Long-distance dispersal of pigeons and doves generated new ecological opportunities for host-switching and adaptive radiation by their parasites.

Adaptive radiation is an important mechanism of organismal diversification and can be triggered by new ecological opportunities. Although poorly studied in this regard, parasites are an ideal group in which to study adaptive radiations because of their close associations with host species. Both experimental and comparative studies suggest that the ectoparasitic wing lice of pigeons and doves have adaptively radiated, leading to differences in body size and overall coloration. Here, we show that long-distance dispersal by dove hosts was central to parasite diversification because it provided new ecological opportunities for parasites to speciate after host-switching. We further show that among extant parasite lineages host-switching decreased over time, with cospeciation becoming the more dominant mode of parasite speciation. Taken together, our results suggest that host dispersal, followed by host-switching, provided novel ecological opportunities that facilitated adaptive radiation by parasites

The SAMI Galaxy Survey: Cubism and covariance, putting round pegs into square holes

We present a methodology for the regularization and combination of sparse sampled and irregularly gridded observations from fibre-optic multiobject integral field spectroscopy. The approach minimizes interpolation and retains image resolution on combining subpixel dithered data. We discuss the methodology in the context of the Sydney-AAO multiobject integral field spectrograph (SAMI) Galaxy Survey underway at the Anglo-Australian Telescope. The SAMI instrument uses 13 fibre bundles to perform high-multiplex integral field spectroscopy across a 1° diameter field of view. The SAMI Galaxy Survey is targeting ~3000 galaxies drawn from the full range of galaxy environments. We demonstrate the subcritical sampling of the seeing and incomplete fill factor for the integral field bundles results in only a 10 per cent degradation in the final image resolution recovered. We also implement a new methodology for tracking covariance between elements of the resulting data cubes which retains 90 per cent of the covariance information while incurring only a modest increase in the survey data volume

The SAMI galaxy survey: the third and final data release

Galaxie

The SAMI Galaxy Survey: The third and final data release

We have entered a new era where integral-field spectroscopic surveys of galaxies are sufficiently large to adequately sample large-scale structure over a cosmologically significant volume. This was the primary design goal of the SAMI Galaxy Survey. Here, in Data Release 3, we release data for the full sample of 3068 unique galaxies observed. This includes the SAMI cluster sample of 888 unique galaxies for the first time. For each galaxy, there are two primary spectral cubes covering the blue (370-570 nm) and red (630-740 nm) optical wavelength ranges at spectral resolving power of R = 1808 and 4304, respectively. For each primary cube, we also provide three spatially binned spectral cubes and a set of standardized aperture spectra. For each galaxy, we include complete 2D maps from parametrized fitting to the emission-line and absorption-line spectral data. These maps provide information on the gas ionization and kinematics, stellar kinematics and populations, and more. All data are available online through Australian Astronomical Optics Data Central

The SAMI Galaxy Survey: Data Release One with emission-line physics value-added products

We present the first major release of data from the SAMI Galaxy Survey. This data release focuses on the emission-line physics of galaxies. Data Release One includes data for 772 galaxies, about 20 per cent of the full survey. Galaxies included have the redshift range 0.004 < z < 0.092, a large mass range (7.6 < logM*/M⊙ < 11.6), and star formation rates of ~10-4 to ~101M⊙ yr-1. For each galaxy, we include two spectral cubes and a set of spatially resolved 2D maps: single- and multi-component emission-line fits (with dust-extinction corrections for strong lines), local dust extinction, and star formation rate. Calibration of the fibre throughputs, fluxes, and differential atmospheric refraction has been improved over the Early Data Release. The data have average spatial resolution of 2.16 arcsec (full width at half-maximum) over the 15 arcsec diameter field of view and spectral (kinematic) resolution of R = 4263 (σ = 30 km s-1) around Ha. The relative flux calibration is better than 5 per cent, and absolute flux calibration has an rms of 10 per cent. The data are presented online through the Australian Astronomical Observatory's Data Central

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