Palaeoenvironmental control on distribution of crinoids in the Bathonian (Middle Jurassic) of England and France

Bulk sampling of a number of different marine and marginal marine lithofacies in the British Bathonian has allowed us to assess the palaeoenvironmental distribution of crinoids for the first time. Although remains are largely fragmentary, many species have been identified by comparison with articulated specimens from elsewhere, whilst the large and unbiased sample sizes allowed assessment of relative proportions of different taxa. Results indicate that distribution of crinoids well corresponds to particular facies. Ossicles of Chariocrinus and Balanocrinus dominate in deeper-water and lower-energy facies,with the former extending further into shallower-water facies than the latter. Isocrinus dominates in shallower water carbonate facies, accompanied by rarer comatulids, and was also present in the more marine parts of lagoons. Pentacrinites remains are abundant in very high-energy oolite shoal lithofacies. The presence of millericrinids within one, partly allochthonous lithofacies suggests the presence of an otherwise unknown hard substrate from which they have been transported. These results are compared to crinoid assemblages from other Mesozoic localities, and it is evident that the same morphological ad-aptations are present within crinoids from similar lithofacies throughout the Jurassic and Early Cretaceous

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Host mating system and the prevalence of disease in a plant population

A modified susceptible–infected–recovered (SIR) host–pathogen model is used to determine the influence of plant mating system on the outcome of a host–pathogen interaction. Unlike previous models describing how interactions between mating system and pathogen infection affect individual fitness, this model considers the potential consequences of varying mating systems on the prevalence of resistance alleles and disease within the population. If a single allele for disease resistance is sufficient to confer complete resistance in an individual and if both homozygote and heterozygote resistant individuals have the same mean birth and death rates, then, for any parameter set, the selfing rate does not affect the proportions of resistant, susceptible or infected individuals at equilibrium. If homozygote and heterozygote individual birth rates differ, however, the mating system can make a difference in these proportions. In that case, depending on other parameters, increased selfing can either increase or decrease the rate of infection in the population. Results from this model also predict higher frequencies of resistance alleles in predominantly selfing compared to predominantly outcrossing populations for most model conditions. In populations that have higher selfing rates, the resistance alleles are concentrated in homozygotes, whereas in more outcrossing populations, there are more resistant heterozygotes