How sensory drive can promote speciation

Some of the most spectacular and diverse traits in animals are the signals used to attract mates. Closely related species often differ dramatically in signaling traits, in spite of similarity in other morphological traits. The idea that reproductive isolation arises when male mating signals and female preferences differ among populations is an old one. However, until recently, there was almost no information on what generates diversity in mating signals and preferences. This is beginning to change, with emerging results that highlight the importance of habitat differences in generating this diversity. Such differences in ecology are at the root of one hypothesis for divergence in sexual signaling – sensory drive. The sensory drive hypothesis focuses on how communication systems adapt to local environments and predicts that divergence in communication systems will occur when environments differ. Reproductive isolation can arise as a byproduct of this adaptive divergence in behavior.     

Sensory drive in cichlid speciation

The role of selection in speciation is a central yet poorly understood problem in evolutionary biology. The rapid radiations of extremely colorful cichlid fish in African lakes have fueled the hypothesis that sexual selection can drive species divergence without geographical isolation. Here we present experimental evidence for a mechanism by which sexual selection becomes divergent: in two sibling species from Lake Victoria, female mating preferences for red and blue male nuptial coloration coincide with their context-independent sensitivities to red and blue light, which in turn correspond to a difference in ambient light in the natural habitat of the species. These results suggest that natural selection on visual performance, favoring different visual properties in different spectral environments, may lead to divergent sexual selection on male nuptial coloration. This interplay of ecological and sexual selection along a light gradient may provide a mechanism of rapid speciation through divergent sensory drive.     

Role of duplicate genes in robustness against deleterious human mutations

It is now widely recognized that robustness is an inherent property of biological systems [1],[2],[3]. The contribution of close sequence homologs to genetic robustness against null mutations has been previously demonstrated in simple organisms [4],[5]. In this paper we investigate in detail the contribution of gene duplicates to back-up against deleterious human mutations. Our analysis demonstrates that the functional compensation by close homologs may play an important role in human genetic disease. Genes with a 90% sequence identity homolog are about 3 times less likely to harbor known disease mutations compared to genes with remote homologs. Moreover, close duplicates affect the phenotypic consequences of deleterious mutations by making a decrease in life expectancy significantly less likely. We also demonstrate that similarity of expression profiles across tissues significantly increases the likelihood of functional compensation by homologs.     

Chaotic gene regulatory networks can be robust against mutations and noise

Robustness to mutations and noise has been shown to evolve through stabilizing selection for optimal phenotypes in model gene regulatory networks. The ability to evolve robust mutants is known to depend on the network architecture. How do the dynamical properties and state-space structures of networks with high and low robustness differ? Does selection operate on the global dynamical behavior of the networks? What kind of state-space structures are favored by selection? We provide damage propagation analysis and an extensive statistical analysis of state spaces of these model networks to show that the change in their dynamical properties due to stabilizing selection for optimal phenotypes is minor. Most notably, the networks that are most robust to both mutations and noise are highly chaotic. Certain properties of chaotic networks, such as being able to produce large attractor basins, can be useful for maintaining a stable gene-expression pattern. Our findings indicate that conventional measures of stability, such as damage propagation, do not provide much information about robustness to mutations or noise in model gene regulatory networks.     

How humans drive speciation as well as extinction

A central topic for conservation science is evaluating how human activities influence global species diversity. Humanity exacerbates extinction rates. But by what mechanisms does humanity drive the emergence of new species? We review human-mediated speciation, compare speciation and known extinctions, and discuss the challenges of using net species diversity as a conservation objective. Humans drive rapid evolution through relocation, domestication, hunting and novel ecosystem creation—and emerging technologies could eventually provide additional mechanisms. The number of species relocated, domesticated and hunted during the Holocene is of comparable magnitude to the number of observed extinctions. While instances of human-mediated speciation are known, the overall effect these mechanisms have upon speciation rates has not yet been quantified. We also explore the importance of anthropogenic influence upon divergence in microorganisms. Even if human activities resulted in no net loss of species diversity by balancing speciation and extinction rates, this would probably be deemed unacceptable. We discuss why, based upon ‘no net loss’ conservation literature—considering phylogenetic diversity and other metrics, risk aversion, taboo trade-offs and spatial heterogeneity. We conclude that evaluating speciation alongside extinction could result in more nuanced understanding of biosphere trends, clarifying what it is we actually value about biodiversity.     

Sexual selection can constrain sympatric speciation

Recent theory has suggested that sympatric speciation can occur quite easily when individuals that are ecologically similar mate assortatively. Although many of these models have assumed that individuals have equal mating success, in nature rare phenotypes may often suffer decreased mating success. Consequently, assortative mating may often generate stabilizing sexual selection. We show that this effect can substantially impede sympatric speciation. Our results emphasize the need for data on the strength of the stabilizing component of selection generated by mating in natural populations.     

pH对不同富集能力植物根际土壤溶液中镉形态的影响

为了解不同p H对土壤溶液中Cd形态分布的影响,采用Visual MINTEQ 3.0模型和阳极溶出伏安法(ASV)研究土壤p H分别为4.0、5.5、7.0和8.5时镉超富集植物东南景天和非富集植物垂盆草根际土壤溶液中Cd的形态分布。模型计算结果表明:随着p H的升高,2种植物土壤溶液中Cd2+的比例均逐渐减小,其中东南景天根际土壤溶液中Cd2+占总溶解性Cd的比例为46.1%~3.2%,垂盆草为60.9%~9.9%;当土壤p H≥5.5时,土壤溶液中Cd形态主要以有机络合态(Cd-DOM)为主;2种植物相比,4个p H水平下垂盆草土壤溶液中Cd2+比例均高于东南景天,但东南景天中有机络合态Cd所占比例较大。基于ASV法的测定结果表明:东南景天土壤溶液中电活性Cd占总溶解性Cd的比例从最小(p H 8.5时)的5.5%到最大(p H 4.0时)的79.6%,而垂盆草的变化范围为11.8%~86.7%;电活性Cd的测定结果与Visual MINTEQ 3.0模型计算结果显著相关(R2=0.80),从而互相验证了实验测量和模拟计算的可靠性。     

Peptides from aminoacyl-tRNA synthetases can cure the defects due to mutations in mt tRNA genes

Recent results from several laboratories have confirmed that human and yeast leucyl- and valyl-tRNA synthetases can rescue the respiratory defects due to mutations in mitochondrial tRNA genes. In this report we show that this effect cannot be ascribed to the catalytic activity per se and that isolated domains of aminoacyl-tRNA synthetases and even short peptides thereof have suppressing effects.     

Trichome cell growth in Arabidopsis thaliana can be derepressed by mutations in at least five genes

Leaf trichomes in Arabidopsis are unicellular epidermal hairs with a branched morphology. They undergo successive endoreduplication rounds early during cell morphogenesis. Mutations affecting trichome nuclear DNA content, such as triptychon or glabra3, alter trichome branching. We isolated new mutants with supernumerary trichome branches, which fall into three unlinked complementation groups: KAKTUS and the novel loci, POLYCHOME and RASTAFARI. They map to chromosomes IV, II, and V, respectively. The trichomes of these mutants presented an increased DNA content, although to a variable extent. The spindly-5 mutant, which displays a constitutive gibberellin response, also produces overbranched trichomes containing more nuclear DNA. We analyzed genetic interactions using double mutants and propose that two independent pathways, defined by SPINDLY and TRIPTYCHON, act to limit trichome growth. KAKTUS and POLYCHOME might have redundant actions mediating gibberellin control via SPINDLY. The overall leaf polysomaty was not notably affected by these mutations, suggesting that they affect the control of DNA synthesis in a tissue- or cell type-specific manner. Wild-type tetraploids also produce overbranched trichomes; they displayed a shifted polysomaty in trichomes and in the whole leaf, suggesting a developmental program controlling DNA increases via the counting of endoreduplication rounds.     

Reinforcement can overcome gene flow during speciation in Drosophila

Reinforcement, the strengthening of prezygotic reproductive isolation by natural selection in response to maladaptive hybridization [1-3], is one of the few processes in which natural selection directly favors the evolution of species as discrete groups (e.g., [4-7]). The evolution of reproductive barriers via reinforcement is expected to evolve in regions where the ranges of two species overlap and hybridize as an evolutionary solution to avoiding the costs of maladaptive hybridization [2,3,8]. The role of reinforcement in speciation has, however, been highly controversial because population-genetic theory suggests that the process is severely impeded by both hybridization [8-11] and migration of individuals from outside the contact zone [12,13]. To determine whether reinforcement could strengthen the reproductive barriers between two sister species of Drosophila in the face of these impediments, I initiated experimental populations of these two species that allowed different degrees of hybridization, as well as migration from outside populations. Surprisingly, even in the face of gene flow, reinforcement could promote the evolution of reproductive isolation within only five generations. As theory predicts, high levels of hybridization (and/or strong selection against hybrids) and migration impeded this evolution. These results suggest that reinforcement can help complete the process of speciation.     

Courtship song genes and speciation in sand flies

Lutzomyia longipalpis (Lutz & Neiva, 1912) (Diptera: Psychodidae: Phlebotominae) is a vector of visceral leishmaniasis in the Americas and it might represent a complex of sibling species. Reproductive isolation between closely related species often involves differences in courtship behaviour. cacophony (cac) and period (per) are two Drosophila genes that control features of the "lovesong" males produce during courtship that has been implicated in the sexual isolation between closely related species. We are using gene fragments from L. longipalpis' homologues of these two genes to study the speciation process in this putative species complex.     

DNA-binding domain mutations in SMAD genes yield dominant-negative proteins or a neomorphic protein that can activate WG target genes in Drosophila

Mutations in SMAD tumor suppressor genes are involved in approximately 140,000 new cancers in the USA each year. At this time, how the absence of a functional SMAD protein leads to a tumor is unknown. However, clinical and biochemical studies suggest that all SMAD mutations are loss-of-function mutations. One prediction of this hypothesis is that all SMAD mutations cause tumors via a single mechanism. To test this hypothesis, we expressed five tumor-derived alleles of human SMAD genes and five mutant alleles of Drosophila SMAD genes in flies. We found that all of the DNA-binding domain mutations conferred gain-of-function activity, thereby falsifying the hypothesis. Furthermore, two types of gain-of-function mutation were identified - dominant negative and neomorphic. In numerous assays, the neomorphic allele SMAD4(100T) appears to be capable of activating the expression of WG target genes. These results imply that SMAD4(100T) may induce tumor formation by a fundamentally different mechanism from other SMAD mutations, perhaps via the ectopic expression of WNT target genes - an oncogenic mechanism associated with mutations in Adenomatous Polyposis Coli. Our results are likely to have clinical implications, because gain-of-function mutations may cause tumors when heterozygous, and the life expectancy of individuals with SMAD4(100T) is likely to be different from those with other SMAD mutations. From a larger perspective, our study shows that the genetic characterization of missense mutations, particularly in modular proteins, requires experimental verification.     

A DNA fragment containing the groE genes can suppress mutations in the Escherichia coli dnaA gene

Summary An 8.2 kb fragment of E. coli chromosomal DNA, when cloned in increased copy number, suppresses the dnaA46 mutation, and an abundant protein of about 68 kd (60 kd when measured by us), encoded by the fragment, is essential for the suppression (Takeda and Hirota 1982). Mapping experiments show that the fragment originates from the 94 min region of the chromosome. It encodes several proteins but only one abundant polypeptide of the correct size, the product of the groEL gene. Suppression by the fragment is allele specific; those mutations which map to the centre of the gene are suppressed. Other initiation mutants including dnaA203, dnaA204, dnaA508, dnaAam, dnaC, dnaP and dnaB252 are not suppressed. Most suppressed strains are cold-sensitive suggesting an interaction between the mutant proteins (or their genes) and the suppressing protein or proteins.     

Selection intensity against deleterious mutations in RNA secondary structures and rate of compensatory nucleotide substitutions

A two-locus model of reversible mutations with compensatory fitness interactions is presented; single mutations are assumed to be deleterious but neutral in appropriate combinations. The expectation of the time of compensatory nucleotide substitutions is calculated analytically for the case of tight linkage between sites. It is shown that selection increases the substitution time dramatically when selection intensity Ns > 1, where N is the diploid population size and s the selection coefficient. Computer simulations demonstrate that recombination increases the substitution time, but the effect of recombination is small when selection is weak. The amount of linkage disequilibrium generated in the process of compensatory substitution is also investigated. It is shown that significant linkage disequilibrium is expected to be rare in natural populations. The model is applied to the mRNA secondary structure of the bicoid 3' untranslated region of Drosophila. It is concluded that average selection intensity Ns against single deleterious mutations is not likely to be much larger than 1.     

Mobile DNA can drive lineage extinction in prokaryotic populations

Natural selection ultimately acts on genes and other DNA sequences. Adaptations that are good for the gene can have adverse effects at higher levels of organization, including the individual or the population. Mobile genetic elements illustrate this principle well, because they can self‐replicate within a genome at a cost to their host. As they are costly and can be transmitted horizontally, mobile elements can be seen as genomic parasites. It has been suggested that mobile elements may cause the extinction of their host populations. In organisms with very large populations, such as most bacteria, individual selection is highly effective in purging genomes of deleterious elements, suggesting that extinction is unlikely. Here we investigate the conditions under which mobile DNA can drive bacterial lineages to extinction. We use a range of epidemiological and ecological models to show that harmful mobile DNA can invade, and drive populations to extinction, provided their transmission rate is high and that mobile element‐induced mortality is not too high. Population extinction becomes more likely when there are more elements in the population. Even if elements are costly, extinction can still occur because of the combined effect of horizontal gene transfer, a mortality induced by mobile elements. Our study highlights the potential of mobile DNA to be selected at the population level, as well as at the individual level.     

Aquatic polymers can drive pathogen transmission in coastal ecosystems

Gelatinous polymers including extracellular polymeric substances (EPSs) are fundamental to biophysical processes in aquatic habitats, including mediating aggregation processes and functioning as the matrix of biofilms. Yet insight into the impact of these sticky molecules on the environmental transmission of pathogens in the ocean is limited. We used the zoonotic parasite Toxoplasma gondii as a model to evaluate polymer-mediated mechanisms that promote transmission of terrestrially derived pathogens to marine fauna and humans. We show that transparent exopolymer particles, a particulate form of EPS, enhance T. gondii association with marine aggregates, material consumed by organisms otherwise unable to access micrometre-sized particles. Adhesion to EPS biofilms on macroalgae also captures T. gondii from the water, enabling uptake of pathogens by invertebrates that feed on kelp surfaces. We demonstrate the acquisition, concentration and retention of T. gondii by kelp-grazing snails, which can transmit T. gondii to threatened California sea otters. Results highlight novel mechanisms whereby aquatic polymers facilitate incorporation of pathogens into food webs via association with particle aggregates and biofilms. Identifying the critical role of invisible polymers in transmission of pathogens in the ocean represents a fundamental advance in understanding and mitigating the health impacts of coastal habitat pollution with contaminated runoff.     

The genes underlying the process of speciation

The long-standing goal of finding genes causing reproductive isolation is being achieved. To better link the genetics with the process of speciation, we propose that 'speciation gene' be defined as any gene contributing to the evolution of reproductive isolation. Characterizing a speciation gene involves establishing that the gene affects a component of reproductive isolation; demonstrating that divergence at the locus occurred before completion of speciation; and quantifying the effect size of the gene (i.e. the increase in total reproductive isolation caused by its divergence). Review of a sample of candidate speciation genes found that few meet these criteria. Improved characterization of speciation genes will clarify how numerous they are, their properties and how they affect genome-wide patterns of divergence.