Genome dynamics最新文献

We present an overview of comparative genomics of ATP-dependent DNA packaging systems of viruses. Several distinct ATPase motors and accessory proteins have been identified in DNA-packaging systems of viruses such as terminase-portal systems, the 29-like packaging apparatus, and packaging systems of lipid inner-membrane-containing viruses. Sequence and structure analysis of these proteins suggest that there were two major independent innovations of ATP-dependent DNA packaging systems in the viral universe. The first of these utilizes a HerA/FtsK superfamily ATPase and is seen in prokaryotic viruses with inner lipid membranes, large eukaryotic nucleo-cytoplasmic DNA viruses (including poxviruses) and a group of eukaryotic mobile DNA transposons. We show that ATPases of the 29-like packaging system are also divergent versions of the HerA/FtsK superfamily that functions in viruses without an inner membrane. The second system, the terminase-portal system, is dominant in prokaryotic tailed viruses and typically functions with linear chromosomes. The large subunit of this system contains a distinct ATPase domain and a C-terminal nuclease domain of the RNAse H fold. We discuss the classification of these ATPases within the P-loop NTPases, genomic demography and positioning of their genes in the viral chromosome. We show that diverse portal proteins utilized by these systems share a common evolutionary origin and might have frequently displaced each other in evolution. Examination of conserved gene neighborhoods indicates repeated acquisition of Helix-turn-Helix domain-containing terminase small subunits and a third accessory component, the MuF protein. Adenoviruses appear to have evolved a third packaging ATPase, unique to their lineage. Relationship between one major type of packaging ATPases and cellular chromosome pumps like FtsK suggests an ancient common origin for viral packaging and cellular chromosome partitioning systems.

Comparative genomics is rapidly bringing to light the manifold differences that exist within and between species on the molecular level. Of fundamental interest are the absolute and relative amounts of the genome dedicated to protein coding regions. Results thus far have shown surprising variation on both the polymorphism and divergence levels. As a result, there has been an increase in efforts aimed to characterize the underlying genetic mechanisms and evolutionary forces that continue to alter genomic architecture. In this review we discuss the formation of chimeric genes generated at the DNA level. While the formation of chimeric genes has been shown to be an important way in which coding regions of the genome evolve, many of the detailed studies have been limited to chimeric genes formed through retroposition events (through an RNA intermediate step). Here we provide a short review of the reported mechanisms that have been identified for chimeric gene formations, excluding retroposition-related cases, and discuss several of the evolutionary analyses carried out on them. We emphasize the utility chimeric genes provide for the study of novel function. We also emphasize the importance of studying chimeric genes that are evolutionarily young.

The activity of transposable elements (TEs) has had a profound impact on the evolution of eukaryotic genomes. Once thought to be purely selfish genomic entities, TEs are now recognized to occupy a continuum of relationships, ranging from parasitic to mutualistic, with their host genomes. One of the many ways that TEs contribute to the function and evolution of the genomes in which they reside is through the donation of host protein coding sequences (CDSs). In this chapter, we will describe several notable examples of eukaryotic host CDSs that are derived from TEs. Despite the existence of a number of such well-established cases, the overall extent and significance of this phenomenon remains a matter of controversy. Genome-scale computational analyses have yielded vastly different estimates for the fraction of host CDSs that are derived from TEs. We explain how these seemingly contradictory findings are the result of specific ascertainment biases introduced by the different methods used to detect TE-related sequences. In light of this problem, we propose a comprehensive and systematic framework for definitively characterizing the contribution of TEs to eukaryotic CDSs.

Gene expression in organisms is controlled by regulatory proteins termed transcription factors, which recognize and bind to specific nucleotide sequences. Over the years, considerable information has accumulated on the regulatory interactions between transcription factors and their target genes in various model prokaryotes, such as Escherichia coli and Bacillus subtilis. This has allowed the representation of this information in the form of a directed graph, which is commonly referred to as the transcriptional regulatory network. The network representation provides us with an excellent conceptual framework to understand the structure of the transcriptional regulation, both at local and global levels of organization. Several studies suggest that the transcriptional network inferred from model organisms may be approximated by a scale-free topology, which in turn implies the presence of a relatively small group of highly connected regulators (hubs or global regulators). While the graph theoretical principles have been applied to infer various properties of such networks, there have been few studies that have actually investigated the evolution of the transcriptional regulatory networks across diverse organisms. Using recently developed computational methods that exploit various evolutionary principles, we have attempted to reconstruct and compare these networks across a wide-range of prokaryotes. This has provided several insights on the modification and diversification of network structures of various organisms in course of evolution. Firstly, we observed that target genes show a much higher level of conservation than their transcriptional regulators. This in turn suggested that the same set of functions could be differently controlled across diverse organisms, contributing significantly to their adaptive radiations. In particular, at the local level of network structure, organism-specific optimization of the transcription network has evolved primarily via tinkering of individual regulatory interactions rather than whole scale reuse or deletion of network motifs (local structure). In turn, as phylogenetic diversification proceeds, this process appears to have favored repeated convergence to scale-free-like structures, albeit with different regulatory hubs.

Interspersed repetitive sequences are major components of eukaryotic genomes. They comprise about 50% of the mammalian genome. They interact with the whole genome and influence its evolution. They do this in many ways, e.g. by serving as recombination hotspots, providing a mechanism for genomic shuffling and a source of 'ready-to-use' motifs for new transcriptional regulatory elements, polyadenylation signals, and protein-coding sequences. In this review we discuss the consequences of exaptation of sequences originated in tansposable elements with focus on events that influence protein coding genes.

Protein-protein interactions (PPIs) are one of the most important components of biological networks. It is important to understand the evolutionary process of PPIs in order to elucidate how the evolution of biological networks has contributed to diversification of the existent organisms. We focused on the evolutionary rates of proteins involved with PPIs, because it had been shown that for a given protein-coding gene the number of its PPIs in a biological network was one of the important factors in determining the evolutionary rate of the gene. We studied the evolutionary rates of duplicated gene products that were involved with PPIs, reviewing the current situation of this subject. In addition, we focused on how the evolutionary rates of proteins were influenced by the characteristic features of PPIs. We, then, concluded that the evolutionary rates of the proteins in the PPI networks were strongly influenced by their PPI partners. Finally, we emphasized that evolutionary considerations of the PPI proteins were very important for understanding the building up of the current PPI networks.

Bacterial flagella at first sight appear uniquely sophisticated in structure, so much so that they have even been considered 'irreducibly complex' by the intelligent design movement. However, a more detailed analysis reveals that these remarkable pieces of molecular machinery are the product of processes that are fully compatible with Darwinian evolution. In this chapter we present evidence for such processes, based on a review of experimental studies, molecular phylogeny and microbial genomics. Several processes have played important roles in flagellar evolution: self-assembly of simple repeating subunits, gene duplication with subsequent divergence, recruitment of elements from other systems ('molecular bricolage'), and recombination. We also discuss additional tentative new assignments of homology (FliG with MgtE, FliO with YscJ). In conclusion, rather than providing evidence of intelligent design, flagellar and non-flagellar Type III secretion systems instead provide excellent case studies in the evolution of complex systems from simpler components.

Duplicated genes can undergo different fates, from nonfunctionalization to subfunctionalization and neofunctionalization. In particular, changes in regulatory sequences affecting the expression domain of genes seem to be responsible for the latter two fates. In this study we used in silico motif detection to show how alterations in the composition of regulatory motifs between paralogous genes in zebrafish and Tetraodon might reflect the functional divergence of duplicates.

The domestic cat has a long history of informing human biology, from early studies of comparative anatomy to the present genetic characterization of many feline genetic disease models. Nearly half of these diseases have homologous counterparts in human. Difficulties studying these defects in humans provide model organisms, like the domestic cat, with a unique opportunity to further inform human hereditary and infectious disease. Here I review the progress in the development of genomic mapping resources, the recent acquisition of a feline 2x genome sequence, and how these tools now equip feline geneticists to identify and characterize genes in cats causing comparable diseases or phenotypes in other species. The availability of such a mapping resource will enable positional cloning approaches and stimulate further development and use of the domestic cat as a model for human disease, while also enhancing the health of the species itself. The cat gene map also provides a useful tool in multispecies comparative genomic analyses to better understand the causes and consequences of chromosome breakage and evolution.