Ancient Darwinian replicators nested within eubacterial genomes

Integrative mobile genetic elements (MGEs), such as transposons and insertion sequences, propagate within bacterial genomes, but persistence times in individual lineages are short. For long-term survival, MGEs must continuously invade new hosts by horizontal transfer. Theoretically, MGEs that persist for millions of years in single lineages, and are thus subject to vertical inheritance, should not exist. Here we draw attention to an exception – a class of MGE termed REPIN. REPINs are non-autonomous MGEs whose duplication depends on non-jumping RAYT transposases. Comparisons of REPINs and typical MGEs show that replication rates of REPINs are orders of magnitude lower, REPIN population size fluctuations correlate with changes in available genome space, REPIN conservation depends on RAYT function, and REPIN diversity accumulates within host lineages. These data lead to the hypothesis that REPINs form enduring, beneficial associations with eubacterial chromosomes. Given replicative nesting, our hypothesis predicts conflicts arising from the diverging effects of selection acting simultaneously on REPINs and host genomes. Evidence in support comes from patterns of REPIN abundance and diversity in two distantly related bacterial species. Together this bolsters the conclusion that REPINs are the genetic counterpart of mutualistic endosymbiotic bacteria

How sequence populations persist inside bacterial genomes

Compared to their eukaryotic counterparts, bacterial genomes are small and contain extremely tightly packed genes. Therefore, discovering a large number of short repetitive sequences in the genomes of Pseudomonads and Enterobacteria is unexpected. These sequences can independently replicate in the host genome and form populations that persist for millions of years. Here we model the interactions of intragenomic sequence populations with the bacterial host. In a simple model, sequence populations either expand until they drive the host to extinction or the sequence population gets purged from the genome. Including horizontal gene transfer does not change the qualitative outcome of the model and leads to the extinction of the sequence population. However, a sequence population can be stably maintained, if each sequence provides a benefit that decreases with increasing sequence population size. But concurrently, the replication of the sequence population needs to be costly to the host. Surprisingly, in regimes where horizontal gene transfer plays a role, the benefit conferred by the sequence population does not have to exceed the damage it causes. Together, our analyses provide a plausible scenario for the persistence of sequence populations in bacterial genomes. More importantly, we hypothesize a limited biologically relevant parameter range, which can be tested in future experiments

Transposable elements promote the evolution of genome streamlining

Eukaryotes and prokaryotes have distinct genome architectures, withmarked differences in genome size, the ratio of coding/non-coding DNA,and the abundance of transposable elements (TEs). As TEs replicate inde-pendently of their hosts, the proliferation of TEs is thought to have drivengenome expansion in eukaryotes. However, prokaryotes also have TEs inintergenic spaces, so why do prokaryotes have small, streamlined genomes?Using anin silicomodel describing the genomes of single-celled asexualorganisms that coevolve with TEs, we show that TEs acquired from theenvironment by horizontal gene transfer can promote the evolution ofgenome streamlining. The process depends on local interactions and isunderpinned by rock–paper–scissors dynamics in which populations ofcells with streamlined genomes beat TEs, which beat non-streamlinedgenomes, which beat streamlined genomes, in continuous and repeatingcycles. Streamlining is maladaptive to individual cells, but improves lineageviability by hindering the proliferation of TEs. Streamlining does not evolvein sexually reproducing populations because recombination partially freesTEs from the deleterious effects they cause.This article is part of the theme issue‘The secret lives of microbial mobilegenetic elements’

An Experimental Microarchitecture for a Superconducting Quantum Processor

Quantum computers promise to solve certain problems that are intractable for classical computers, such as factoring large numbers and simulating quantum systems. To date, research in quantum computer engineering has focused primarily at opposite ends of the required system stack: devising high-level programming languages and compilers to describe and optimize quantum algorithms, and building reliable low-level quantum hardware. Relatively little attention has been given to using the compiler output to fully control the operations on experimental quantum processors. Bridging this gap, we propose and build a prototype of a flexible control microarchitecture supporting quantum-classical mixed code for a superconducting quantum processor. The microarchitecture is based on three core elements: (i) a codeword-based event control scheme, (ii) queue-based precise event timing control, and (iii) a flexible multilevel instruction decoding mechanism for control. We design a set of quantum microinstructions that allows flexible control of quantum operations with precise timing. We demonstrate the microarchitecture and microinstruction set by performing a standard gate-characterization experiment on a transmon qubit.Comment: 13 pages including reference. 9 figure

hArtes: Hardware-Software Codesign for Heterogeneous Multicore Platforms

Developing heterogeneous multicore platforms requires choosing the best hardware configuration for mapping the application, and modifying that application so that different parts execute on the most appropriate hardware component. The hArtes toolchain provides the option of automatic or semi-automatic support for this mapping. During test and validation on several computation-intensive applications, hArtes achieved substantial speedups and drastically reduced development times

Genomic analysis of the kiwifruit pathogen Pseudomonas syringae pv. actnidiae provides insight into the origins of an emergent plant disease

The origins of crop diseases are linked to domestication of plants. Most crops were domesticated centuries – even millennia – ago, thus limiting opportunity to understand the concomitant emergence of disease. Kiwifruit (Actinidia spp.) is an exception: domestication began in the 1930s with outbreaks of canker disease caused by P. syringae pv. actinidiae (Psa) first recorded in the 1980s. Based on SNP analyses of two circularized and 34 draft genomes, we show that Psa is comprised of distinct clades exhibiting negligible within-clade diversity, consistent with disease arising by independent samplings from a source population. Three clades correspond to their geographical source of isolation; a fourth, encompassing the Psa-V lineage responsible for the 2008 outbreak, is now globally distributed. Psa has an overall clonal population structure, however, genomes carry a marked signature of within-pathovar recombination. SNP analysis of Psa-V reveals hundreds of polymorphisms; however, most reside within PPHGI-1-like conjugative elements whose evolution is unlinked to the core genome. Removal of SNPs due to recombination yields an uninformative (star-like) phylogeny consistent with diversification of Psa-V from a single clone within the last ten years. Growth assays provide evidence of cultivar specificity, with rapid systemic movement of Psa-V in Actinidia chinensis. Genomic comparisons show a dynamic genome with evidence of positive selection on type III effectors and other candidate virulence genes. Each clade has highly varied complements of accessory genes encoding effectors and toxins with evidence of gain and loss via multiple genetic routes. Genes with orthologs in vascular pathogens were found exclusively within Psa-V. Our analyses capture a pathogen in the early stages of emergence from a predicted source population associated with wild Actinidia species. In addition to candidate genes as targets for resistance breeding programs, our findings highlight the importance of the source population as a reservoir of new disease

The hArtes Tool Chain

This chapter describes the different design steps needed to go from legacy code to a transformed application that can be efficiently mapped on the hArtes platform

Quantitative Analysis of Situation Awareness (QASA): modelling and measuring situation awareness using signal detection theory

This paper presents a model of situation awareness (SA) that emphasises that SA is necessarily built using a subset of available information. A technique (Quantitative Analysis of Situation Awareness – QASA), based around signal detection theory, has been developed from this model that provides separate measures of actual SA (ASA) and perceived SA (PSA), together with a feature unique to QASA, a measure of bias (information acceptance). These measures allow the exploration of the relationship between actual SA, perceived SA and information acceptance. QASA can also be used for the measurement of dynamic ASA, PSA and bias. Example studies are presented and full details of the implementation of the QASA technique are provided