No abstract

Aim Size is one of the most important and obvious traits of an organism. Both small and large sizes have adaptive advantages and disadvantages. Body size–frequency distributions of most large clades are unimodal and right skewed. Species larger than the mean or range midpoint of body sizes are relatively scarce. Theoretical models suggest evolutionary rates are higher in small organisms with short generation times. Therefore diversification rates are usually thought to be maximal at relatively small body sizes. Empirical studies of the rates of molecular evolution and clade diversification, however, have usually indicated that both are unrelated to body size. Furthermore, it has been claimed that because snakes are longer than lizards, the size–frequency distribution of all squamate species is bimodal overall. We examined the shape of the size–frequency distribution of nearly all Squamata and Rhynchocephalia species, and investigated how size affected diversification rates. Location Global. Methods We collected data on maximum body length for 9805 lepidosaur (squamates and the tuatara) species (99.7% of all species) and converted them to mass using clade‐specific allometric equations. Using methods that test for relationships between continuous traits and speciation and extinction rates on a large, dated phylogeny (4155 species), we investigated the relationship between diversification rates and body size. Results Living squamates span six orders of magnitude in body size, eight when giant extinct snakes and mosasaurs are included. The body size–frequency distributions of snakes and lizards separately, and of all lepidosaur species combined, are unimodal and right skewed. Nonetheless, we find neither linear nor hump‐shaped relationships between size and diversification rates, except in snakes, where speciation and diversification are hump shaped. Main conclusions  Despite a clear modality and skew in the body sizes of lepidosaurs, we find little evidence for faster diversification of modal‐sized taxa, perhaps implying that larger‐sized clades are relatively young.

Polyploidy is commonly thought to be associated with the domestication process because of its concurrence with agriculturally favourable traits and because it is widespread among the major plant crops(1-4). Furthermore, the genetic consequences of polyploidy(5-7) might have increased the adaptive plasticity of those plants, enabling successful domestication(6-8). Nevertheless, a detailed phylogenetic analysis regarding the association of polyploidy with the domestication process, and the temporal order of these distinct events, has been lacking(3). Here, we have gathered a comprehensive data set including dozens of genera, each containing one or more major crop species and for which sufficient sequence and chromosome number data exist. Using probabilistic inference of ploidy levels conducted within a phylogenetic framework, we have examined the incidence of polyploidization events within each genus. We found that domesticated plants have gone through more polyploidy events than their wild relatives, with monocots exhibiting the most profound difference: 54% of the crops are polyploids versus 40% of the wild species. We then examined whether the preponderance of polyploidy among crop species is the result of two, non-mutually-exclusive hypotheses: (1) polyploidy followed by domestication, and (2) domestication followed by polyploidy. We found support for the first hypothesis, whereby polyploid species were more likely to be domesticated than their wild relatives, suggesting that the genetic consequences of polyploidy have conferred genetic preconditions for successful domestication on many of these plants.

Transcription is a highly regulated process, and stress-induced changes in gene transcription have been shown to play a major role in stress responses and adaptation. Genome-wide studies reveal prevalent transcription beyond known protein-coding gene loci, generating a variety of RNA classes, most of unknown function. One such class, termed downstream of gene-containing transcripts (DoGs), was reported to result from transcriptional readthrough upon osmotic stress in human cells. However, how widespread the readthrough phenomenon is, and what its causes and consequences are, remain elusive. Here we present a genome-wide mapping of transcriptional readthrough, using nuclear RNA-Seq, comparing heat shock, osmotic stress, and oxidative stress in NIH 3T3 mouse fibroblast cells. We observe massive induction of transcriptional readthrough, both in levels and length, under all stress conditions, with significant, yet not complete, overlap of readthrough-induced loci between different conditions. Importantly, our analyses suggest that stress-induced transcriptional readthrough is not a random failure process, but is rather differentially induced across different conditions. We explore potential regulators and find a role for HSF1 in the induction of a subset of heat shock-induced readthrough transcripts. Analysis of public datasets detected increases in polymerase II occupancy in DoG regions after heat shock, supporting our findings. Interestingly, DoGs tend to be produced in the vicinity of neighboring genes, leading to a marked increase in their antisense-generating potential. Finally, we examine genomic features of readthrough transcription and observe a unique chromatin signature typical of DoG-producing regions, suggesting that readthrough transcription is associated with the maintenance of an open chromatin state.transcriptional readthrough | stress response | transcription regulation

Prokaryotic genomes are small and compact. Either this feature is caused by neutral evolution or by natural selection favoring small genomes—genome streamlining. Three separate prior lines of evidence argue against streamlining for most prokaryotes. We find that the same three lines of evidence argue for streamlining in the genomes of thermophile bacteria. Specifically, with increasing habitat temperature and decreasing genome size, the proportion of genomic DNA in intergenic regions decreases. Furthermore, with increasing habitat temperature, generation time decreases. Genome-wide selective constraints do not decrease as in the reduced genomes of host-associated species. Reduced habitat variability is not a likely explanation for the smaller genomes of thermophiles. Genome size may be an indirect target of selection due to its association with cell volume. We use metabolic modeling to demonstrate that known changes in cell structure and physiology at high temperature can provide a selective advantage to reduce cell volume at high temperatures.

New protein-coding genes can originate either through modification of existing genes or de novo. Recently, the importance of de novo origination has been recognized in eukaryotes, although eukaryotic genes originated de novo are relatively rare and difficult to identify. In contrast, viruses contain many de novo genes , namely those in which an existing gene has been “overprinted” by a new open reading frame, a process that generates a new protein-coding gene overlapping the ancestral gene. We analyzed the evolution of 12 experimentally validated viral genes that originated de novo and estimated their relative ages. We found that young de novo genes have a different codon usage from the rest of the genome. They evolve rapidly and are under positive or weak purifying selection. Thus, young de novo genes might have strain-specific functions, or no function, and would be difficult to detect using current genome annotation methods that rely on the sequence signature of purifying selection. In contrast to young de novo genes, older de novo genes have a codon usage that is similar to the rest of the genome. They evolve slowly and are under stronger purifying selection. Some of the oldest de novo genes evolve under stronger selection pressure than the ancestral gene they overlap, suggesting an evolutionary tug of war between the ancestral and the de novo gene.

Published estimates of the proportion of positively selected genes (PSGs) in human vary over three orders of magnitude. In mammals, estimates of the proportion of PSGs cover an even wider range of values. We used 2,980 orthologous protein-coding genes from human, chimpanzee, macaque, dog, cow, rat, and mouse as well as an established phylogenetic topology to infer the fraction of PSGs in all seven terminal branches. The inferred fraction of PSGs ranged from 0.9% in human through 17.5% in macaque to 23.3% in dog. We found three factors that influence the fraction of genes that exhibit telltale signs of positive selection: the quality of the sequence, the degree of misannotation, and ambiguities in the multiple sequence alignment. The inferred fraction of PSGs in sequences that are deficient in all three criteria of coverage, annotation, and alignment is 7.2 times higher than that in genes with high trace sequencing coverage, “known” annotation status, and perfect alignment scores. We conclude that some estimates on the prevalence of positive Darwinian selection in the literature may be inflated and should be treated with caution.

It has recently been claimed that older genes tend to evolve more slowly than newer ones (Alba and Castresana 2005). By simulation of genes of equal age, we show that the inverse correlation between age and rate is an artifact caused by our inability to detect homology when evolutionary distances are large. Since evolutionary distance increases with time of divergence and rate of evolution, homologs of fast-evolving genes are frequently undetected in distantly related taxa and are, hence, misclassified as "new." This misclassification causes the mean genetic distance of 'new' genes to be overestimated and the mean genetic distance of "old" genes to be underestimated.