A future for soil ecology

Abstract not availabl

The origins of multicellularity

is celebrating his 50th year in biology at Princeton University. His major research has been in experimental studies on the development of cellular slime molds. He also has broad interests in various aspects of evolutionary biology, which had led to a series of books from Morphogenesis in 1952 to Sixty Years of Biology in 1996. The Origins of Multicellularity JOHN TYLER BONNER There is great interest in the invention of multicellularity because it is one of the major transitions during the course of early evolution. 1 Most of the emphasis has been on why it occurred. For instance, recently Gerhart and Kirschner 2 have argued that a multicellular organism has gained the advantage of a unicellular ancestor because it can more effectively shield itself from the vagaries of the environment by producing its own internal environment. In broader terms, this is Dawkins' 3 argument that a competitively effective way of carrying the genes from one generation to the next is by building a complex soma that safely sees to it that the germ plasm survives

The origins of multicellularity

The Origins of Multicellularity JOHN TYLER BONNER There is great interest in the invention of multicellularity because it is one of the major transitions during the course of early evolution. 1 Most of the emphasis has been on why it occurred. For instance, recently Gerhart and Kirschner 2 have argued that a multicellular organism has gained the advantage of a unicellular ancestor because it can more effectively shield itself from the vagaries of the environment by producing its own internal environment. In broader terms, this is Dawkins' 3 argument that a competitively effective way of carrying the genes from one generation to the next is by building a complex soma that safely sees to it that the germ plasm survives

Writing in Britain and Ireland, c. 400 to c. 800

No abstract available

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 hospitalization2–4 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

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

OBSERVATIONS ON POLARITY IN THE SLIME MOLD DICTYOSTELIUM DISCOIDEUM

Volume: 99Start Page: 143End Page: 15

The Evolution of Complexity

xii,260 hal,;ill,23 c

Induction of Stalk Cell Differentiation by Cyclic AMP in the Cellular Slime Mold Dictyostelium discoideum

Cyclic AMP, which is a cell attractant (acrasin) for Dictyostelium discoideum, will cause isolated, unaggregated cells to turn directly into stalk cells containing thick celluloselike walls and large vacuoles. From previous work we know that in the cell mass, acrasin is produced solely in the region of stalk formation during fruiting, that stalk formation involves a high level of catabolism, and that cyclic AMP stimulates catabolic enzymes in other systems. These facts obviously suggest that in the development of D. discoideum, cyclic AMP might be a key factor in stalk cell differentiation