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Abstract The evolution of multicellularity led to the origin of new kinds of organisms and, in several lineages, massive adaptive radiations through the formation of entirely new ecosystems. This paper examines three key mechanisms underpinning parallel adaptive radiations within the five clades of ‘complex’ multicellularity: animals, land plants, fungi, red algae, and brown algae. First, the evolution of key multicellular innovations permitted diversification into new ecological roles. Second, the evolution of large multicellular organisms with strong genetic bottlenecks between generations fundamentally changed the population genetic context of evolution, greatly reducing effective population size and increasing the role of genetic drift. This may be beneficial during adaptive radiations, underpinning nonadaptive expansions of genome size and allowing broader exploration of multicellular trait space. Finally, we explore how evolutionary priority effects provide a first-mover advantage, maintaining ancient adaptive radiations over long time periods by suppressing competition from convergently evolving multicellular taxa. Investigating parallel patterns of diversification across independent origins of complex multicellularity provides insight into the principles underpinning these crucially important adaptive radiations. 

SARS-CoV2 has caused the current pandemic of new coronavirus disease 2019 (COVID-19) worldwide. Clinical outcomes of COVID-19 illness range broadly from asymptotic and mild to a life-threatening situation. This casts uncertainties for defining host determinants underlying the disease severity. Recent genetic analyses based on extensive clinical sample cohorts using genome-wide association studies (GWAS) and high throughput sequencing curation revealed genetic errors and gene loci associated with about 20% of life-threatening COVID-19 cases. Significantly, most of these critical genetic loci are enriched in two immune signaling pathways, i.e., interferon-mediated antiviral signaling and chemokine-mediated/inflammatory signaling. In line with these genetic profiling studies, the broad spectrum of COVID-19 illness could be explained by immuno-pathological regulation of these critical immunogenetic pathways through various epigenetic mechanisms, which further interconnect to other vital components such as those in the renin–angiotensin–aldosterone system (RAAS) because of its direct interaction with the virus causing COVID-19. Together, key genes unraveled by genetic profiling may provide targets for precisely early risk diagnosis and prophylactic design to relieve severe COVID-19. The confounding epigenetic mechanisms may be key to understanding the clinical broadness of COVID-19 illness.