The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before ∼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by ∼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged ∼20 to ∼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from ∼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections.phylogeny | cohort immunity | pathogenicity | virulence | reassortment

Zoonotic infectious diseases such as influenza continue to pose a grave threat to human health1. However, the factors that mediate the emergence of RNA viruses like influenza A virus (IVA) remain incompletely understood2,3. Phylogenetic inference is crucial to reconstructing the origins and tracing the flow of influenza A virus within and between hosts3-8. Here, we show that explicitly allowing IVA host lineages to have independent rates of molecular evolution is necessary for reliable phylogenetic inference of IVA and that methods that do not do so, including ‘relaxed’ molecular clock models9, can positively mislead. A phylogenomic analysis using a host-specific local clock model recovers extremely consistent evolutionary histories across all genomic segments and demonstrates that the equine H7N7 lineage is a sister clade to strains from birds—as well as those from humans, swine, and the equine H3N8 lineage— sharing an ancestor with them in the mid- to late-1800s. Moreover, major Western and Eastern Hemisphere avian influenza lineages inferred for each gene coalesce in the late 1800s. Based on these phylogenies and the synchrony of these key nodes, we infer that the internal genes of avian influenza virus (AIV) underwent a global selective sweep beginning in the late 1800s, a process that continued throughout the 20th century and up to the present. The resulting western hemispheric AIV lineage subsequently contributed most of the genomic segments to the 1918 pandemic virus and, independently, the 1963 equine H3N8 panzootic lineage. This approach provides a surprisingly clear resolution of IVA evolutionary patterns and processes, including the flow of viral genes and genomes within and between host lineages.

Plant hormones modulate plant growth, development, and defense. However, many aspects of the origin and evolution of plant hormone signaling pathways remain obscure. Here, we use a comparative genomic and phylogenetic approach to investigate the origin and evolution of nine major plant hormone (abscisic acid, auxin, brassinosteroid, cytokinin, ethylene, gibberellin, jasmonate, salicylic acid, and strigolactone) signaling pathways. Our multispecies genome-wide analysis reveals that: (1) auxin, cytokinin, and strigolactone signaling pathways originated in charophyte lineages; (2) abscisic acid, jasmonate, and salicylic acid signaling pathways arose in the last common ancestor of land plants; (3) gibberellin signaling evolved after the divergence of bryophytes from land plants; (4) the canonical brassinosteroid signaling originated before the emergence of angiosperms but likely after the split of gymnosperms and angiosperms; and (5) the origin of the canonical ethylene signaling pathway postdates shortly the emergence of angiosperms. Our findings might have important implications in understanding the molecular mechanisms underlying the emergence of land plants.

Quantitative trait locus (QTL) analysis of kernel shape and weight in common wheat was conducted using a set of 131 recombinant inbred lines (RIL) derived from 'Chuan 35050' 9 'Shannong 483'. The RIL and their two parental genotypes were evaluated for kernel length (KL), kernel width (KW), thousand-kernel weight (TKW), and test weight (TW) in four different environments. Twenty QTL were located on 12 chromosomes, 1A, 1B, 1D, 2A, 2B, 3B, 4A, 4B, 5D, 6A, 6B, and 7B, with single QTL in different environments explaining 5.9-26.4% of the phenotypic variation. Six, three, four, and seven QTL were detected for KL, KW, TKW, and TW, respectively. The additive effects for 17 QTL were positive with Chuan 35050 increasing the QTL effects, whereas the remaining three QTL were negative with Shannong 483 increasing the effects. Eight QTL (40%) were detected in two or more environments. Two QTL clusters relating to KW, TKW, and TW were located on chromosomes 2A and 5D, and the co-located QTL on chromosome 6A involved a QTL for KW found in two environments and a QTL for TKW detected in four environments.

Contents Summary70I.Introduction70II.Ancient associations between plants and microbes72III.Evolutionary dynamics of plant–pathogen interactions74IV.Evolutionary signature of plant–pathogen interactions74V.Origin and evolution of RLK proteins75VI.Origin and evolution of NLR proteins77VII.Origin and evolution of SA signaling78VIII.Origin and evolution of RNA‐based defense79IX.Perspectives79Acknowledgements80References80 Summary Microbes have engaged in antagonistic associations with plants for hundreds of millions of years. Plants, in turn, have evolved diverse immune strategies to combat microbial pathogens. The conflicts between plants and pathogens result in everchanging coevolutionary cycles known as ‘Red Queen’ dynamics. These ancient and ongoing plant–pathogen interactions have shaped the evolution of both plant and pathogen genomes. With the recent explosion of plant genome‐scale data, comparative analyses provide novel insights into the coevolutionary dynamics of plants and pathogens. Here, we discuss the ancient associations between plants and microbes as well as the evolutionary principles underlying plant–pathogen interactions. We synthesize and review the current knowledge on the origin and evolution of key components of the plant immune system. We also highlight the importance of studying algae and nonflowering land plants in understanding the evolution of the plant immune system.

During plant-pathogen interactions, plants use intracellular proteins with nucleotide-binding site and Leu-rich repeat (NBS-LRR) domains to detect pathogens. NBS-LRR proteins represent a major class of plant disease resistance genes (-genes). Whereas -genes have been well characterized in angiosperms, little is known about their origin and early diversification. Here, we perform comprehensive evolutionary analyses of-genes in plants and report the identification of -genes in basal-branching streptophytes, including charophytes, liverworts, and mosses. Phylogenetic analyses suggest that plant-genes originated in charophytes and R-proteins diversified into TIR-NBS-LRR proteins and non-TIR-NBS-LRR proteins in charophytes. Moreover, we show that plant R-proteins evolved in a modular fashion through frequent gain or loss of protein domains. Most of the -genes in basal-branching streptophytes underwent adaptive evolution, indicating an ancient involvement of-genes in plant-pathogen interactions. Our findings provide novel insights into the origin and evolution of -genes and the mechanisms underlying colonization of terrestrial environments by plants.

Little is known about the origin and long-term evolutionary mode of retroviruses. Retroviruses can integrate into their hosts' genomes, providing a molecular fossil record for studying their deep history. Here we report the discovery of an endogenous foamy virus-like element, which we designate ‘coelacanth endogenous foamy-like virus’ (CoeEFV), within the genome of the coelacanth (Latimeria chalumnae). Phylogenetic analyses place CoeEFV basal to all known foamy viruses, strongly suggesting an ancient ocean origin of this major retroviral lineage, which had previously been known to infect only land mammals. The discovery of CoeEFV reveals the presence of foamy-like viruses in species outside the Mammalia. We show that foamy-like viruses have likely codiverged with their vertebrate hosts for more than 407 million years and underwent an evolutionary transition from water to land with their vertebrate hosts. These findings suggest an ancient marine origin of retroviruses and have important implications in understanding foamy virus biology.

Jasmonates are phytohormones that modulate a wide spectrum of plant physiological processes, especially defense against herbivores and necrotrophs. The molecular mechanisms of jasmonate biosynthesis and signaling have been well characterized in model plants. In this review, we provide an in-depth analysis and overview of the origin and evolution of the jasmonate biosynthesis and signaling pathways. Furthermore, we discuss the striking parallels between jasmonate and auxin signaling mechanisms, which reveals a common ancestry of these signaling mechanisms. Finally, we highlight the importance of studying jasmonate biosynthesis and signaling in lower plants.