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Orphans are genes restricted to a single phylogenetic lineage and emerge at high rates. While this predicts an accumulation of genes, the gene number has remained remarkably constant through evolution. This paradox has not yet been resolved. Because orphan genes have been mainly analyzed over long evolutionary time scales, orphan loss has remained unexplored. Here we study the patterns of orphan turnover among close relatives in the Drosophila obscura group. We show that orphans are not only emerging at a high rate, but that they are also rapidly lost. Interestingly, recently emerged orphans are more likely to be lost than older ones. Furthermore, highly expressed orphans with a strong male-bias are more likely to be retained. Since both lost and retained orphans show similar evolutionary signatures of functional conservation, we propose that orphan loss is not driven by high rates of sequence evolution, but reflects lineage-specific functional requirements. New genes are added to most genomes on a steady basis. A new gene can either begin as a copy of an existing gene from elsewhere in the genome, or is created entirely ‘from scratch’ from a DNA sequence that had not previously encoded for a protein. New genes that are not found in other related species are called orphan genes—and these genes can account for up to 30% of all the genes in the well-studied genomes. However, for reasons that are not fully understood, the total number of genes in most genomes remains fairly constant despite these regular additions. Now, Palmieri et al. have investigated this paradox by following the evolutionary fate of orphan genes in a small group of related species of fruit fly. Palmieri et al. discovered that most orphan genes are very short-lived, even though they showed clear signals of carrying out important functions. Most orphan genes died out quickly due to mutations that made them unable to be expressed as functional proteins, and a small number were deleted entirely from the genome. Unexpectedly, new orphan genes were more likely to die out than those that had been around for a while. Palmieri et al. also found that the expression levels of orphan genes determined their probability of dying with those genes that were expressed to the highest levels being most likely to persist longer. Furthermore, genes that were expressed more in males than in females were also less likely to die. The next challenge will be to identify the mechanisms that determine which orphan genes survive and which do not.

Background The endosymbiosis of the bacterial progenitors of the mitochondrion and the chloroplast are landmark events in the evolution of life on Earth. While both organelles have retained substantial proteomic and biochemical complexity, this complexity is not reflected in the content of their genomes. Instead, the organellar genomes encode fewer than 5% of the genes found in living relatives of their ancestors. While many of the 95% of missing organellar genes have been discarded, others have been transferred to the host nuclear genome through a process known as endosymbiotic gene transfer. Results Here, we demonstrate that the difference in the per-cell copy number of the organellar and nuclear genomes presents an energetic incentive to the cell to either delete organellar genes or transfer them to the nuclear genome. We show that, for the majority of transferred organellar genes, the energy saved by nuclear transfer exceeds the costs incurred from importing the encoded protein into the organelle where it can provide its function. Finally, we show that the net energy saved by endosymbiotic gene transfer can constitute an appreciable proportion of total cellular energy budgets and is therefore sufficient to impart a selectable advantage to the cell. Conclusion Thus, reduced cellular cost and improved energy efficiency likely played a role in the reductive evolution of mitochondrial and chloroplast genomes and the transfer of organellar genes to the nuclear genome.

As one of the most successful group of organisms, mammals occupy a variety of niches on Earth as a result of macroevolution. Transcription factors (TFs), the fundamental regulators of gene expression, may also have evolved. To examine the relationship between TFs and mammalian macroevolution, we analyzed 140,821 de novo-identified TFs and their birth and death histories from 96 mammalian species. Gene tree vs. species tree reconciliation revealed that placental mammals experienced an upsurge in TF losses around 100 million years ago (Mya) and also near the Cretaceous–Paleogene boundary (K–Pg boundary, 66 Mya). Early Euarchontoglires, Laurasiatheria and marsupials appeared between 100 and 95 Mya and underwent initial diversification. The K-Pg boundary was associated with the massive extinction of dinosaurs, which lead to adaptive radiation of mammals. Surprisingly, TF loss decelerated, rather than accelerated, molecular evolutionary rates of their target genes. As the rate of molecular evolution is affected by the mutation rate, the proportion of neutral mutations and the population size, the decrease in molecular evolution may reflect increased functional constraints to survive target genes.

Background The genus Cuscuta L. (Convolvulaceae), commonly known as dodder, is a holoparasite plant that relies on host plants for nutrition, leading to significant genomic changes, particularly in plastomes. This dependency has led to significant reductions and modifications in their plastomes compared to autotrophic plants. In contrast to the well-conserved plastomes of photosynthetic plants, Cuscuta exhibits substantial genomic reductions reflecting the loss of photosynthetic functions and associated genes. Result This study examines eight plastomes within Cuscuta and reconstructs the phylogenetic relationships among 40 Cuscuta taxa using five other genera as an outgroup. The size of plastid genome varies significantly, with the smallest being 60 kb and the largest 121 kb, highlighting extensive genomic reduction. In special cases, the subgenera Cuscuta exhibit the loss of inverted repeats, distinguishing from them other subge within the Cuscuta genus. This reduction is most pronounced in genes related to photosynthesis, such as atp , pet , psa , psb , and ycf genes, particularly in the subg. Grammica (Lour.) Peter. The study also notes the frequent and independent loss of the plastid genes inf A, rpl 23, rpl 32 , rps 15, and rps 16 across various angiosperm lineages, often involving transfer to the nuclear genome. In parasitic plants like Cuscuta , the ndh genes, crucial for photosynthesis, are often lost. The study also highlights that in the subg. Grammica , the mat K and rpo genes, along with trn R-ACG genes, are lost in parallel, indicating that these parasitic plants do not need mat K and rpo genes after the loss of ndh genes for survival. Analysis of selective relaxation pressure on plastid genes shows a reductive trend, with genes such as atp , pet , psa, psb, rpo , and ycf progressively becoming pseudogenes over time, with housekeeping genes like rpl and rps expected to follow. However, the pseudogenization process is specific to the subg. Grammica , Pachystigma (Engelm.) Baker & C.H.Wright, and Cuscuta , rather than in the subg. Monogynella (Des Moul.) Peter, Engl. & Prantl (ancient clade species). Conclusion The study of Cuscuta plastomes reveals the profound impact of parasitism on genome evolution, highlighting the complex interplay of gene retention and loss through phylogenomic approaches. This research enriches our understanding of plant genome evolution and the intricate host-parasite relationships. It also sheds light on the evolutionary history and genomic adaptations of Cuscuta , illustrating the diverse strategies enabling subg. Grammica , Pachystigma , Cuscuta , and Monogynella thrive as parasitic species. These findings provide valuable insights into the molecular mechanisms underlying parasitism and its impact on plastid genome organization.

An ordered draft sequence of the 17-gigabase hexaploid bread wheat (Triticum aestivum) genome has been produced by sequencing isolated chromosome arms. We have annotated 124,201 gene loci distributed nearly evenly across the homeologous chromosomes and subgenomes. Comparative gene analysis of wheat subgenomes and extant diploid and tetraploid wheat relatives showed that high sequence similarity and structural conservation are retained, with limited gene loss, after polyploidization. However, across the genomes there was evidence of dynamic gene gain, loss, and duplication since the divergence of the wheat lineages. A high degree of transcriptional autonomy and no global dominance was found for the subgenomes. These insights into the genome biology of a polyploid crop provide a springboard for faster gene isolation, rapid genetic marker development, and precise breeding to meet the needs of increasing food demand worldwide.

Polyploidization has provided much genetic variation for plant adaptive evolution, but the mechanisms by which the molecular evolution of polyploid genomes establishes genetic architecture underlying species differentiation are unclear. Brassica is an ideal model to increase knowledge of polyploid evolution. Here we describe a draft genome sequence of Brassica oleracea, comparing it with that of its sister species B. rapa to reveal numerous chromosome rearrangements and asymmetrical gene loss in duplicated genomic blocks, asymmetrical amplification of transposable elements, differential gene co-retention for specific pathways and variation in gene expression, including alternative splicing, among a large number of paralogous and orthologous genes. Genes related to the production of anticancer phytochemicals and morphological variations illustrate consequences of genome duplication and gene divergence, imparting biochemical and morphological variation to B. oleracea. This study provides insights into Brassica genome evolution and will underpin research into the many important crops in this genus.

The nucleocytoplasmic large DNA viruses (NCLDVs) are a monophyletic group of diverse eukaryotic viruses that reproduce primarily in the cytoplasm of the infected cells and include the largest viruses currently known: the giant mimiviruses, pandoraviruses, and pithoviruses. With virions measuring up to 1.5 μm and genomes of up to 2.5 Mb, the giant viruses break the now-outdated definition of a virus and extend deep into the genome size range typical of bacteria and archaea. Additionally, giant viruses encode multiple proteins that are universal among cellular life forms, particularly components of the translation system, the signature cellular molecular machinery. These findings triggered hypotheses on the origin of giant viruses from cells, likely of an extinct fourth domain of cellular life, via reductive evolution. However, phylogenomic analyses reveal a different picture, namely multiple origins of giant viruses from smaller NCLDVs via acquisition of multiple genes from the eukaryotic hosts and bacteria, along with gene duplication. Thus, with regard to their origin, the giant viruses do not appear to qualitatively differ from the rest of the virosphere. However, the evolutionary forces that led to the emergence of virus gigantism remain enigmatic.

In order to understand the evolution of the orchid plastome, we annotated and compared 124 complete plastomes of Orchidaceae representing all the major lineages in their structures, gene contents, gene rearrangements, and IR contractions/expansions. Forty-two of these plastomes were generated from the corresponding author's laboratory, and 24 plastomes-including nine genera ( , , , , , , , and )-are new in this study. All orchid plastomes, except and have a quadripartite structure consisting of a large single copy (LSC), two inverted repeats (IRs), and a small single copy (SSC) region. The IR region was completely lost in the plastomes. The SSC is lost in the plastome. The smallest plastome size was 19,047 bp, in and the largest plastome size was 178,131 bp, in . The small plastome sizes are primarily the result of gene losses associated with mycoheterotrophic habitats, while the large plastome sizes are due to the expansion of noncoding regions. The minimal number of common genes among orchid plastomes to maintain minimal plastome activity was 15, including the three subunits of (14, 16, and 36), seven subunits of (2, 3, 4, 7, 8, 11, and 14), three subunits of (5, 16, and 23), C-GCA, and P genes. Three stages of gene loss were observed among the orchid plastomes. The first was gene loss, which is widespread in Apostasioideae, Vanilloideae, Cypripedioideae, and Epidendroideae, but rare in the Orchidoideae. The second stage was the loss of photosynthetic genes ( , and ) and gene subunits, which are restricted to and some species of and . The third stage was gene loss related to prokaryotic gene expression ( , , and others), which was observed in , , and In addition, an intermediate stage between the second and third stage was observed in (Vanilloideae). The majority of intron losses are associated with the loss of their corresponding genes. In some orchid taxa, however, introns have been lost in 16 16, and P(2) without their corresponding gene being lost. A total of 104 gene rearrangements were counted when comparing 116 orchid plastomes. Among them, many were concentrated near the IRa/b-SSC junction area. The plastome phylogeny of 124 orchid species confirmed the relationship of {Apostasioideae [Vanilloideae (Cypripedioideae (Orchidoideae, Epidendroideae))]} at the subfamily level and the phylogenetic relationships of 17 tribes were also established. Molecular clock analysis based on the whole plastome sequences suggested that Orchidaceae diverged from its sister family 99.2 mya, and the estimated divergence times of five subfamilies are as follows: Apostasioideae (79.91 mya), Vanilloideae (69.84 mya), Cypripedioideae (64.97 mya), Orchidoideae (59.16 mya), and Epidendroideae (59.16 mya). We also released the first nuclear ribosomal (nr) DNA unit (18S-ITS1-5.8S-ITS2-28S-NTS-ETS) sequences for the 42 species of Orchidaceae. Finally, the phylogenetic tree based on the nrDNA unit sequences is compared to the tree based on the 42 identical plastome sequences, and the differences between the two datasets are discussed in this paper.

Monkeypox is a zoonotic disease caused by monkeypox virus (MPXV), which is a member of orthopoxvirus genus. The reemergence of MPXV in 2017 (at Bayelsa state) after 39 years of no reported case in Nigeria, and the export of travelers’ monkeypox (MPX) from Nigeria to other parts of the world, in 2018 and 2019, respectively, have raised concern that MPXV may have emerged to occupy the ecological and immunological niche vacated by smallpox virus. This review X-rays the current state of knowledge pertaining the infection biology, epidemiology, and evolution of MPXV in Nigeria and worldwide, especially with regard to the human, cellular, and viral factors that modulate the virus transmission dynamics, infection, and its maintenance in nature. This paper also elucidates the role of recombination, gene loss and gene gain in MPXV evolution, chronicles the role of signaling in MPXV infection, and reviews the current therapeutic options available for the treatment and prevention of MPX. Additionally, genome-wide phylogenetic analysis was undertaken, and we show that MPXV isolates from recent 2017 outbreak in Nigeria were monophyletic with the isolate exported to Israel from Nigeria but do not share the most recent common ancestor with isolates obtained from earlier outbreaks, in 1971 and 1978, respectively. Finally, the review highlighted gaps in knowledge particularly the non-identification of a definitive reservoir host animal for MPXV and proposed future research endeavors to address the unresolved questions.

Background The growing importance of the ubiquitous fungal genus Trichoderma (Hypocreales, Ascomycota) requires understanding of its biology and evolution. Many Trichoderma species are used as biofertilizers and biofungicides and T. reesei is the model organism for industrial production of cellulolytic enzymes. In addition, some highly opportunistic species devastate mushroom farms and can become pathogens of humans. A comparative analysis of the first three whole genomes revealed mycoparasitism as the innate feature of Trichoderma . However, the evolution of these traits is not yet understood. Results We selected 12 most commonly occurring Trichoderma species and studied the evolution of their genome sequences. Trichoderma evolved in the time of the Cretaceous-Palaeogene extinction event 66 (±15) mya, but the formation of extant sections ( Longibrachiatum, Trichoderma ) or clades ( Harzianum/Virens ) happened in Oligocene. The evolution of the Harzianum clade and section Trichoderma was accompanied by significant gene gain, but the ancestor of section Longibrachiatum experienced rapid gene loss. The highest number of genes gained encoded ankyrins, HET domain proteins and transcription factors. We also identified the Trichoderma core genome, completely curated its annotation, investigated several gene families in detail and compared the results to those of other fungi. Eighty percent of those genes for which a function could be predicted were also found in other fungi, but only 67% of those without a predictable function. Conclusions Our study presents a time scaled pattern of genome evolution in 12 Trichoderma species from three phylogenetically distant clades/sections and a comprehensive analysis of their genes . The data offer insights in the evolution of a mycoparasite towards a generalist.