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.
We identified 275 differentially expressed circRNAs and the expression level of two circRNAs was confirmed using real-time quantitative PCR.
The deep history and early diversification of retroviruses remains elusive, largely because few retroviruses have been characterized in vertebrates other than mammals and birds. Endogenous retroviruses (ERVs) documented past retroviral infections and thus provide ‘molecular fossils’ for studying the deep history of retroviruses. Here we perform a comprehensive phylogenomic analysis of ERVs within the genomes of 92 non-avian/mammalian vertebrates, including 72 fishes, 4 amphibians, and 16 reptiles. We find that ERVs are present in all the genomes of jawed vertebrates, revealing the ubiquitous presence of ERVs in jawed vertebrates. We identify a total of >8,000 ERVs and reconstruct ~450 complete or partial ERV genomes, which dramatically expands the phylogenetic diversity of retroviruses and suggests that the diversity of exogenous retroviruses might be much underestimated in non-avian/mammalian vertebrates. Phylogenetic analyses show that retroviruses cluster into five major groups with different host distributions, providing important insights into the classification and diversification of retroviruses. Moreover, we find retroviruses mainly underwent frequent host switches in non-avian/mammalian vertebrates, with exception of spumavirus-related viruses that codiverged with their ray-finned fish hosts. Interestingly, ray-finned fishes and turtles appear to serve as unappreciated hubs for the transmission of retroviruses. Finally, we find retroviruses underwent many independent water-land transmissions, indicating the water-land interface is not a strict barrier for retrovirus transmission. Our analyses provide unprecedented insights into and valuable resources for studying the diversification, key evolutionary transitions, and macroevolution of retroviruses.
Ovarian cancer remains the most fatal gynecologic malignancy worldwide due to delayed diagnosis as well as recurrence and drug resistance. Thus, the development of new tumor-related molecules with high sensitivity and specificity to replace or supplement existing tools is urgently needed. Cancer-testis antigens (CTAs) are exclusively expressed in normal testis tissues but abundantly found in several types of cancers, including ovarian cancer. Numerous novel CTAs have been identified by high-throughput sequencing techniques, and some aberrantly expressed CTAs are associated with ovarian cancer initiation, clinical outcomes and chemotherapy resistance. More importantly, CTAs are immunogenic and may be novel targets for antigen-specific immunotherapy in ovarian cancer. In this review, we attempt to characterize the expression of candidate CTAs in ovarian cancer and their clinical significance as biomarkers, activation mechanisms, function in malignant phenotypes and applications in immunotherapy.
Zika virus (ZIKV) has caused explosive epidemics in the Pacific and the Americas, posing a serious threat to public health. Conventional opinion advocates that ZIKV evolved into two distinct lineages, namely, African and Asian. Descendants of this latter lineage dispersed globally causing major epidemics. However, based on shared amino acid replacements and phylogenetic analyses, it was recently contentiously proposed that the Asian lineage was a direct descendant of the African lineage. To address this contentious issue, we reconstructed a phylogenetic tree of ZIKV using the method based on shared amino acid replacements and found that ZIKV evolved into two distinct lineages. This supports the conventional phylogenetic divergence pattern of ZIKV. Evidence of recombination and sequencing errors was identified among the large collection of ZIKV. As such problematic sequences could confound the phylogenetic analyses, they were removed. Bayesian phylogenetic analyses using the improved sequence data enabled estimates for the divergence time in the past of the African and Asian lineages of ∼180 years ago. Moreover, we found that the Asian lineage viruses did not evolve at an elevated rate. Our findings provide additional support for the conventional opinion that the Asian lineage of ZIKV diverged from the African lineage.
ABSTARCT The NLR protein ZAR1 (HOPZ-ACTIVATED RESISTANCE 1), an immune receptor, interacts with HOPZ-ETI-DEFICIENT 1 (ZED1)-related kinases (ZRKs) and AVRPPHB SUSCEPTIBLE 1 (PBS1)-like proteins to form a pentameric resistosome, triggering immune responses. Here, we show that ZAR1 emerged through gene duplication and that ZRKs were derived from the cell surface immune receptors wall-associated protein kinases (WAKs) through the loss of the extracellular domain before the split of eudicots and monocots during the Jurassic period. Many angiosperm ZAR1 orthologs, but not ZAR1 paralogs, are capable of oligomerization in the presence of AtZRKs and triggering cell death, suggesting that the functional ZAR1 resistosome might have originated during the early evolution of angiosperms. Surprisingly, inter-specific pairing of ZAR1 and AtZRKs sometimes results in the formation of a resistosome in the absence of pathogen stimulation, suggesting within-species compatibility between ZAR1 and ZRKs as a result of co-evolution. Numerous concerted losses of ZAR1 and ZRKs occurred in angiosperms, further supporting the ancient co-evolution between ZAR1 and ZRKs. Our findings provide insights into the origin of new plant immune surveillance networks.
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