The lack of genes assigned to the common ancestor of branch 3 (with the obvious exception of the RdRp) prevents development of a coherent evolutionary scenario for the entire branch. In the case of the clade encompassing the “alphavirus supergroup” and related viruses, a potential common ancestor could be a simple virus that encoded only an RdRp and a SJR-CP, a CP fold most broadly represented in this clade, including diverse tombusviruses, nodaviruses and members of Bromoviridae, and Tymoviridae within the “alphavirus supergroup.” Proposal of such an ancestor for the ﬂavivirus clade is challenged by the lack of viruses with short and simple genomes among ﬂaviviruses. Indeed, the lengths of the genomes in this clade range from ⬃ 9 kb to ⬃ 26 kb, with even the shortest ones encoding at least three of the ﬂavivirus signature genes (serine protease [Spro], S2H, and RdRp). One potential clue, how- ever, is provided by “jı ngménviruses,” with tetrapartite genomes in which the protease-helicase modules and the RdRps are encoded by separate genome segments; two other segments apparently encode structural proteins of unclear provenance (38). This genome architecture could hint at an ancestral ﬂavivirus genome that was assembled from genes borrowed from preexisting viruses, one of which possessed a divergent “tombus-like virus” RdRp. Although the origins of branch 3 are murky, major trends in its subsequent evolution clearly included lineage-speciﬁc gene capture, starting with helicases and CapEs in the ancestors of the major lineages and followed by diverse genes in smaller groups (Fig. 4B).
notably, bipedalism, a large brain, susceptibility to AIDS, We tackle this problem by comparing the rate of pro- speech, and higher-order cognitive function (Boyd and tein sequence evolution in the human lineage (since Silk 2000; McConkey et al. 2000; Varki 2000; Gagneux the human-chimpanzee split) with that in nonhuman and Varki 2001). Understanding how and why these mammals. This comparison is useful because pheno- and other features unique to humans evolved is a key type-affecting genetic modifications can be subject to to disclosing the mystery of human origins and is of sub- positive Darwinian selection, under which the rate of stantial medical importance (Gibbons 1998; McConkey amino acid substitution can be greatly enhanced (Nei et al. 2000; Varki 2000). Fortunately, most of the genetic and Kumar 2000). A change in substitution rate may bases of these features lie somewhere in the ⵑ3 billion also result when the function of a protein shifts so that nucleotides of our genome, a huge, albeit limited, pool the selective pressure is either enhanced or relaxed (Nei in which to look for answers. Gagneux and Varki and Kumar 2000). In the following, we report identifi- (2000) recently reviewed genetic differences between cation of two genes with significant rate enhancements humans and great apes. Although many genetic changes in the hominid lineage and discuss their relevance to that have occurred in the human lineage have been the origins of human-specific features.
This report only highlights a few of the many intriguing presentations that were offered at this year’s SICB Annual meeting. Clearly the availability of new gene/ genome sequencing technologies continues to make a major impact in the field of evolutionary development. Also, many labs are creatively adapting classical approaches to gain fascinating new insights on an expanding number of new biological systems. As these laboratories continue to examine the evolution of devel- opmental systems, understanding of this field and the origins of biological diversity continues to grow. It should be exciting to learn what has been gained by the 2013 meeting in San Francisco, California.
A major challenge is to identify the genetic changes respon- sible for appearance of new animal groups during the course of evolution. To our knowledge, we now provide the first evidence that origins of regulatory elements in a homeotic gene, Cdx1, correspond with evolutionary transitions between vertebrate groups. The Cdx genes, as upstream regulators of Hox genes, seem ideally suited for effecting large scale evolutionary changes in body plan. It is unlikely that modifications in expression of Cdx1 alone could have resulted in the morphological changes that we have discussed. Cdx1 modification may have been one of several changes, each acquired step-wise and providing some selective advantage. Sexual reproduction will have accelerated the accu- mulation of changes necessary for large scale morphological evolution.
Here, we performed whole exome-based mutational analyses for eight synchronous pairs of colorectal adenomas and carcinomas. Adenoma tissues were separated from accompanying carcinomas using microdissection and subjected to whole-exome sequencing (WES). Given the unique molecular pathogenic features between microsatellite- stable (MSS) and microsatellite-unstable (MSU) CRCs , adenoma-carcinoma pairs from both MSS and MSU CRCs were explored in this study. We show that the mutational architecture supports a parallel evolution, with clonal origins of synchronous benign and malignant lesions instead of the traditional adenoma-to-carcinoma sequence. We also observed that sequential acquisition of key somatic mutations during colorectal malignant transformation is largely consistent with previous reports (e.g., the early, clonal appearance of APC and KRAS mutations in microsatellite- stable CRC), but this might often be context-dependent.
ABSTRACT The vertebrate head is a complex assemblage of cranial specializations, including the central and peripheral nervous systems, viscero- and neurocranium, musculature and connective tissue. The primary differences that exist between vertebrates and other chordates relate to their craniofacial organization. Therefore, evolution of the head is considered fundamental to the origins of vertebrates (Gans and Northcutt, 1983). The transition from invertebrate to vertebrate chordates was a multistep process, involving the formation and patterning of many new cell types and tissues. The evolution of early vertebrates, such as jawless fish, was accompanied by the emergence of a specialized set of cells, called neural crest cells which have long held a fascination for developmental and evolutionary biologists due to their considerable influence on the complex development of the vertebrate head. Although it has been classically thought that protochordates lacked neural crest counterparts, the recent identification and characterization of amphioxus and ascidian genes homologous to those involved in vertebrate neural crest development challenges this idea. Instead it suggests that the neural crest may not be a novel vertebrate cell population, but could have in fact originated from the protochordate dorsal midline epidermis. Consequently, the evolution of the neural crest cells could be reconsidered in terms of the acquisition of new cell properties such as delamination-migration and also multipotency which were key innovations that contributed to craniofacial development. In this review we discuss recent findings concerning the inductive origins of neural crest cells, as well as new insights into the mechanisms patterning this cell population and the subsequent influence this has had on craniofacial evolution.
Quite what the world where these ancient virus-like replica- tors resided looked like is open to debate, and there are a number of rather different versions of the pre-LUCA theory. One important idea is that there was an “ancient virus world” of primordial replicators that existed before any cellular or- ganisms and that both RNA (first) and DNA (later) viruses originated at this time, donating some features to the first cellular organisms (24, 26). The obligatory parasitic behavior of contemporary viruses therefore represents a more recent adaptation. A competing theory is that RNA cells existed be- fore the LUCA and that RNA viruses were parasites on these RNA cells that later evolved DNA as a way of escaping host cell responses (13, 14). As such, viruses were responsible for one of the major innovations in evolutionary history. Given that we are attempting to reconstruct events that happened billions of years ago, such that the trace of common ancestry has all but disappeared, it is always going to be extremely challenging to choose between theories of pre-LUCA life. In- deed, it is patently easier to create theories for viral origins than to test them. These fundamental limitations notwith- standing, I believe Koonin’s argument that a “precellular stage of evolution must have involved genetic elements of virus-like size and complexity” is a compelling one (27). Indeed, as I will argue below, a consideration of how RNA viruses evolve today strongly suggests that the earliest replicating molecules shared some clear similarities with viruses.
The paper proposes that the four-component structure of political order con- sists of state, imagination, rule, and accountability whose mental origins are the social brain, theory of mind, the rational brain, and the empirical brain, respectively. The rational brain and the empirical brain are from the thinking brain. This paper posits that in the evolution of political order, the main function of political order is to pacify changed social structure derived from technological revolution. Therefore, the four technological revolutions (the Upper Paleolithic, Agricultural-Bronze, Iron, and Industrial Revolutions) pro- duce the four changed social structures (linked bands, tribe, mega empire, and modern nation, respectively) whose internal conflicts are pacified by the four political revolutions (the imaginative, hierarchical, thinking, bottom-up political revolutions, respectively) to form the four politics (the imaginative ega- litarianism, decentralized hierarchical tribalism, centralized top-down thinking, and multilateral bottom-up thinking politics, respectively). In the competitive West originated from Greece and Middle East, the rule of law is the rational rule of competition among competitors, and the accountability of election is the empirical accountability of competition among competitors. In the coop- erative East originated from India and China, the rule of relation is the ra- tional rule of cooperation among kin-friends, and the accountability of pro- fessional qualification is the empirical accountability of cooperation among kin-friends. For political order, the two viable politics are competitive liberal democracy based on liberty and cooperative well-off democracy (well-off so- cialism) based on wellbeing. The direction of political order is middle democra- cy between liberal democracy and well-off democracy based on the multila- teral bottom-up thinking politics.
In accordance with the INA, employment-based preference visas (and family-sponsored visas) are issued to eligible immigrants in the order in which petitions have been filed under that specific preference category for that specific country. Spouses and children of prospective LPRs are entitled to the same status, and the same order of consideration as the person qualifying as the principal LPR, if accompanying or following to join the LPR (referred to as derivative status). When visa demand exceeds the per-country limit, visas are prorated according to the preference system allocations (detailed in Table 1) for the oversubscribed foreign state or dependent area.
duplications (Fig. 3 and Supplementary Fig. S1, available at JXB online). The three most recent copies, namely ppc-1E1c, ppc-1E1d, and ppc-1E1e, are all characterized by increased rates of amino acid substitutions (Fig. 3 and Table 2). The Portulacineae encompass species with different degrees of CAM metabolism (Guralnick and Jackson, 2001; Nyffeler et al., 2008). The high number of ppc-1E1 copies could have promoted neo- functionalization of the genes by relaxing selective constraints, facilitating the diversification of photosynthetic types in this group. A gradual upregulation of the CCM over time would have triggered successive periods of adaptive genetic changes in response to modifications of the catalytic environment, explain- ing the high rates of amino acid substitutions sustained in the entire clade (Fig. 3). For instance, the accumulation of muta- tions on the branches leading to ppc-1E1c of CAM-constitutive cacti (Cactoideae and Opuntioideae; Fig. 3) could be linked to the evolution of a more efficient CAM pathway in these taxa. This contrasts with the evolution of C 4 -specific PEPC where
Below we discuss the ﬁrst two key assumptions—asexual reproduction and adaptation from de novo mutations—in more detail. First, consider our assumption of asexual re- production. Our results rely strongly on compensatory evo- lution, and empirical data (Meer et al. 2010), as well as the simulation results presented here, suggest that compensa- tory evolution is common in the absence of recombination. The key issue is whether high rates of compensatory evolu- tion are also expected among cryptic sequences in sexual populations. Unfortunately, comparable sexual simulations would require the tracking of a far larger number of geno- types, making such simulations computationally inaccessi- ble. However, some heuristic predictions can be made, based on previous analytical theory on this topic. Consider the simple example of a segregating pair of loci with mutu- ally compensatory phenotypic effects. When recombination breaks up compensatory pairings, alleles from rare pairs are likely eliminated. This will initially select against new com- pensatory allele pairs (when their component alleles are rare) but may later favor them if they survive to become common. On the other hand, two alleles that would form a compensatory pair but appeared in different individuals may sometimes be brought together by recombination. The net result of these effects is complex, but theory shows that in the slightly different case where the pair of compensatory alleles is more ﬁt than the original genotype, pairs ﬁx more frequently with low recombination and equally frequently with either high or zero recombination, so long as selection against cryptic alleles is weak (Weissman et al. 2010). This theoretical ﬁnding suggests that our results may apply to sexual populations as well. Indeed, empirically, compensa- tory evolution seems to occur despite frequent recombina- tion in sexual species, as suggested by QTL mapping studies that have reported alleles with opposite phenotypic effects at different loci (Rieseberg et al. 1999; Brem and Kruglyak 2005; Carlborg et al. 2006; Visscher 2008).
To further explore the evolution of LASV within and between hosts, we investigated how often iSNVs become fixed in other consensus sequences. We defined an iSNV as ‘fixed’ if its minor allelic variant was observed in one or more LASV consensus sequences. We observed a significantly higher nonsynonymous to synonymous ratio (N/S) for unfixed compared to fixed iSNVs (Figure 7A), suggesting a selective bias against the fixation of nonsynonymous iSNVs. LASV and EBOV both have similar numbers of unfixed iSNVs, but LASV has many more fixed iSNVs, likely due to higher rates of iSNV fixation (or transmission) in LASV than EBOV (Figure 7B). However, the putative transmitted (fixed) iSNVs tend to be biased toward synonymous mutations. This bias is much stronger in LASV (Figure 7C, top panel) but still detectable in EBOV (Figure 7C, middle panel). The bias cannot be attributed to differences in minor allele frequencies between nonsynonymous and synonymous iSNVs (P-value > 0.1, Kolmogorov-Smirnov test), or to a correlation between MAF and prevalence in consensus sequences (P-value > 0.1 for both N and S, Pearson's correlation); therefore, it is best attributed to selection against transmission and/or fixation of nonsynonymous iSNVs.
Breast cancer is not a single disease, but rather is composed of distinct subtypes associated with different clinical outcomes. Understanding this heterogeneity is key for the development of target- ed cancer-preventative and -therapeutic interventions. Current models explaining inter- and intra- tumoral diversity are the cancer stem cell and the clonal evolution hypotheses. Although tumor initiation and progression are predominantly driven by acquired genetic alterations, recent data implicate a role for microenvironmental and epigenetic changes as well. Comprehensive unbiased studies of tumors and patient populations have significantly advanced our molecular understand- ing of breast cancer, but translating these findings into clinical practice remains a challenge.
dissimilar in sequence to even very close relatives - are almost certainly simply rapidly evolving. Yet their rate of evolution is astonishingly fast - their protein sequences are as unique to D. melanogaster as any “true” orphan. The fourth chapter describes a set of genes that are in whole or part specific to D. melanogaster and its relatives. Surprisingly, RNAi knockdown of some of these genes led to total lethality, implying these genes are essential. The genes are expressed in the testes and also in developing larvae, lending credence to Kaessmann’s (2010) “out of the testes” hypothesis for the evolution of novel functions for new genes. Finally, chapter five describes two putative protein-coding genes that apparently have evolved from previously non-coding RNAs. One of these is apparently essential, though we hypothesize that the essential function is more likely due to the function of the older RNA gene than the new ORF. Together with chapter four, this result implies that the evolutionary trajectories of de novo genes are diverse, even while disrupting their function leads to surprisingly similar results.