Are long‐unburnt eucalypt forest patches important for the conservation of plant species diversity?

Question: Are long‐unburnt patches of eucalypt forest important for maintaining floristic diversity? Location: Eucalyptus forests of southeastern New South Wales, Australia. Methods: Data from 976 sites representing a range of fire history from three major vegetation formations – shrubby dry sclerophyll forest (SF), grassy dry SF and wet SF – were analysed. Generalized linear models were used to examine changes in species richness with increasing time since wildfire and analysis of similarities to examine changes in community composition. Chi‐squared tests were conducted to examine the distribution of individual species across four time since fire categories. Results: Plant species relationships to fire varied between the three formations. Shrubby dry SF supported lower plant species richness with increasing time since wildfire and this was associated with shifts in community composition. Grassy dry SF showed significant shifts in community composition and species richness in relation to time, with a peak in plant species richness 20–30 yr post fire (either prescribed fire or wildfire). Wet SF increased in species richness until 10–20 yr post wildfire then displayed a general declining trend. Species richness in each vegetation type was not related to the fire frequencies and fire intervals observed in this study. Conclusions: Long‐unburnt (30–50 yr post wildfire) forests appeared to play a minor role in the maintenance of plant species diversity in dry forest systems, although this was more significant in wet forests. Maintenance of a range of fire ages within each vegetation formation will assist in maintaining floristic diversity within regions.     

What is the risk‐benefit ratio of long‐term antipsychotic treatment in people with schizophrenia?

The long‐term benefit‐to‐risk ratio of sustained antipsychotic treatment for schizophrenia has recently been questioned. In this paper, we critically examine the literature on the long‐term efficacy and effectiveness of this treatment. We also review the evidence on the undesired effects, the impact on physical morbidity and mortality, as well as the neurobiological correlates of chronic exposure to antipsychotics. Finally, we summarize factors that affect the risk‐benefit ratio. There is consistent evidence supporting the efficacy of antipsychotics in the short term and mid term following stabilization of acute psychotic symptoms. There is insufficient evidence supporting the notion that this effect changes in the long term. Most, but not all, of the long‐term cohort studies find a decrease in efficacy during chronic treatment with antipsychotics. However, these results are inconclusive, given the extensive risk of bias, including increasing non‐adherence. On the other hand, long‐term studies based on national registries, which have lower risk of bias, find an advantage in terms of effectiveness during sustained antipsychotic treatment. Sustained antipsychotic treatment has been also consistently associated with lower mortality in people with schizophrenia compared to no antipsychotic treatment. Nevertheless, chronic antipsychotic use is associated with metabolic disturbance and tardive dyskinesia. The latter is the clearest undesired clinical consequence of brain functioning as a potential result of chronic antipsychotic exposure, likely from dopaminergic hypersensitivity, without otherwise clear evidence of other irreversible neurobiological changes. Adjunctive psychosocial interventions seem critical for achieving recovery. However, overall, the current literature does not support the safe reduction of antipsychotic dosages by 50% or more in stabilized individuals receiving adjunctive psychosocial interventions. In conclusion, the critical appraisal of the literature indicates that, although chronic antipsychotic use can be associated with undesirable neurologic and metabolic side effects, the evidence supporting its long‐term efficacy and effectiveness, including impact on life expectancy, outweighs the evidence against this practice, overall indicating a favorable benefit‐to‐risk ratio. However, the finding that a minority of individuals diagnosed initially with schizophrenia appear to be relapse free for long periods, despite absence of sustained antipsychotic treatment, calls for further research on patient‐level predictors of positive outcomes in people with an initial psychotic presentation.     

Habitat fragmentation,genetic diversity,and inbreeding depression in a threatened grassland legume: is genetic rescue necessary?

Kincaid’s lupine (Lupinus oreganus), a threatened perennial legume of western Oregon grasslands, is composed of small, fragmented populations that have consistently low natural seed set, suggesting they may have accumulated high enough levels of genetic load to be candidates for genetic rescue. We used simple sequence repeat (SSR) loci, both nuclear DNA and chloroplast DNA, to screen populations throughout the species’ range for evidence of severe inbreeding and recent genetic bottlenecks due to habitat fragmentation. After genotyping about 40% of the known populations, only one of 24 populations had strong statistical evidence for a recent genetic bottleneck (H _e > H _eq). Both mean nSSR fixation coefficients and genetic diversity did not statistically differ between very small, small, medium, and large lupine population size classes. Within population chloroplast DNA haplotype number was high for an animal pollinated species, ≈4.2 haplotypes/population, and within population haplotype diversity was also relatively evenly distributed. Within population patterns of nSSR and cpSSR genetic diversity suggest that genetic diversity has not been lost over the last century of habitat fragmentation. With genet lifespan thought to exceed 100 years, overlap of several to many generations, and substantial reductions in seed set from inbreeding depression that shifts cohort composition towards those generated by outcrossing events, Kincaid’s lupine is likely maintain the currently high levels of within population genetic diversity. The case of Kincaid’s lupine provides an example of how the assumptions of severe inbreeding depression with small population size and habitat fragmentation can be inaccurate.     

Within‐season increase in parental investment in a long‐lived bird species: investment shifts to maximize successful reproduction?

In nest‐building species predation of nest contents is a main cause of reproductive failure and parents have to trade off reproductive investment against antipredatory behaviours. While this trade‐off is modified by lifespan (short‐lived species prioritize current reproduction; long‐lived species prioritize future reproduction), it may vary within a breeding season, but this idea has only been tested in short‐lived species. Yet, life history theory does not make any prediction how long‐lived species should trade off current against future reproductive investment within a season. Here, we investigated this trade‐off through predator‐exposure experiments in a long‐lived bird species, the brown thornbill. We exposed breeding pairs that had no prior within‐season reproductive success to the models of a nest predator and a predator of adults during their first or second breeding attempt. Overall, parents reduced their feeding rate in the presence of a predator, but parents feeding second broods were more risk sensitive and almost ceased feeding when exposed to both types of predators. However, during second breeding attempts, parents had larger clutches and a higher feeding rate in the absence of predators than during first breeding attempts and approached both types of predators closer when mobbing. Our results suggest that the trade‐off between reproductive investment and risk‐taking can change in a long‐lived species within a breeding season depending on both prior nest predation and renesting opportunities. These patterns correspond to those in short‐lived species, raising the question of whether a within‐season shift in reproductive investment trade‐offs is independent of lifespan.     

How important is long‐distance seed dispersal for the regional survival of plant species?

Long‐distance seed dispersal is generally assumed to be important for the regional survival of plant species. In this study, we quantified the importance of long‐distance seed dispersal for regional survival of plant species using wind dispersal as an example. We did this using a new approach, by first relating plant species’ dispersal traits to seed dispersal kernels and then relating the kernels to regional survival of the species. We used a recently developed and tested mechanistic seed dispersal model to calculate dispersal kernels from dispersal traits. We used data on 190 plant species and calculated their regional survival in two ways, using species distribution data from 36,800 1 km²‐grid cells and 10,754 small plots covering the Netherlands during the largest part of the 20th century. We carried out correlation and stepwise multiple regression analyses to quantify the importance of long‐distance dispersal, expressed as the 99‐percentile dispersal distance of the dispersal kernels, relative to the importance of median‐distance dispersal and other plant traits that are likely to contribute to the explanation of regional survival: plant longevity (annual, biennial, perennial), seed longevity, and plant nutrient requirement. Results show that long‐distance dispersal plays a role in determining regional survival, and is more important than median‐distance dispersal and plant longevity. However, long‐distance dispersal by wind explains only 1–3% of the variation in regional survival between species and is equally important as seed longevity and much less important than nutrient requirement. In changing landscapes such as in the Netherlands, where large‐scale eutrophication and habitat destruction took place in the 20th century, plant traits indicating ability to grow under the changed, increasingly nutrient‐rich conditions turn out to be much more important for regional survival than seed dispersal.     

When can refuges mediate the genetic effects of fire regimes? A simulation study of the effects of topography and weather on neutral and adaptive genetic diversity in fire‐prone landscapes

Understanding how landscape heterogeneity mediates the effects of fire on biodiversity is increasingly important under global changes in fire regimes. We used a simulation experiment to investigate how fire regimes interact with topography and weather to shape neutral and selection‐driven genetic diversity under alternative dispersal scenarios, and to explore the conditions under which microrefuges can maintain genetic diversity of populations exposed to recurrent fire. Spatial heterogeneity in simulated fire frequency occurred in topographically complex landscapes, with fire refuges and fire‐prone “hotspots” apparent. Interannual weather variability reduced the effect of topography on fire patterns, with refuges less apparent under high weather variability. Neutral genetic diversity was correlated with long‐term fire frequency under spatially heterogeneous fire regimes, being higher in fire refuges than fire‐prone areas, except under high dispersal or low fire severity (low mortality). This generated different spatial genetic structures in fire‐prone and fire‐refuge components of the landscape, despite similar dispersal. In contrast, genetic diversity was only associated with time since the most recent fire in flat landscapes without predictable refuges and hotspots. Genetic effects of selection driven by fire‐related conditions depended on selection pressure, migration distance and spatial heterogeneity in fire regimes. Allele frequencies at a locus conferring higher fitness under successional environmental conditions followed a pattern of “temporal adaptation” to contemporary conditions under strong selection pressure and high migration. However, selected allele frequencies were correlated with spatial variation in long‐term mean fire frequency (relating to environmental predictability) under weak dispersal, low selection pressure and strong spatial heterogeneity in fire regimes.     

5‐HTTLPR S‐allele: a genetic plasticity factor regarding the effects of life events on personality?

The S-allele of the 5-HTTLPR has been identified as a genetic vulnerability factor, being associated with an increased risk for affective disorders and/or maladaptive traits (e.g. neuroticism), especially after exposition to negative life-events (LEs). Alternatively, it has been hypothesized that this genetic risk factor might constitute a genetic plasticity factor. That is, S-allele carriers are not only vulnerable to the negative effects of a preponderance of stressful LEs but also disproportionally benefit from a preponderance of positive environmental influences. We tested this hypothesis in 357 subjects who were genotyped for the 5-HTTLPR and provided self-reports of neuroticism, life-satisfaction and LEs. Results showed a relatively increased number of positive LEss to be associated with reduced neuroticism (men: β = -0.501, P < 0.05, women: β = -0.369, P < 0.005) and increased life satisfaction (β = 0.494, P < 0.001) within SS-homozygotes. Within SL-heterozygotes, similar tendencies were found. No associations were detected in LL-homozygotes. Extreme Group comparisons revealed a genotype × LE interaction (F(2,198) = 5.593, P < 0.005), with SS-homozygotes having experienced predominantly positive LEs exhibiting reduced neuroticism (women: F(1,34) = 4.764, P < 0.05; men: F(1,17) = 2.092, P = 0.17), and increased life satisfaction (F(1,53) = 4.057, P < 0.05), as compared to LL-homozygotes having experienced predominantly positive LEs. Our data support the idea that the S-allele of the 5-HTTLPR is associated with an overall increased reactivity to environmental influences, be they positive or negative in nature. These findings constitute a promising add-on to earlier data and support the plasticity hypothesis.     

Extinction and time help drive the marine‐terrestrial biodiversity gradient: is the ocean a deathtrap?

The marine‐terrestrial richness gradient is among Earth's most dramatic biodiversity patterns, but its causes remain poorly understood. Here, we analyse detailed phylogenies of amniote clades, paleontological data and simulations to reveal the mechanisms underlying low marine richness, emphasising speciation, extinction and colonisation. We show that differences in diversification rates (speciation minus extinction) between habitats are often weak and inconsistent with observed richness patterns. Instead, the richness gradient is explained by limited time for speciation in marine habitats, since all extant marine clades are relatively young. Paleontological data show that older marine invasions have consistently ended in extinction. Simulations show that marine extinctions help drive the pattern of young, depauperate marine clades. This role for extinction is not discernible from molecular phylogenies alone, and not predicted by most previously hypothesised explanations for this gradient. Our results have important implications for the marine‐terrestrial biodiversity gradient, and studies of biodiversity gradients in general.     

Bryophyte diaspore bank: a genetic memory? Genetic structure and genetic diversity of surface populations and diaspore bank in the liverwort Mannia fragrans (Aytoniaceae)

Propagule banks are assumed to be able to store considerable genetic variability. Bryophyte populations are expected to rely more heavily on stored propagules than those of seed plants due to the vulnerability of the haploid gametophyte. This reliance has important implications for the genetic structure and evolutionary potential of surface populations. A liverwort, Mannia fragrans, was used to test whether the bryophyte diaspore bank functions as a "genetic memory." If a diaspore bank is capable of conserving genetic variability over generations, the levels of genetic diversity in the soil are expected to be similar or higher than at the surface. Surface and diaspore bank constituents of two populations of M. fragrans were investigated. Genetic structure and diversity measured as unbiased heterozygosity were analyzed using three ISSR markers. Similar genetic diversities were found in the soil (H(s) = 0.067) and at the surface (H(s)= 0.082). However, more haplotypes and specific haplotype lineages were present in soil samples. The results suggest that the bryophyte diaspore bank has an important role in accumulating genetic variability over generations and seasons. It is postulated that the role of the diaspore bank as a "genetic memory" is especially important in species of temporarily available habitats that have long-lived spores and genetically variable populations.     

Population structure of long‐finned pilot whales in the North Atlantic: a correlation with sea surface temperature?

The long-finned pilot whale, Globicephala melas, is a social, pelagic odontocete distributed widely in the cold temperate waters of the North Atlantic. Despite genetic, morphometric, physiological and observational studies, it remains unclear whether any population substructure exists. We have used eight highly polymorphic microsatellite loci to analyse samples from four disparate sampling sites: USA East Coast (Cape Cod), West Greenland, the Faeroe Islands and the UK. Our results indicate that substructure does exist, and is particularly pronounced between West Greenland and other sites. The magnitudes of the various pairwise comparisons do not support a simple isolation-by-distance model. Instead, the patterns of genetic differentiation suggest that population isolation occurs between areas of the ocean which differ in sea surface temperature. Such a mechanism is supported by the observation that temperature is a primary factor determining the relative distributions of two short-finned pilot whale (G. macrorhynchus) populations off the Pacific coast of Japan.     

Prenatal genetic screening and the evolving quest for “perfect babies”: at what cost for genetic diversity?

Commercial screening services for inheritable diseases raise concerns about pressure on parents to terminate “imperfect babies”. Subject Categories: S&S: Economics & Business, Molecular Biology of Disease

Nearly two decades have passed since the first draft sequences of the human genome were published at the eyewatering cost of nearly US$3 billion for the publicly funded project. Sequencing costs have dropped drastically since, and a range of direct‐to‐consumer genetics companies now offer partial sequencing of your individual genome in the US$100 price range, and whole‐genome sequencing for less than US$1,000.While such tests are mainly for personal peruse, there have also been substantial drops in price in clinical genome sequencing, which has greatly enabled the study of and screening for inheritable disorders. This has both advanced our understanding of these diseases in general, and benefitted early diagnosis of many genetic disorders, which is crucial for early and efficient treatment. Such detection can, in fact, now occur long before birth: from cell‐free DNA testing during the first trimester of pregnancy, to genetic testing of embryos generated by in vitro fertilization, to preconception carrier screening of parents to find out if both are carriers of an autosomal recessive condition. While such prenatal testing of foetuses or embryos primarily focuses on diseases caused by chromosomal abnormalities, technological advances allow also for the testing of an increasing number of heritable monogenic conditions in cases where the disease‐causing variants are known.The medical benefits of such screening are obvious: I personally have lost two pregnancies, one to Turner''s syndrome and the other to an extremely rare and lethal autosomal recessive skeletal dysplasia, and I know first‐hand the heartbreak and devastation involved in finding out that you will lose the child you already love so much. It should be noted though that, very rarely, Turner syndrome is survivable and the long‐term outlook is typically good in those cases (GARD, 2021). In addition, I have Kallmann syndrome, a highly genetically complex dominant endocrine disorder (Maoine et al, 2018), and early detection and treatment make a difference in outcome. Being able to screen early during pregnancy or childhood therefore has significant benefits for affected children. Many other genetic disorders similarly benefit from prenatal screening and detection.But there is also obvious cause for concern: the concept of “designer babies” selected for sex, physical features, or other apparent benefits is well entrenched in our society – and indeed culture – as a product from a dystopian future. Just as a recent example, Philipp Ball, writing for the Guardian in 2017, described designer babies as “an ethical horror waiting to happen” (Ball, 2017). In addition, various commercial enterprises hope to capitalize on these screening technologies. Orchid Inc claims that their preconception screening allows you to “… safely and naturally, protect your baby from diseases that run in your family”. The fact that this is hugely problematic if not impossible from a technological perspective has already been extensively clarified by Lior Pachter, a computational biologist at Caltech (Pachter, 2021). George Church at Harvard University suggested creating a DNA‐based dating app that would effectively prevent people who are both carriers for certain genetic conditions from matching (Flynn, 2019). Richard Dawkins at Oxford University recently commented that “…the decision to deliberately give birth to a Down [syndrome] baby, when you have the choice to abort it early in the pregnancy, might actually be immoral from the point of view of the child’s own welfare” (Dawkins, 2021).These are just a few examples, and as screening technology becomes cheaper, more companies will jump on the bandwagon of perfect “healthy” babies. Conversely, this creates a risk that parents come under pressure to terminate pregnancies with “imperfect babies” as I have experienced myself. What does this mean for people with rare diseases? From my personal moral perspective, the ethics are clear in cases where the pregnancy is clearly not viable. Yet, there are literally thousands of monogenic conditions and even chromosomal abnormalities, not all of which are lethal, and we are making constant strides in treating conditions that were previously considered untreatable. In addition, there is still societal prejudice against people with genetic disorders, and ignorance about how it is to live with a rare disease. In reality, however, all rare disease patients I have encountered are happy to be alive and here, even those whose conditions have significant impact on their quality of life. Many of us also don''t like the term “disorder” or “syndrome”, as we are so much more than merely a disorder or a syndrome.Unfortunately, I also see many parents panic about the results of prenatal testing. Without adequate genetic counselling, they do not understand that their baby’s condition may have actually a quite good prognosis without major impact on the quality of life. Following from this, a mere diagnosis of a rare disease – many of which would not even necessarily have been detectable until later in life, if at all – can be enough to make parents consider termination, due to social stigma.This of course raises the thorny issue of regulation, which range from the USA where there is little to no regulation of such screening technologies (ACOG, 2020), to Sweden where such screening technologies are banned with the exception of specific high‐risk/lethal medical conditions both parents are known carriers for (SMER, 2021). As countries come to grips with both the potential and the risks involved in new screening technologies, medical ethics board have approached this issue. And as screening technologies advance, we will need to ask ourselves difficult questions as a society. I know that in the world of “perfect babies” that some of these companies and individuals are trying to promote, I would not exist, nor would my daughter. I have never before had to find myself so often explaining to people that our lives have value, and I do not want to continue having to do so. Like other forms of diversity, genetic diversity is important and makes us richer as a society. As these screening technologies quickly advance and become more widely available, regulation should at least guarantee that screening must involve proper genetic counselling from a trained clinical geneticist so that parents actually understand the implications of the test results. More urgently, we need to address the problem of societal attitudes towards rare diseases, face the prejudice and fear towards patients, and understand that abolishing genetic diversity in a quest for perfect babies would impoverish humanity and make the world a much poorer place.     

Baculovirus‐induced tree‐top disease: how extended is the role of egt as a gene for the extended phenotype?

Many parasites alter host behaviour to enhance their chance of transmission. Recently, the ecdysteroid UDP‐glucosyl transferase (egt) gene from the baculovirus Lymantria dispar multiple nucleopolyhedrovirus (LdMNPV) was identified to induce tree‐top disease in L. dispar larvae. Infected gypsy moth larvae died at elevated positions (hence the term tree‐top disease), which is thought to promote dissemination of the virus to lower foliage. It is, however, unknown whether egt has a conserved role among baculoviruses in inducing tree‐top disease. Here, we studied tree‐top disease induced by the baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in two different host insects, Trichoplusia ni and Spodoptera exigua, and we investigated the role of the viral egt gene therein. AcMNPV induced tree‐top disease in both T. ni and S. exigua larvae, although in S. exigua a moulting‐dependent effect was seen. Those S. exigua larvae undergoing a larval moult during the infection process died at elevated positions, while larvae that did not moult after infection died at low positions. For both T. ni and S. exigua, infection with a mutant AcMNPV lacking egt did not change the position where the larvae died. We conclude that egt has no highly conserved role in inducing tree‐top disease in lepidopteran larvae. The conclusion that egt is a ‘gene for an extended phenotype’ is therefore not generally applicable for all baculovirus–host interactions. We hypothesize that in some baculovirus–host systems (including LdMNPV in L. dispar), an effect of egt on tree‐top disease can be observed through indirect effects of egt on moulting‐related climbing behaviour.     

Evolution of antigenic diversity in the tick‐transmitted bacterium Borrelia afzelii: a role for host specialization?

Antigenic diversity in pathogenic microbes can be a result of at least three different processes: diversifying selection by acquired immunity, host–pathogen coevolution and/or host specialization. Here, we investigate whether host specialization drives diversity at ospC (which encodes an immunodominant surface protein) in the tick‐transmitted bacterium Borrelia afzelii. We determined prevalence and infection intensity of ospC strains in naturally infected wild mammals (rodents and shrews) by 454 amplicon sequencing in combination with qPCR. Neither prevalence nor infection intensity of specific ospC strains varied in a species‐specific manner (i.e. there were no significant ospC × host species interactions). Rankings of ospC prevalences were strongly positively correlated across host species. Rankings of ospC infection intensities were correlated more weakly, but only in one case significantly < 1. ospC prevalences in the studied mammals were similar to those in ticks sampled at the study site, indicating that we did not miss any mammal species that are important hosts for specific ospC strains. Based on this, we conclude that there is at best limited host specialization in B. afzelii and that other processes are likely the main drivers of ospC diversity.     

Modelling the evolution of common cuckoo host‐races: speciation or genetic swamping?

Co‐evolutionary arms races have provided clear evidence for evolutionary change, especially in host–parasite systems. The evolution of host‐specific races in the common cuckoo (Cuculus canorus), however, is also an example where sexual conflict influences the outcome. Cuckoo females benefit from better adaptation to overcome host defences, whereas cuckoo males face a trade‐off between the benefits of better adaptation to a host and the benefits of multiple mating with females from other host‐races. The outcome of this trade‐off might be genetic differentiation or prevention of it by genetic swamping. We use a simulation model to test which outcome is more likely with three sympatric cuckoo host‐races. We assume a cost for cuckoo chicks that express a host adaptation allele not suited to their foster host species and that cuckoo males that switch to another host‐race experience either a fitness benefit or cost. Over most of the parameter space, cuckoo male host‐race fidelity increases significantly with time, and gene flow between host‐races ceases within a few thousand to a hundred thousand generations. Our results hence support the idea that common cuckoo host‐races might be in the incipient stages of speciation.