Modelling the structure and evolution of cultural information as quasispecies.

We present a novel mode of cultural evolution whereby some forms of transmission may be modelled as quasispecies. The model incorporates the effect of high rates of error in certain forms of communication; while also building on the structural similarities between biological molecules and written language. Firstly, both written language and key biological molecules, such as RNA and proteins, are modular. Within these molecules, structural domains may be recombined, while retaining their function. Likewise, sentences are structured as combinations of clauses, in which each clause contains a domain of information. The clausal structure permits the recombination of information to adopt different meanings, while allowing each unit to retain its identity. Secondly, by virtue of intrinsically-high error rates, we show that some, but not all, aspects of communicated culture information exists as rapidly evolving clouds within the population. These clouds of cultural information behave as quasispecies, which we model with varying mutation rates and suitable selection coefficients. We then integrate these ideas with the application of Shannon Diversity Index to produce a more holistic view of culture that is centred on the evolution of its information. Re-imagining culture, as evolving clouds of information, unifies the mode in which information is stored culturally and biologically, and opens up new avenues of comparative analysis.

Listeria monocytogenes GlmR Is an Accessory Uridyltransferase Essential for Cytosolic Survival and Virulence.

The cytosol of eukaryotic host cells is an intrinsically hostile environment for bacteria. Understanding how cytosolic pathogens adapt to and survive in the cytosol is critical to developing novel therapeutic interventions against these pathogens. The cytosolic pathogen Listeria monocytogenes requires glmR (previously known as yvcK), a gene of unknown function, for resistance to cell-wall stress, cytosolic survival, inflammasome avoidance, and, ultimately, virulence in vivo. In this study, a genetic suppressor screen revealed that blocking utilization of UDP N-acetylglucosamine (UDP-GlcNAc) by a nonessential wall teichoic acid decoration pathway restored resistance to lysozyme and partially restored virulence of ΔglmR mutants. In parallel, metabolomic analysis revealed that ΔglmR mutants are impaired in the production of UDP-GlcNAc, an essential peptidoglycan and wall teichoic acid (WTA) precursor. We next demonstrated that purified GlmR can directly catalyze the synthesis of UDP-GlcNAc from GlcNAc-1P and UTP, suggesting that it is an accessory uridyltransferase. Biochemical analysis of GlmR orthologues suggests that uridyltransferase activity is conserved. Finally, mutational analysis resulting in a GlmR mutant with impaired catalytic activity demonstrated that uridyltransferase activity was essential to facilitate cell-wall stress responses and virulence in vivo. Taken together, these studies indicate that GlmR is an evolutionary conserved accessory uridyltransferase required for cytosolic survival and virulence of L. monocytogenes. IMPORTANCE Bacterial pathogens must adapt to their host environment in order to cause disease. The cytosolic bacterial pathogen Listeria monocytogenes requires a highly conserved protein of unknown function, GlmR (previously known as YvcK), to survive in the host cytosol. GlmR is important for resistance to some cell-wall stresses and is essential for virulence. The ΔglmR mutant is deficient in production of an essential cell-wall metabolite, UDP-GlcNAc, and suppressors that increase metabolite levels also restore virulence. Purified GlmR can directly catalyze the synthesis of UDP-GlcNAc, and this enzymatic activity is conserved in both Bacillus subtilis and Staphylococcus aureus. These results highlight the importance of accessory cell wall metabolism enzymes in responding to cell-wall stress in a variety of Gram-positive bacteria.

A New Ecological and Evolutionary Perspective on the Emergence of Oxygenic Photosynthesis.

In this hypothesis article, we propose that the timing of the evolution of oxygenic photosynthesis and the diversification of cyanobacteria is firmly tied to the geological evolution of Earth in the Mesoarchean to Neoarchean. Specifically, the diversification of species capable of oxygenic photosynthesis is tied to the growth of subaerial (above sea-level/terrestrial) continental crust, which provided niches for their diversification. Moreover, we suggest that some formerly aerobic bacterial lineages evolved to become anoxygenic photosynthetic as a result of changes in selection following the reintroduction of ferruginous conditions in the oceans at 1.88 GYa. Both conclusions are fully compatible with phylogenetic evidence. The hypothesis carries with it a predictive component-at least for terrestrial organisms-that the development and expansion of photosynthesis species was dependent on the geological evolution of Earth.

Regional Features of Long-Term Exposure to PM2.5 Air Quality over Asia under SSP Scenarios Based on CMIP6 Models.

This study investigates changes in fine particulate matter (PM2.5) concentration and air-quality index (AQI) in Asia using nine different Coupled Model Inter-Comparison Project 6 (CMIP6) climate model ensembles from historical and future scenarios under shared socioeconomic pathways (SSPs). The results indicated that the estimated present-day PM2.5 concentrations were comparable to satellite-derived data. Overall, the PM2.5 concentrations of the analyzed regions exceeded the WHO air-quality guidelines, particularly in East Asia and South Asia. In future SSP scenarios that consider the implementation of significant air-quality controls (SSP1-2.6, SSP5-8.5) and medium air-quality controls (SSP2-4.5), the annual PM2.5 levels were predicted to substantially reduce (by 46% to around 66% of the present-day levels) in East Asia, resulting in a significant improvement in the AQI values in the mid-future. Conversely, weak air pollution controls considered in the SSP3-7.0 scenario resulted in poor AQI values in China and India. Moreover, a predicted increase in the percentage of aged populations (>65 years) in these regions, coupled with high AQI values, may increase the risk of premature deaths in the future. This study also examined the regional impact of PM2.5 mitigations on downward shortwave energy and surface air temperature. Our results revealed that, although significant air pollution controls can reduce long-term exposure to PM2.5, it may also contribute to the warming of near- and mid-future climates.

Biogeographical Modeling of Alien Worlds.

In this article, we partially quantify the biological potential of an exoplanet. We employ a variety of biogeographical analyses, placing biological evolution in the context of the geological evolution of the planet as a whole. Terrestrial (as in Earthly) biodiversity is tightly constrained in terms of species richness by its environment. An organism's habitable environment may be considered its niche space or hypervolume in terms of the physical characteristics in which that organism can survive and reproduce. This fundamental niche forms the broader space in which the organism realizes its true niche in terms of its interactions with other species. Many of the physical characteristics can be determined from astrophysical constraints and are thus amenable for dissection. However, the geographical space that organisms occupy is driven by the geological evolution of a sizable telluric planet. In turn, this is driven by the progressive differentiation of its interior to produce increasingly felsic crust. Using a variety of available models, we can then constrain the available space that species can inhabit using species-area relationships. By considering a combination of astrophysical constraints and geographical space, we partially quantify the numbers of species that can inhabit the landscape that geology provides. Finally, we also identify a correlation between geomorphological scale and speciation, which, if validated, will allow further dissection of species diversity on alien worlds.

A chronology of global air quality.

Air pollution has been recognized as a threat to human health since the time of Hippocrates, ca 400 BC. Successive written accounts of air pollution occur in different countries through the following two millennia until measurements, from the eighteenth century onwards, show the growing scale of poor air quality in urban centres and close to industry, and the chemical characteristics of the gases and particulate matter. The industrial revolution accelerated both the magnitude of emissions of the primary pollutants and the geographical spread of contributing countries as highly polluted cities became the defining issue, culminating with the great smog of London in 1952. Europe and North America dominated emissions and suffered the majority of adverse effects until the latter decades of the twentieth century, by which time the transboundary issues of acid rain, forest decline and ground-level ozone became the main environmental and political air quality issues. As controls on emissions of sulfur and nitrogen oxides (SO2 and NOx) began to take effect in Europe and North America, emissions in East and South Asia grew strongly and dominated global emissions by the early years of the twenty-first century. The effects of air quality on human health had also returned to the top of the priorities by 2000 as new epidemiological evidence emerged. By this time, extensive networks of surface measurements and satellite remote sensing provided global measurements of both primary and secondary pollutants. Global emissions of SO2 and NOx peaked, respectively, in ca 1990 and 2018 and have since declined to 2020 as a result of widespread emission controls. By contrast, with a lack of actions to abate ammonia, global emissions have continued to grow. This article is part of a discussion meeting issue 'Air quality, past present and future'.

The effect of future ambient air pollution on human premature mortality to 2100 using output from the ACCMIP model ensemble.

Ambient air pollution from ground-level ozone and fine particulate matter (PM2.5) is associated with premature mortality. Future concentrations of these air pollutants will be driven by natural and anthropogenic emissions and by climate change. Using anthropogenic and biomass burning emissions projected in the four Representative Concentration Pathway scenarios (RCPs), the ACCMIP ensemble of chemistry-climate models simulated future concentrations of ozone and PM2.5 at selected decades between 2000 and 2100. We use output from the ACCMIP ensemble, together with projections of future population and baseline mortality rates, to quantify the human premature mortality impacts of future ambient air pollution. Future air pollution-related premature mortality in 2030, 2050 and 2100 is estimated for each scenario and for each model using a health impact function based on changes in concentrations of ozone and PM2.5 relative to 2000 and projected future population and baseline mortality rates. Additionally, the global mortality burden of ozone and PM2.5 in 2000 and each future period is estimated relative to 1850 concentrations, using present-day and future population and baseline mortality rates. The change in future ozone concentrations relative to 2000 is associated with excess global premature mortality in some scenarios/periods, particularly in RCP8.5 in 2100 (316 thousand deaths/year), likely driven by the large increase in methane emissions and by the net effect of climate change projected in this scenario, but it leads to considerable avoided premature mortality for the three other RCPs. However, the global mortality burden of ozone markedly increases from 382,000 (121,000 to 728,000) deaths/year in 2000 to between 1.09 and 2.36 million deaths/year in 2100, across RCPs, mostly due to the effect of increases in population and baseline mortality rates. PM2.5 concentrations decrease relative to 2000 in all scenarios, due to projected reductions in emissions, and are associated with avoided premature mortality, particularly in 2100: between -2.39 and -1.31 million deaths/year for the four RCPs. The global mortality burden of PM2.5 is estimated to decrease from 1.70 (1.30 to 2.10) million deaths/year in 2000 to between 0.95 and 1.55 million deaths/year in 2100 for the four RCPs, due to the combined effect of decreases in PM2.5 concentrations and changes in population and baseline mortality rates. Trends in future air pollution-related mortality vary regionally across scenarios, reflecting assumptions for economic growth and air pollution control specific to each RCP and region. Mortality estimates differ among chemistry-climate models due to differences in simulated pollutant concentrations, which is the greatest contributor to overall mortality uncertainty for most cases assessed here, supporting the use of model ensembles to characterize uncertainty. Increases in exposed population and baseline mortality rates of respiratory diseases magnify the impact on premature mortality of changes in future air pollutant concentrations and explain why the future global mortality burden of air pollution can exceed the current burden, even where air pollutant concentrations decrease.

Health burdens of surface ozone in the UK for a range of future scenarios.

Exposure to surface ozone (O3), which is influenced by emissions of precursor chemical species, meteorology and population distribution, is associated with excess mortality and respiratory morbidity. In this study, the EMEP-WRF atmospheric chemistry transport model was used to simulate surface O3 concentrations at 5km horizontal resolution over the British Isles for a baseline year of 2003, for three anthropogenic emissions scenarios for 2030, and for a +5°C increase in air temperature on the 2003 baseline. Deaths brought forward and hospitalisation burdens for 12 UK regions were calculated from population-weighted daily maximum 8-hour O3. The magnitude of changes in annual mean surface O3 over the UK for +5°C temperature (+1.0 to +1.5ppbv, depending on region) was comparable to those due to inter-annual meteorological variability (-1.5 to +1.5ppbv) but considerably less than changes due to precursor emissions changes by 2030 (-3.0 to +3.5ppbv, depending on scenario and region). Including population changes in 2030, both the 'current legislation' and 'maximum feasible reduction' scenarios yield greater O3-attributable health burdens than the 'high' emission scenario: +28%, +22%, and +16%, respectively, above 2003 baseline deaths brought forward (11,500) and respiratory hospital admissions (30,700), using O3 exposure over the full year and no threshold for health effects. The health burdens are greatest under the 'current legislation' scenario because O3 concentrations increase as a result of both increases in background O3 concentration and decreases in UK NOx emissions. For the +5°C scenario, and no threshold (and not including population increases), total UK health burden increases by 500 premature deaths (4%) relative to the 2003 baseline. If a 35ppbv threshold for O3 effects is assumed, health burdens are more sensitive to the current legislation and +5°C scenarios, although total health burdens are roughly an order of magnitude lower. In all scenarios, the assumption of a threshold increases the proportion of health burden in the south and east of the UK compared with the no threshold assumption. The study highlights that the total, and geographically-apportioned, O3-attributable health burdens in the UK are highly sensitive to the future trends of hemispheric, regional and local emissions of O3 precursors, and to the assumption of a threshold for O3 effect.

Enhanced chemistry-climate feedbacks in past greenhouse worlds.

Trace greenhouse gases are a fundamentally important component of Earth's global climate system sensitive to global change. However, their concentration in the pre-Pleistocene atmosphere during past warm greenhouse climates is highly uncertain because we lack suitable geochemical or biological proxies. This long-standing issue hinders assessment of their contribution to past global warmth and the equilibrium climate sensitivity of the Earth system (E(ss)) to CO(2). Here we report results from a series of three-dimensional Earth system modeling simulations indicating that the greenhouse worlds of the early Eocene (55 Ma) and late Cretaceous (90 Ma) maintained high concentrations of methane, tropospheric ozone, and nitrous oxide. Modeled methane concentrations were four- to fivefold higher than the preindustrial value typically adopted in modeling investigations of these intervals, even after accounting for the possible high CO(2)-suppression of biogenic isoprene emissions on hydroxyl radical abundance. Higher concentrations of trace greenhouse gases exerted marked planetary heating (> 2 K), amplified in the high latitudes (> 6 K) by lower surface albedo feedbacks, and increased E(ss) in the Eocene by 1 K. Our analyses indicate the requirement for including non-CO(2) greenhouse gases in model-based E(ss) estimates for comparison with empirical paleoclimate assessments, and point to chemistry-climate feedbacks as possible amplifiers of climate sensitivity in the Anthropocene.

Current and future climate- and air pollution-mediated impacts on human health.

BACKGROUND: We describe a project to quantify the burden of heat and ozone on mortality in the UK, both for the present-day and under future emission scenarios. METHODS: Mortality burdens attributable to heat and ozone exposure are estimated by combination of climate-chemistry modelling and epidemiological risk assessment. Weather forecasting models (WRF) are used to simulate the driving meteorology for the EMEP4UK chemistry transport model at 5 km by 5 km horizontal resolution across the UK; the coupled WRF-EMEP4UK model is used to simulate daily surface temperature and ozone concentrations for the years 2003, 2005 and 2006, and for future emission scenarios. The outputs of these models are combined with evidence on the ozone-mortality and heat-mortality relationships derived from epidemiological analyses (time series regressions) of daily mortality in 15 UK conurbations, 1993-2003, to quantify present-day health burdens. RESULTS: During the August 2003 heatwave period, elevated ozone concentrations > 200 microg m-3 were measured at sites in London and elsewhere. This and other ozone photochemical episodes cause breaches of the UK air quality objective for ozone. Simulations performed with WRF-EMEP4UK reproduce the August 2003 heatwave temperatures and ozone concentrations. There remains day-to-day variability in the high ozone concentrations during the heatwave period, which on some days may be explained by ozone import from the European continent.Preliminary calculations using extended time series of spatially-resolved WRF-EMEP4UK model output suggest that in the summers (May to September) of 2003, 2005 & 2006 over 6000 deaths were attributable to ozone and around 5000 to heat in England and Wales. The regional variation in these deaths appears greater for heat-related than for ozone-related burdens.Changes in UK health burdens due to a range of future emission scenarios will be quantified. These future emissions scenarios span a range of possible futures from assuming current air quality legislation is fully implemented, to a more optimistic case with maximum feasible reductions, through to a more pessimistic case with continued strong economic growth and minimal implementation of air quality legislation. CONCLUSION: Elevated surface ozone concentrations during the 2003 heatwave period led to exceedences of the current UK air quality objective standards. A coupled climate-chemistry model is able to reproduce these temperature and ozone extremes. By combining model simulations of surface temperature and ozone with ozone-heat-mortality relationships derived from an epidemiological regression model, we estimate present-day and future health burdens across the UK. Future air quality legislation may need to consider the risk of increases in future heatwaves.

The contribution from shipping emissions to air quality and acid deposition in Europe.

A global three-dimensional Lagrangian chemistry-transport model STOCHEM is used to describe the European regional acid deposition and ozone air quality impacts along the Atlantic Ocean seaboard of Europe, from the SO2, NOx, VOCs and CO emissions from international shipping under conditions appropriate to the year 2000. Model-derived total sulfur deposition from international shipping reaches over 200 mg S m(-2) yr(-1) over the southwestern approaches to the British Isles and Brittany. The contribution from international shipping to surface ozone concentrations during the summertime, peaks at about 6 ppb over Ireland, Brittany and Portugal. Shipping emissions act as an external influence on acid deposition and ozone air quality within Europe and may require control actions in the future if strict deposition and air quality targets are to be met.

Chromatin silencing: RNA in the driving seat.

Recent studies have provided major new insights into the mechanism by which eukaryotic organisms initiate heterochromatin formation. Surprisingly, RNA appears to be a central component of the chromatin silencing machinery.

Co-evolution of the genetic code and ribozyme replication.

The origin of translation has stimulated much discussion since the basic processes involved were deciphered during the 1960s and 1970s. One strand of thought suggested that the process originated from RNA replication in the RNA world (Weiner & Maizels, 1987, 1994). In this paper I seek to extend this model. The mRNA originates as a replication intermediate of minus-strand ribozyme replication and thus contains all the genetic information contained in both the ribozyme portion and the putative tRNA-like portion of the RNA molecule. Qualitatively, this is similar to the model for the origin of chromosomes (Szathmary & Maynard-Smith, 1993, Maynard-Smith & Szathmary, 1993). This model explicitly describes the evolution of early chromosomes and the role replication played in generating the modern mRNA. Moreover, by pursuing this model, the START and STOP codons were derived and their original function with regard to the primitive 23S ribosomal RNA is suggested. Co-evolution of the genetic code (Wong, 1975) is also contained within the model. Lastly, I address some of the benefits and costs that the process may have for the organism in the context of autotrophy in the RNA world.