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cDNA sequence of a human skeletal muscle ADP/ATP translocator: lack of a leader peptide, divergence from a fibroblast translocator cDNA, and coevolution with mitochondrial DNA genes.

We have characterized a 1400-nucleotide cDNA for the human skeletal muscle ADP/ATP translocator. The deduced amino acid sequence is 94% homologous to the beef heart ADP/ATP translocator protein and contains only a single additional amino-terminal methionine. This implies that the human translocator lacks an amino-terminal targeting peptide, a conclusion substantiated by measuring the molecular weight of the protein synthesized in vitro. A 1400-nucleotide transcript encoding the skeletal muscle translocator was detected on blots of total RNA from human heart, kidney, skeletal muscle, and HeLa cells by hybridization with oligonucleotide probes homologous to the coding region and 3' noncoding region of the cDNA. However, the level of this mRNA varied substantially among tissues. Comparison of our skeletal muscle translocator sequence with that of a recently published human fibroblast translocator cognate revealed that the two proteins are 88% identical and diverged about 275 million years ago. Hence, tissues vary both in the level of expression of individual translocator genes and in differential expression of cognate translocator genes. Comparison of the base substitution rates of the ADP/ATP translocator and the oxidative phosphorylation genes encoded by mitochondrial DNA revealed that the mitochondrial DNA genes fix 10 times more synonymous substitutions and 12 times more replacement substitutions; yet, these nuclear and cytoplasmic respiration genes experience comparable evolutionary constraints. This suggests that the mitochondrial DNA genes are highly prone to deleterious mutations.

Base Sequence↗

Coevolution of host and pathogen populations in the Hordeum vulgare-Rhynchosporium secalis pathosystem.

Isolates of Rhynchosporium secalis collected from two experimental barley populations were scored for putative isozyme, colony color, and virulence loci. Allelic frequencies, multilocus haplotype frequencies, and multilocus genetic structure differed in the two populations of R. secalis; haplotypes also differed widely from each other in virulence. The average virulence of isolates collected from the more resistant host population was greater than the average virulence of the isolates collected from the less resistant host population; also the least virulent haplotype, which made up 19% of the pathogen population collected from the less resistant host population, accounted for only 0.3% of the isolates collected from the more resistant host population. It was concluded that the genetic systems of the barley host and fungal pathogen interacted in a complementary fashion and that the genetic structures of both the host and pathogen populations were shaped by coevolutionary processes featuring interactions among loci affecting many different traits, including interactions among host resistance genes and pathogen virulence genes.

Biological Evolution↗

Gene-culture coevolution: toward a general theory of vertical transmission.

A general formulation of cultural and genetic transmission is developed. The cultural transmission is vertical and the genetics may involve multiple loci. Each individual is represented by a phenogenotype, and conditions are given under which the evolutionary dynamics of phenogenotype frequencies are reducible to phenogametic or phenoallelic frequencies. The interaction between genes and culture is specified by an association measure, and results on the order of magnitude of this association at equilibrium are presented.

Biological Evolution↗

Coevolution of persistently infecting small DNA viruses and their hosts linked to host-interactive regulatory domains.

Although most RNA viral genomes (and related cellular retroposons) can evolve at rates a millionfold greater than that of their host genomes, some of the small DNA viruses (polyomaviruses and papillomaviruses) appear to evolve at much slower rates. These DNA viruses generally cause host species-specific inapparent primary infections followed by life-long, benign persistent infections. Using global progressive sequence alignments for kidney-specific Polyomaviridae (mouse, hamster, primate, human), we have constructed parsimonious evolutionary trees for the viral capsid proteins (VP1, VP2/VP3) and the large tumor (T) antigen. We show that these three coding sequences can yield phylogenetic trees similar to each other and to that of their host species. Such virus-host "co-speciation" appears incongruent with some prevailing views of viral evolution, and we suggest that inapparent persistent infections may link virus and most host evolution. Similarity analysis identified three specific regions of polyoma regulatory gene products (T antigens) as highly conserved, and two of these regions correspond to binding sites for host regulatory proteins (p53, the retinoblastoma gene product p105, and the related protein p107). The p53 site overlaps with a conserved ATPase domain and the retinoblastoma site corresponds to conserved region 1 of E1A protein of adenovirus type 5. We examined the local conservation of these binding sequences and show that the conserved retinoblastoma binding domain is characteristic and inclusive of the entire polyomavirus family, but the conserved p53-like binding domain is characteristic and inclusive of three entire families of small DNA viruses: polyomaviruses, papillomaviruses, and parvoviruses. The evolution of small-DNA-virus families may thus be tightly linked to host evolution and speciation by interaction with a subset of host regulatory proteins.

Amino Acid Sequence↗

Monophyletic origin of beta-division proteobacterial endosymbionts and their coevolution with insect trypanosomatid protozoa Blastocrithidia culicis and Crithidia spp.

Some trypanosomatid protozoa (order Kinetoplastida) are well known to harbor bacterial endosymbionts. Their phylogenetic positions and evolutionary relationships with the hosts were deduced by comparing the rRNA gene sequences. Earlier, we observed that these symbionts from three Crithidia spp. are identical and are closely related to Bordetella bronchiseptica. We have now sequenced the genes of another endosymbiont and the host protozoan Blastocrithidia culicis. The 16S rRNA genes of the Blastocrithidia and Crithidia symbionts share approximately 97% identity and form a distinct group, branching off the B. bronchiseptica lineage in the beta-division of Proteobacteria. Comparison of their secondary structures in the stem regions suggests compensatory mutations of the symbiont sequences, contributing to their biased base transitions from G to A and C to T. Two putative genes encoding tRNA(Ile) and tRNA(Ala) are highly conserved in the otherwise variable internal transcribed spacer region. Comparisons of the host rRNA gene sequences suggest that the symbiont-containing Crithidia and Blastocrithidia are more akin to each other than to other trypanosomatids. The evidence suggests that Blastocrithidia and Crithidia symbionts descend from a common ancestor, which had presumably entered an ancestral host and thence coevolved with it into different species. We therefore propose naming the symbionts Kinetoplastibacterium blastocrithidii and Kinetoplastibacterium crithidii.

Animals↗

Ninety-seven million years of angiosperm-insect association: paleobiological insights into the meaning of coevolution.

From well preserved leaf damage of the mid-Cretaceous Dakota Flora (97 million years ago), three distinctive, insect-mediated feeding traces have been identified and assigned to two extant genera and one subfamily. These taxa are the leaf miners Stigmella and Ectoedemia of the Nepticulidae and Phyllocnistinae of the Gracillariidae. These fossils indicate that within 25 million years of early angiosperm radiation, the organs of woody dicots already were exploited in intricate and modern ways by insect herbivores. For Ectoedemia and its platanoid host, we document 97 million years of continuity for a plant-insect interaction. The early occurrence during the mid-Cretaceous of diverse and extensive herbivory on woody angiosperms may be associated with the innovation of deciduousness, in which a broadleafed angiosperm provided an efficient, but disposable, photosynthetic organ that with-stood the increased cost of additional insect herbivory. Moreover, the group represented in this study, the leaf-mining Lepidoptera, exhibits a wide range of subordinal taxonomic differentiation and includes the Gracillariidae, a member of the most derived lepidopteran suborder, the Ditrysia. Ditrysian presence during the mid-Cretaceous, in addition to lepidopteran body-fossil evidence from Early Cretaceous and Late Jurassic deposits, suggests that the radiation of major lepidopteran lineages probably occurred during the Late Jurassic on a gymnosperm-dominated flora.

Journal Article↗

Molecular coevolution of mammalian ribosomal gene terminator sequences and the transcription termination factor TTF-I.

Both the DNA elements and the nuclear factors that direct termination of ribosomal gene transcription exhibit species-specific differences. Even between mammals--e.g., human and mouse--the termination signals are not identical and the respective transcription termination factors (TTFs) which bind to the terminator sequence are not fully interchangeable. To elucidate the molecular basis for this species-specificity, we have cloned TTF-I from human and mouse cells and compared their structural and functional properties. Recombinant TTF-I exhibits species-specific DNA binding and terminates transcription both in cell-free transcription assays and in transfection experiments. Chimeric constructs of mouse TTF-I and human TTF-I reveal that the major determinant for species-specific DNA binding resides within the C terminus of TTF-I. Replacing 31 C-terminal amino acids of mouse TTF-I with the homologous human sequences relaxes the DNA-binding specificity and, as a consequence, allows the chimeric factor to bind the human terminator sequence and to specifically stop rDNA transcription.

Amino Acid Sequence↗

Specificity in cholesterol regulation of gene expression by coevolution of sterol regulatory DNA element and its binding protein.

When demand for cholesterol rises in mammalian cells, the sterol regulatory element (SRE) binding proteins (SREBPs) are released from their membrane anchor through proteolysis. Then, the N-terminal region enters the nucleus and activates genes of cholesterol uptake and biosynthesis. Basic helix-loop-helix (bHLH) proteins such as SREBPs bind to a palindromic DNA sequence called the E-box (5'-CANNTG-3'). However, SREBPs are special because they also bind direct repeat elements called SREs. Importantly, sterol regulation of all promoters studied thus far is mediated by SREBP binding only to SREs. To study the reason for this we converted the direct repeat SRE from the sterol-regulated low-density lipoprotein receptor promoter into an E-box. In this report we show that SREBPs are still able to bind and activate this promoter however, sterol regulation is lost. The results are consistent with the mutant promoter being a target for promiscuous activation by constitutively expressed E-box binding bHLH proteins that are not regulated by cholesterol. Kim and coworkers [Kim, J. B., Spotts, G. D., Halvorsen, Y.-D., Shih, H.-M., Ellenberger, T., Towle, H. C. & Spiegelman, B. M. (1995) Mol. Cell. Biol. 15, 2582-2588] demonstrated that the dual DNA binding specificity of SREBPs is caused by a specific tyrosine in the conserved basic region of the DNA binding domain that corresponds to an arginine in all other bHLH proteins that recognize only E-boxes. Taken together the data suggest an evolutionary mechanism where a DNA binding protein along with its recognition site have coevolved to ensure maximal specificity and sensitivity in a crucial nutritional regulatory response.

Animals↗

Experimental removal of sexual selection reverses intersexual antagonistic coevolution and removes a reproductive load.

Although sexual selection can provide benefits to both sexes, it also can be costly because of expanded opportunities for intersexual conflict. We evaluated the role of sexual selection in a naturally promiscuous species, Drosophila melanogaster. In two replicate populations, sexual selection was removed through enforced monogamous mating with random mate assignment or retained in promiscuous controls. Monogamous mating constrains the reproductive success of mates to be identical, thereby converting prior conflicts between mates into opportunities for mutualism. Random mate assignment removes the opportunity for females to choose beneficial qualities in their mate. The mating treatments were maintained for 47 generations, and evolution was allowed to proceed naturally within the parameters of the design. In the monogamous populations, males evolved to be less harmful to their mates, and females evolved to be less resistant to male-induced harm. The monogamous populations also evolved a greater net reproductive rate than their promiscuous controls. These results indicate a potentially widespread cost of sexual selection caused by conflicts inherent to promiscuity.

Animals↗

Identification of amino acid residues that direct differential ligand selectivity of mammalian and nonmammalian V1a type receptors for arginine vasopressin and vasotocin. Insights into molecular coevolution of V1a type receptors and their ligands.

Arginine vasotocin (VT) is the ortholog in all nonmammalian vertebrates of arginine vasopressin (AVP) in mammals. We have previously cloned an amphibian V1atype vasotocin receptor (VT1R) that exhibited higher sensitivity for VT than AVP, while the mammalian V1a type receptor (V1aR) responded better to AVP than VT. In the present study, we identified the amino acid residues that confer differential ligand selectivity for AVP and VT between rat V1aR and bullfrog VT1R (bfVT1R). A chimeric rat V1aR having transmembrane domain (TMD) VI to the carboxyl-terminal tail (C-tail) of bfVT1R showed a reverse ligand preference for AVP and VT, whereas a chimeric VT1R with TMD VI to the C-tail of rat V1aR showed a great increase in sensitivity for AVP. A single mutation (Ile(315(6.53)) to Thr) in TMD VI of V1aR increased the sensitivity for VT, while a single mutation (Phe(313(6.51)) to Tyr or Pro(334(7.33)) to Thr) reduced sensitivity toward AVP. Interestingly the triple mutation (Phe(313(6.51)) to Tyr, Ile(6.53) to Thr, and Pro(7.33) to Thr) of V1aR increased sensitivity to VT but greatly reduced sensitivity to AVP, behaving like bfVT1R. Further, like V1aR, a double mutant (Tyr(306(6.51)) to Phe and Thr(327(7.33)) to Pro) of bfVT1R showed an increased sensitivity to AVP. These results suggest that Phe/Tyr(6.51), Ile/Thr(6.53), and Pro/Thr(7.33) are responsible for the differential ligand selectivity between rat V1aR and bfVT1R. This information regarding the molecular interaction of VT/AVP with their receptors may have important implications for the development of novel AVP analogs.

Amino Acid Sequence↗

Seabird and louse coevolution: complex histories revealed by 12S rRNA sequences and reconciliation analyses.

We investigated the coevolutionary history of seabirds (orders Procellariiformes and Sphenisciformes) and their lice (order Phthiraptera). Independent trees were produced for the seabirds (tree derived from 12S ribosomal RNA, isoenzyme, and behavioral data) and their lice (trees derived from 12S rRNA data). Brook's parsimony analysis (BPA) supported a general history of cospeciation (consistency index = 0.84, retention index = 0.81). We inferred that the homoplasy in the BPA was caused by one intrahost speciation, one potential host-switching, and eight or nine sorting events. Using reconciliation analysis, we quantified the cost of fitting the louse tree onto the seabird tree. The reconciled trees postulated one host-switching, nine cospeciation, three or four intrahost speciation, and 11 to 14 sorting events. The number of cospeciation events was significantly more than would be expected from chance alone (P < 0.01). The sequence data were used to test for rate heterogeneity for both seabirds and lice. Neither data set displayed significant rate heterogeneity. An examination of the codivergent nodes revealed that seabirds and lice have cospeciated synchronously and that lice have evolved at approximately 5.5 times the rate of seabirds. The degree of sequence divergence supported some of the postulated intrahost speciation events (e.g., Halipeurus predated the evolution of their present hosts). The sequence data also supported some of the postulated host-switching events. These results demonstrate the value of sequence data and reconciliation analyses in unraveling complex histories between hosts and their parasites.

Animals↗

Interspecific Competition, Environmental Gradients, Gene Flow, and the Coevolution of Species' Borders.

Darwin viewed species range limits as chiefly determined by an interplay between the abiotic environment and interspecific interactions. Haldane argued that species' ranges could be set intraspecifically when gene flow from a species' populous center overwhelms local adaptation at the periphery. Recently, Kirkpatrick and Barton have modeled Haldane's process with a quantitative genetic model that combines density-dependent local population growth with dispersal and gene flow across a linear environmental gradient in optimum phenotype. To address Darwin's ideas, we have extended the Kirkpatrick and Barton model to include interspecific competition and the frequency-dependent selection that it generates, as well as stabilizing selection on a quantitative character. Our model includes local population growth, movements over space, natural selection, and gene flow. It simultaneously addresses the evolution of character displacement and species borders. It reproduces the Kirkpatrick and Barton single-species result that limited ranges can be produced with sufficiently steep environmental gradients and strong dispersal. Further, in the absence of environmental gradients or barriers to dispersal, interspecific competition will not limit species ranges at evolutionary equilibrium. However, interspecific competition can interact with environmental gradients and gene flow to generate limited ranges with much less extreme gradient and dispersal parameters than in the single-species case. Species display character displacement in sympatry, yet the reduction in competition that results from this displacement does not necessarily allow the two species to become sympatric everywhere. When species meet, competition reduces population densities in the region of overlap, which, in turn, intensifies the asymmetry in gene flow from center to margin. This reduces the ability of each species to adapt to local physical conditions at their range limits. If environmental gradients are monotonic but not linear, the transition zone between species at coevolutionary equilibrium occurs where the environmental gradient is steepest. If productivity gradients are also introduced into the model, then patterns similar to Rapoport's rule emerge. Interacting species respond to climate change, as it affects the optimal phenotype over space, by a combination of range shifts and local evolution in mean phenotype, while solitary species respond solely by range shifts. Finally, we compare empirical estimates for intrinsic growth rates and diffusion coefficients for several species to those needed by the single-species model to produce a stable limited range. These empirical values are generally insufficient to produce limited ranges in the model suggesting a role for interspecific interactions.

Journal Article↗

Coevolution of the major histocompatibility complex and the t-complex in the mouse. I. Generation and maintenance of high complementarity associations.

A quantitative model is developed to explore the effects of prezygotic and postzygotic incompatibility on the origin and maintenance of associations between the major histocompatibility complex (MHC) and the t-complex in the mouse. Incompatibility is represented by a reduction in the rate of conception or gestation of offspring derived from sperm bearing MHC antigens in common with the mother. Incompatibility encourages the evolution of associations from a state of complete independence between the two complexes by promoting the invasion of all novel antigens, including those that exhibit associations with the t-complex. Incompatibility can modify the relative numbers of antigens associated with each haplotype by actively promoting the exclusion or invasion of recombinants that bear formerly +-specific or t-specific antigens on the alternative haplotype. The results of the analysis indicate that the state of complete independence between the MHC and the t-complex is not preserved over evolutionary time in the presence of incompatibility. Further, the expression of incompatibility maintains fully associated states that include a single antigen associated with the t-haplotype and up to three to five antigens associated with the +-haplotype within a single population.

Animals↗

Coevolution of the major histocompatibility complex and the t-complex in the mouse. II. Modification of response to sharing of histocompatibility antigens.

Selective pressures imposed by high complementarity associations between the major histocompatibility complex (MHC) and the t-complex on a locus that modifies the expression of prezygotic and postzygotic incompatibility are investigated through the analysis of a quantitative model. Sharing of MHC antigens between mates or between mother and offspring elicits weak inhibition of conception or gestation. In the presence of high complementarity associations between the MHC and the t-complex, weak incompatibility depresses the mean fitness of the population. Nevertheless, natural selection favors the enhancement of the expression of incompatibility if the number of antigens associated with the +-haplotype exceeds the number associated with the t-haplotype by a sufficient margin. Under absolute linkage between the modifier locus and the t-complex, the number associated with the +-haplotype need only be greater than the number associated with the t-haplotype. In the absence of linkage, a twofold difference is sufficient to ensure the initial increase of modifier alleles that intensify the expression of incompatibility.

Alleles↗

Evidence for redundancy but not trans factor-cis element coevolution in the regulation of Drosophila Yp genes.

In Drosophila melanogaster and the endemic Hawaiian species D. grimshawi three Yolk protein (Yp) genes are expressed in a similar sex- and tissue-specific pattern. In contrast, DNA sequence comparisons of promoter/enhancer regions show low levels of similarity. We tested the functional significance of these observations by transforming D. melanogaster with the genomic region that includes the divergently transcribed D. grimshawi DgYp1 and DgYp2 genes; we found that the introduced genes were expressed in female fat body and in ovaries but not in males. Moreover, we found D. grimshawi proteins in the hemolymph and accumulating in ovaries. Using reporter constructs we showed that the intergenic region from D. grimshawi was sufficient to drive accurate expression, but some low level of ectopic expression was seen in males. Transforming D. melanogaster with constructs bearing deletions within the D. grimshawi intergenic region revealed only subtle effects in the overall level of expression, suggesting a high level of redundancy. Testing mutants in the sex-specific regulator doublesex revealed that it is capable of repressing the DgYp genes in males. Together, these data show that D. melanogaster trans-acting factors can regulate the in vivo pattern of DgYp expression and support the notion of a redundant and complex system of cis-acting elements.

Animals↗

Coevolution of the telomeric retrotransposons across Drosophila species.

As in other eukaryotes, telomeres in Drosophila melanogaster are composed of long arrays of repeated DNA sequences. Remarkably, in D. melanogaster these repeats are produced, not by telomerase, but by successive transpositions of two telomere-specific retrotransposons, HeT-A and TART. These are the only transposable elements known to be completely dedicated to a role in chromosomes, a finding that provides an opportunity for investigating questions about the evolution of telomeres, telomerase, and the transposable elements themselves. Recent studies of D. yakuba revealed the presence of HeT-A elements with precisely the same unusual characteristics as HeT-A(mel) although they had only 55% nucleotide sequence identity. We now report that the second element, TART, is also a telomere component in D. yakuba; thus, these two elements have been evolving together since before the separation of the melanogaster and yakuba species complexes. Like HeT-A(yak), TART(yak) is undergoing concerted sequence evolution, yet they retain the unusual features TART(mel) shares with HeT-A(mel). There are at least two subfamilies of TART(yak) with significantly different sequence and expression. Surprisingly, one subfamily of TART(yak) has >95% sequence identity with a subfamily of TART(mel) and shows similar transcription patterns. As in D. melanogaster, other retrotransposons are excluded from the D. yakuba terminal arrays studied to date.

Animals↗

Coevolution of the S-locus genes SRK, SLG and SP11/SCR in Brassica oleracea and B. rapa.

Brassica self-incompatibility (SI) is controlled by SLG and SRK expressed in the stigma and by SP11/SCR expressed in the anther. We determined the sequences of the S domains of 36 SRK alleles, 13 SLG alleles, and 14 SP11 alleles from Brassica oleracea and B. rapa. We found three S haplotypes lacking SLG genes in B. rapa, confirming that SLG is not essential for the SI recognition system. Together with reported sequences, the nucleotide diversities per synonymous and nonsynonymous site (pi(S) and pi(N)) at the SRK, SLG, and SP11 loci within B. oleracea were computed. The ratios of pi(N):pi(S) for SP11 and the hypervariable region of SRK were significantly >1, suggesting operation of diversifying selection to maintain the diversity of these regions. In the phylogenetic trees of 12 SP11 sequences and their linked SRK alleles, the tree topology was not significantly different between SP11 and SRK, suggesting a tight linkage of male and female SI determinants during the evolutionary course of these haplotypes. Genetic exchanges between SLG and SRK seem to be frequent; three such recent exchanges were detected. The evolution of S haplotypes and the effect of gene conversion on self-incompatibility are discussed.

Amino Acid Sequence↗

Some aspects of the coevolution of virulence and resistance in contact transmission disease processes with ecological constraints.

In this paper, the author constructs a general, continuous-time dynamical model of a coevolutionary host-microparasite interaction, which incorporates host resistance (degree of susceptibility to invasion by the parasite) and parasite virulence (pathogenicity and transmission efficiency). Discrete classes of resistance type and virulence type are allowed. It is assumed that high virulence parasite strains are able to take over hosts already occupied by lower virulence strains. Heritability of host resistance is assumed, but specific assumptions about the genetics of such inheritance are avoided. Instead, a 'neutral' view is adopted, which assumes that the disease process is the sole selective force acting on a disease-free resistance distribution. This allows the dimensionality of the model to be kept lower than corresponding explicitly population-genetic models. Ecological factors are taken into account via density dependence in host encounter rate (which also influences transmission properties of the disease via contact transmission), and by density dependence in host fecundity. Two distinct host types are considered, which we call 'bunchers' and 'separators', characterized by the form of reaction of the encounter rate to changes in host density. Detailed analyses are given for versions of the model having: (a) one resistance class and one virulence class; (b) two resistance classes and one virulence class; (c) two resistance classes and two virulence classes. Sufficient conditions are found in case (c) for the low resistance type to be eliminated by the coevolutionary process. Features which might tend to promote resistance polymorphism are also discussed.

Animals↗