Churyumov-Gerasimenko: an application of the IMEX model. Astron. Astrophys. 583, A18. (doi:10.1051/0004-6361/201526184)) to predict cometary stream traverses by Ulysses and re-analyse the Ulysses dust dataset in order to identify impacts of cometary stream particles detected during such trail traverses. We identify 19 particles compatible with three Ulysses trail traverses on 12 March 1995, 25-27 April 2001 and 16-19 May 2001. The particle origin is compatible with up to five comets, i.e. 10P/Tempel 2, 146P/Shoemaker-LINEAR, 267P/LONEOS and possibly 45P/Honda-Mrkos-Pajdusáková and P/1999 RO28 (LONEOS). We find a dust spatial density in these trails of approximately [Formula: see text]. The radii of the detected cometary stream particles derived from the dust instrument calibration are in the micrometre range. The in situ analysis of meteoroid trail particles in space, which can be traced back to their source bodies, opens a new opportunity for remote compositional analysis of comets and asteroids without the necessity to send a spacecraft to or even land on these celestial bodies, opening new opportunities for future space missions equipped with in situ dust analyzers. This article is part of the theme issue 'Dust in the Solar System and beyond'.

The TLCΦ satellite phage harbors a Xer recombination activation factor.

The circular chromosomes of bacteria can be concatenated into dimers by homologous recombination. Dimers are solved by the addition of a cross-over at a specific chromosomal site, dif, by 2 related tyrosine recombinases, XerC and XerD. Each enzyme catalyzes the exchange of a specific pair of strands. Some plasmids exploit the Xer machinery for concatemer resolution. Other mobile elements exploit it to integrate into the genome of their host. Chromosome dimer resolution is initiated by XerD. The reaction is under the control of a cell-division protein, FtsK, which activates XerD by a direct contact. Most mobile elements exploit FtsK-independent Xer recombination reactions initiated by XerC. The only notable exception is the toxin-linked cryptic satellite phage of Vibrio cholerae, TLCΦ, which integrates into and excises from the dif site of the primary chromosome of its host by a reaction initiated by XerD. However, the reaction remains independent of FtsK. Here, we show that TLCΦ carries a Xer recombination activation factor, XafT. We demonstrate in vitro that XafT activates XerD catalysis. Correspondingly, we found that XafT specifically interacts with XerD. We further show that integrative mobile elements exploiting Xer (IMEXs) encoding a XafT-like protein are widespread in gamma- and beta-proteobacteria, including human, animal, and plant pathogens.

FtsK translocation permits discrimination between an endogenous and an imported Xer/dif recombination complex.

In bacteria, the FtsK/Xer/dif (chromosome dimer resolution site) system is essential for faithful vertical genetic transmission, ensuring the resolution of chromosome dimers during their segregation to daughter cells. This system is also targeted by mobile genetic elements that integrate into chromosomal dif sites. A central question is thus how Xer/dif recombination is tuned to both act in chromosome segregation and stably maintain mobile elements. To explore this question, we focused on pathogenic Neisseria species harboring a genomic island in their dif sites. We show that the FtsK DNA translocase acts differentially at the recombination sites flanking the genomic island. It stops at one Xer/dif complex, activating recombination, but it does not stop on the other site, thus dismantling it. FtsK translocation thus permits cis discrimination between an endogenous and an imported Xer/dif recombination complex.

Assessment of simple sequence repeats signature in hepatitis E virus (HEV) genomes.

BACKGROUND: Hepatitis E virus (HEV) is small (27-34 nm diameter) non-enveloped with positive sense ssRNA genome. Microsatellites or simple sequence repeats (SSR) are short tandem repeat sequences present across coding and non-coding regions of both prokaryotes and eukaryotes. They are involved with genome function and evolution at multiple levels. RESULTS: The complete genome sequences of 22 HEV genomes of the family Hepeviridae and genus Orthohepevirus (21 species) and Piscihepevirus (1 species) were extracted from NCBI database ( http://www.ncbi.nlm.nih.gov/ ). The extraction of microsatellites was done using Imperfect Microsatellite Extractor (IMEx) in 'Advance-Mode'. The average genome size of the studied HEV genomes was 7003nt and it ranged from 6649nt (HEV11) to 7310nt (HEV22). The average GC content of the genomes was ~ 55%. A total of 519 SSRs and 21 cSSRS were extracted from the HEV genomes with an average incidence of 24 per genome ranging from 14 (HEV13) to 34 (HEV19). The cSSR incidence ranged from 0 (eight species) to 4 (HEV19). The genomes with no cSSR incidence had an SSR incidence range from 14 to 28. There were just four hexa-nucleotide repeat motifs and 5 penta-nucleotide repeat motifs observed. The most prevalent mono-, di-, and tri-nucleotide repeat motifs were "C", "GT/TG", and "GAC/CTG" respectively. The studied genomes had a minimum of ~ 90% incident SSRs present in the coding regions. Viruses with same or similar hosts are placed together on the phylogenetic tree implicating viral host being one of the driving forces for evolution. Conclusions Host range in viruses is being decided by multiple factors aided by the unique genome SSR signature and genomes of varied compositions need to be analyzed to forge a widely acceptable rule for predicting the same.

Mobile Element Integration Reveals a Chromosome Dimer Resolution System in Legionellales.

In bacteria, the mechanisms used to repair DNA lesions during genome replication include homologous recombination between sister chromosomes. This can lead to the formation of chromosome dimers if an odd number of crossover events occurs. The dimers must be resolved before cell separation to ensure genomic stability and cell viability. Dimer resolution is achieved by the broadly conserved dif/Xer system, which catalyzes one additional crossover event immediately prior to cell separation. While dif/Xer systems have been characterized or predicted in the vast majority of proteobacteria, no homologs to dif or xer have been identified in the order Legionellales. Here, we report the discovery of a distinct single-recombinase dif/Xer system in the intracellular pathogen Legionella pneumophila. The dif site was uncovered by our analysis of Legionella mobile element-1 (LME-1), which harbors a dif site mimic and integrates into the L. pneumophila genome via site-specific recombination. We demonstrate that lpg1867 (here named xerL) encodes a tyrosine recombinase that is necessary and sufficient for catalyzing recombination at the dif site and that deletion of dif or xerL causes filamentation along with extracellular and intracellular growth defects. We show that the dif/XerL system is present throughout Legionellales and that Coxiella burnetii XerL and its cognate dif site can functionally substitute for the native system in L. pneumophila. Finally, we describe an unexpected link between C. burnetii dif/Xer and the maintenance of its virulence plasmids. IMPORTANCE The maintenance of circular chromosomes depends on the ability to resolve aberrant chromosome dimers after they form. In most proteobacteria, broadly conserved Xer recombinases catalyze single crossovers at short, species-specific dif sites located near the replication terminus. Chromosomal dimerization leads to the formation of two copies of dif within the same molecule, leading to rapid site-specific recombination and conversion back into chromosome monomers. The apparent absence of chromosome dimer resolution mechanisms in Legionellales has been a mystery to date. By studying a phage-like mobile genetic element, LME-1, we have identified a previously unknown single-recombinase dif/Xer system that is not only widespread across Legionellales but whose activity is linked to virulence in two important human pathogens.

Navigating the Global Protein-Protein Interaction Landscape Using iRefWeb.

iRefWeb is a resource that provides web interface to a large collection of protein-protein interactions aggregated from major primary databases. The underlying data-consolidation process, called iRefIndex, implements a rigorous methodology of identifying redundant protein sequences and integrating disparate data records that reference the same peptide sequences, despite many potential differences in data identifiers across various source databases. iRefWeb offers a unified user interface to all interaction records and associated information collected by iRefIndex, in addition to a number of data filters and visual features that present the supporting evidence. Users of iRefWeb can explore the consolidated landscape of protein-protein interactions, establish the provenance and reliability of each data record, and compare annotations performed by different data curator teams. The iRefWeb portal is freely available at http://wodaklab.org/iRefWeb .

Xer Site Specific Recombination: Double and Single Recombinase Systems.

The separation and segregation of newly replicated bacterial chromosomes can be constrained by the formation of circular chromosome dimers caused by crossing over during homologous recombination events. In Escherichia coli and most bacteria, dimers are resolved to monomers by site-specific recombination, a process performed by two Chromosomally Encoded tyrosine Recombinases (XerC and XerD). XerCD recombinases act at a 28 bp recombination site dif, which is located at the replication terminus region of the chromosome. The septal protein FtsK controls the initiation of the dimer resolution reaction, so that recombination occurs at the right time (immediately prior to cell division) and at the right place (cell division septum). XerCD and FtsK have been detected in nearly all sequenced eubacterial genomes including Proteobacteria, Archaea, and Firmicutes. However, in Streptococci and Lactococci, an alternative system has been found, composed of a single recombinase (XerS) genetically linked to an atypical 31 bp recombination site (difSL). A similar recombination system has also been found in 𝜀-proteobacteria such as Campylobacter and Helicobacter, where a single recombinase (XerH) acts at a resolution site called difH. Most Archaea contain a recombinase called XerA that acts on a highly conserved 28 bp sequence dif, which appears to act independently of FtsK. Additionally, several mobile elements have been found to exploit the dif/Xer system to integrate their genomes into the host chromosome in Vibrio cholerae, Neisseria gonorrhoeae, and Enterobacter cloacae. This review highlights the versatility of dif/Xer recombinase systems in prokaryotes and summarizes our current understanding of homologs of dif/Xer machineries.

Potential linkage between compound microsatellites and recombination in geminiviruses: Evidence from comparative analysis.

The compound microsatellites consist of two or more individual microsatellites, originate from mutation or imperfection in simple repeat sequences. The reports on systematic analysis of the occurrence, size and density of compound microsatellite (cSSR) types are very rare. Our study indicates that cSSRs are clustered at specific regions in the begomovirus genomes. cSSRs were overrepresented in majority of begomovirus genomes indicating that they might have some functional significance. Further, non-random distribution pattern of cSSR in begomovirus genomes was significantly correlated with the recombination breakpoint positions in the genome. The analysis of cSSR regions in the viral genome indicates the presence of stem loop (hairpin) secondary structure. The significance of these findings in biology of geminiviruses is discussed based on our present understanding of recombination and repetitive DNA. To our knowledge, this is the first analysis suggesting the possible association between recombination and microsatellites in any viral genome.

Genome-wide scan for analysis of simple and imperfect microsatellites in diverse carlaviruses.

An exhaustive compilation and analysis of incidence, distribution and variation of simple sequence repeats (SSRs) in viruses are required to understand the evolution and functional aspects of repetitive sequences. Present study focuses on the analysis of SSRs in 32 species of carlaviruses. The full length genome sequences were assessed from NCBI (http://www.ncbi.nlm.nih.-gov/) and analyzed using IMEx software. Variance in incidence of SSRs was observed, independent of genome size. Though the conversion of SSRs to imperfect microsatellite or compound SSR is low; compound microsatellites constituted by variant motifs accounted for up to 12.5% of the SSRs. Mononucleotide A/T is most prevalent followed by dinucleotide GT/TG and trinucleotide AAG/GAA in these genomes. The SSR and cSSR are predominantly localized to the coding region RDRP (RNA dependent RNA polymerase) and ORF-6 (open reading frame). The relative frequency of different classes of simple and compound microsatellites has been highlighted in accordance with the biology of carlavirus. Characterization of such variations would be pivotal for deciphering the enigma of these widely used, but incompletely understood sequences.

In- silico exploration of thirty alphavirus genomes for analysis of the simple sequence repeats.

The compilation of simple sequence repeats (SSRs) in viruses and its analysis with reference to incidence, distribution and variation would be instrumental in understanding the functional and evolutionary aspects of repeat sequences. Present study encompasses the analysis of SSRs across 30 species of alphaviruses. The full length genome sequences, assessed from NCBI were used for extraction and analysis of repeat sequences using IMEx software. The repeats of different motif sizes (mono- to penta-nucleotide) observed therein exhibited variable incidence across the species. Expectedly, mononucleotide A/T was the most prevalent followed by dinucleotide AG/GA and trinucleotide AAG/GAA in these genomes. The conversion of SSRs to imperfect microsatellite or compound microsatellite (cSSR) is low. cSSR, primarily constituted by variant motifs accounted for up to 12.5% of the SSRs. Interestingly, seven species lacked cSSR in their genomes. However, the SSR and cSSR are predominantly localized to the coding region ORFs for non structural protein and structural proteins. The relative frequencies of different classes of simple and compound microsatellites within and across genomes have been highlighted.

Incidence, complexity and diversity of simple sequence repeats across potexvirus genomes.

An in-silico analysis of simple sequence repeats (SSRs) in genomes of 32 species of potexviruses was performed wherein a total of 691 SSRs and 33 cSSRs were observed. Though SSRs were present in all the studied genomes their incident frequency ranged from 11 to 30 per genome. Further, 10 potexvirus genomes possessed no cSSRs when extracted at a dMAX of 10 and wherein present, the highest frequency was 3. SSR and cSSR incidence, relative density and relative abundance were non-significantly correlated with genome size and GC content suggesting an ongoing evolutionary and adaptive phase of the virus species. SSRs present primarily ranged from mono- to tri-nucleotide repeat motifs with a greatly skewed distribution across the coding and non-coding regions. Present work is an effort for the undergoing compilation and analysis of incidence, distribution and variation of the viral repeat sequences to understand their evolutionary and functional relevance.

In-silico analysis of simple and imperfect microsatellites in diverse tobamovirus genomes.

An in-silico analysis of simple sequence repeats (SSRs) in 30 species of tobamoviruses was done. SSRs (mono to hexa) were present with variant frequency across species. Compound microsatellites, primarily of variant motifs accounted for up to 11.43% of the SSRs. Motif duplications were observed for A, T, AT, and ACA repeats. (AG)-(TC) was the most prevalent SSR-couple. SSRs were differentially localized in the coding region with ~54% on the 128 kDa protein while 20.37% was exclusive to 186 kDa protein. Characterization of such variations is important for elucidating the origin, sequence variations, and structure of these widely used, but incompletely understood sequences.