Temperature and Photoperiod Effects on Sterility in a Cytoplasmic Male-Sterile Soybean

Manual cross-pollination to produce large quantities of hybrid soybean seed is difficult and time consuming. An environmentally stable sterility system is one of the necessary components to produce large quantities of hybrid seed. The objective of this study was to subject cytoplasmic male-sterile (CMS) BC5F1 plants, from a cross of a Chinese Glycine max wild-type soybean with a Chinese wild annual soybean G. soja (male parent) and controls, to a variety of different temperature and photoperiod treatments to test whether CMS is stable under various environmental conditions. Plants were grown in growth chambers under controlled temperature, photoperiod, and irradiance regimes until pod set, and then they were transferred to a glasshouse until they matured. Plants were evaluated for time of anthesis after photoperiod induction (13 h light/11 h dark) and fertility or sterility. Anther squash and pod set data showed that sterility of the CMS line was stable under all environmental conditions tested, whereas fertility-restored control plants remained fertile. Extreme environmental conditions led to delayed floral induction and/or stunted growth

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