Report On A Study Tour To Examine Symptoms Of Rice Diseases In Southern USA And California

This was the first visit by a pathologist to look at rice diseases overseas since the industry started over 80 years ago. The purpose of my visit to the USA was to become familiar with current research into, and symptoms of, those diseases of rice that are potentially important in Australia. Whilst my major interest was in rice blast, I took the opportunity to look at all diseases that were present at the time

Risk Assessment Of Exotic Plant Diseases To The Australian Rice Industry, With Emphasis on Rice Blast

A pest risk assessment was carried out using all available information found in the literature and also two softwares developed by the CSIRO, CLIMEX and DYMEX. CLIMEX was used to assess the suitability of the climate in Australian rice growing area for each pest/disease and then when necessary and possible, a pest/disease model was created with DYMEX and run with Australian climatic data. The Australian climatic conditions and/or the rice growing practices were found to be unfavourable for the majority of the exotic diseases. However, two diseases of rice (rice blast and kernel smut) and one plant parasitic nematode genus (root nematodes) were identified as having the potential to threaten the Australian rice industry if ever introduced in south eastern Australia

Enhancing survival and subsequent infectivity of conidia of potential mycoherbistats using UV protectants

Ultraviolet radiation (UV) can reduce the effectiveness of fungi used for biological control; therefore, this study examined the photostabilising effect of water- and oil-soluble UV protectants on conidium germination of Plectosporium alismatis and Colletotrichum orbiculare, pathogens with potential as biocontrol agents, and the ability of conidia of C. orbiculare to cause disease. Formulation in riboflavin (1%), proline (1%), propyl gallate (1%), melanin (0.1%) and ascorbic acid (5%) increased the germination of UVB-exposed conidia of P. alismatis to levels found in the dark control without causing a delay in germination. Formulation in (a) pyridoxin (5%), (b) an nC24 mineral oil (5%), and (c) ECCO 1422 (5% in the mineral oil) also resulted in germination similar to the control but germination was delayed. Protection was provided to conidia of C. orbiculare treated with 1% aqueous solutions of proline and folic acid in vitro. Formulation of conidia of C. orbiculare in a 5% aqueous emulsion of the mineral oil and aqueous solutions of melanin (0.01%), proline and tyrosine (both at 1%) significantly increased anthracnose development above control levels on leaf discs of Xanthium spinosum exposed to UVB dose of 16.7 kJ m-2. After exposure to natural sunlight at a UVB dose of 2.2 kJ m-2, anthracnose development was greater on leaf discs inoculated with conidia of C. orbiculare formulated in 1% aqueous solutions of ascorbic acid (1%), proline (1%), tyrosine (1%) and melanin (0.01%), or in 5% aqueous emulsions of a canola-derived oil and the mineral oil than by conidia formulated in water alone. Therefore, a range of compounds can provide conidia with protection from UVB. Of these, propyl gallate and oils similar to the mineral oil are likely to be cost effective. Such formulations can be combined with suitable application times to increase mycoherbisitat efficiency

Effects of ultraviolet radiation, simulated or as natural sunlight, on conidium germination and appressorium formation by fungi with potential as mycoherbistats

Solar radiation, particularly its UV wavelengths, greatly influences conidium survival and this study looked at the impact of radiation and its interactions with temperature on Plectosporium alismatis and Colletotrichum orbiculare, two fungi that are potential mycoherbistats. UV radiation, rather than temperature, was found to be the primary cause of conidium mortality; however, there were interactions between these factors leading to the enhancement of the lethal effects of UVB on conidium germination at high temperatures. C. orbiculare was more sensitive than P. alismatis with conidium germination being halved by UVB doses of 1.47 and 13.1 kJ m-2, respectively, for the two pathogens. Conidium mortality was dose-dependent and for P. alismatis exposed to a dose of 3.7 kJ m-2 reciprocity was observed. However, for C. orbiculare equivalent doses were not reciprocal as higher doses for short periods were more lethal than lower doses of longer duration. Low UVB doses only caused delays in conidium germination, whereas higher doses killed conidia and caused delays in the germination of any survivors. Radiation also affected appressorium formation. Appressorium formation was stimulated by UVA and was dose dependent with P. alismatis requiring a higher dose than C. orbiculare to initiate formation. Microcycle conidiation by P. alismatis was observed following exposure to sunlight. This knowledge of how conidia of these potential mycoherbistats react to climate suggests that rapid conidium germination and appressorium formation could be achieved by manipulation of the time at which they are applied in the field. Conidia could be applied so that they receive sufficient UVA to stimulate appressorium formation but without receiving a dose that would significantly affect conidium germination. However, for this, additional protection from UVB may be needed

Optimising sporulation and virulence in Drechslera avenacea

Studies were conducted on agar media to optimise sporulation of Drechslera avenacea, a fungal pathogen being evaluated as a biological control agent for Avena species (wild oats). Conidium production was affected by nutrition, pH, temperature and light conditions. Of the agar media tested, Czapek Dox agar (CZA) and half-strength oatmeal agar (OMA) were the only media where sporulation occurred at all temperatures tested under a 12-h light:12-h dark photoperiod (L/D). The optimum temperature for conidium production was 20°C on OMA, whereas there was no optimum temperature on CZA. Under a 12-h near-ultraviolet (NUV):12-h dark photoperiod (NUV/D), similar numbers of conidia were produced on CZA at 6.66, 14.56, and 22.78 W m-2, whereas on OMA conidium production was the highest at 14.56 W m-2. When NUV/D and L/D conditions were compared, similar numbers of conidia where produced on CZA, whereas OMA conidium production was superior under the NUV/D photoperiod. Considerable variation in sporulation and degree of violence of D. avenacea was detected among isolates from different geographic areas. The most virulent conidia were obtained on OMA at 20°C incubated under continuous illumination NUV light. Therefore, the most suitable conditions for conidium production of D. avenacea were growth for 1 week on OMA at 20°C under continuous NUV at an intensity of 14.56 W m-2. Under these conditions, 1.1×105 conidia mL-1 were produced which is the highest sporulation yet reported for any Drechslera spp., which are traditionally poor sporulators

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

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