Genetic improvement of resistance to cyclaneusma needle cast in Pinus radiata

Progeny testing of resistance to needle loss caused by Cyclaneusma minus has been included in the needle disease resistance strategy of Pinus radiata in New Zealand since the late 1970s. Data on progeny trials, two in the North Island of New Zealand and one in Tasmania, Australia were available to estimate heritability, between trait genetic correlations and genotype by environment interaction. Resistance to cyclaneusma needle cast had moderate estimates of heritability (0.25 to 0.46) at all sites. Genetic correlations between the assessed traits indicated that selection for faster early growth, i.e. tree height at age four and diameter at breast height at age six favours trees that are prone to Cyclaneusma infection, whilst a favourable genetic association between resistance to cyclaneusma needle cast and productivity was evident at later assessment that was at age nine. No significant genotype by environment interaction was found for resistance to cyclaneusma needle cast, however, stability of genotypes across a wider range of environments and with a high genetic connectedness require more research. Considerable genetic improvement can be achieved for resistance to cyclaneusma needle cast and indirect selection for the trait should be pursued by selecting for productivity and culling susceptible genotypes from breeding.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Data from: Effect of hidden relatedness on single-step genetic evaluation in an advanced open-pollinated breeding program

Open-pollinated (OP) mating is frequently used in forest tree breeding due to the relative temporal and financial efficiency of the approach. The trade-off is the lower precision of the estimated genetic parameters. Pedigree/sib-ship reconstruction has been proven as a tool to correct and complete pedigree information and to improve the precision of genetic parameter estimates. Our study analyzed an advanced generation Eucalyptus population from an OP breeding program using single-step genetic evaluation. The relationship matrix inferred from sib-ship reconstruction was used to rescale the marker-based relationship matrix (G matrix). This was compared with a second scenario that used rescaling based on the documented pedigree. The proposed single-step model performed better with respect to both model fit and the theoretical accuracy of breeding values. We found that the prediction accuracy was superior when using the pedigree information only when compared with using a combination of the pedigree and genomic information. This pattern appeared to be mainly a result of accumulated unrecognized relatedness over several breeding cycles, resulting in breeding values being shrunk toward the population mean. Using biased, pedigree-based breeding values as the base with which to correlate predicted GEBVs, resulted in the underestimation of prediction accuracies. Using breeding values estimated on the basis of sib-ship reconstruction resulted in increased prediction accuracies of the genotyped individuals. Therefore, selection of the correct base for estimation of prediction accuracy is critical. The beneficial impact of sib-ship reconstruction using G matrix rescaling was profound, especially in traits with inbreeding depression, such as stem diameter

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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