Incompatibility Systems in Switchgrass

Switchgrass (Panicum virgatum L.), a cross-pollinated perennial, produces very little or no seed when self-pollinated, indicating the presence of self-incompatibility mechanisms. Knowledge of self-incompatibility mechanisms is required to use germplasm effectively in a breeding program. The objective of this study was to characterize features of the incompatibility systems in switchgrass. Seed set and seed characteristics of reciprocal matings of tetraploid, octaploid, and tetraploid x octaploid plants were used as measures of incompatibility. Both bagged mutual pollination and manual emasculation and pollination methods were used to make crosses. The percentages of self-compatibility in the tetraploid and octaploid parent plants were 0.35 and 1.39%, respectively. Prefertilization incompatibility in switchgrass is apparently under gametophytic control, since there were significant differences in percentage of compatible pollen as measured by percentage of total seed set between reciprocal matings within ploidy levels. Results indicated that the prefertilization incompatibility system in switchgrass is similar to the S-Z incompatibility system found in other members of the Poaceae. A postfertilization incompatibility system also exists that inhibits intermatings among octaploid and tetraploid plants. In these interploidy crosses, two very distinctive types of abnormal seed were found. When the female parent was the tetraploid plant, the resulting seed was small and shriveled, while when the female parent was the octaploid, small seed with floury endosperm was obtained. These results are similar to those obtained for endosperm incompatibility due to the endosperm balance number system found in other species

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

Specification of the primitive myeloid precursor pool requires signaling through Alk8 in zebrafish

In the zebrafish embryo, primitive hematopoiesis initiates in two spatially distinct regions. Rostrally, the cells of the anterior lateral plate mesoderm (ALPM) give rise exclusively to cells of the myeloid lineage in a pu.1-dependent manner [1-5]. Caudally, in the posterior lateral plate mesoderm (PLPM), the expression of gata1 defines a precursor pool that gives rise predominantly to the embryonic erythrocytes [6]. The transcription factor scl acts upstream of both gata1 and pu.1 in these precursor pools, activating a series of conserved transcription factors that cell-autonomously specify either myeloid or erythroid fates [1, 4, 7, 8]. However, the mechanisms underlying the spatial separation of the hematopoietic precursor pools and the induction of differential gene expression within these pools are not well understood. We show here that the Bmp receptor lost-a-fin/alk8 is required for rostral pu.1 expression and myelopoiesis, identifying an early genetic event that distinguishes between the induction of anterior and posterior hematopoiesis. Introducing a constitutively active version of the Alk8 receptor led to increased pu.1 expression, but the role of alk8 was independent of the scl-dependent cell-fate pathway. Furthermore, the role of Alk8 in myelopoiesis was genetically separable from its earlier role in dorsal-ventral embryonic patterning