We analyzed the geographic distribution of the Ixodes ricinus-like ticks in eastern North America by comparing the mitochondrial 16S rDNA sequences of specimens sampled directly from the field during the 1990s. Two distinct lineages are evident. The southern clade includes ticks from the southeastern and middle-eastern regions of the United States. The range of the northern clade, which appears to have been restricted to the northeastern region until the mid-1900s, now extends throughout the northeastern and middle-eastern regions. These phyletic units correspond to northern and southern taxa that have previously been assigned specific status as Ixodes dammini and Ixodes scapularis, respectively. The expanding range of I. dammini appears to drive the present outbreaks of zoonotic disease in eastern North America that include Lyme disease and human babesiosis.
We describe a system of hybrid dysgenesis in Drosophila virilis in which at least four unrelated transposable elements are all mobilized following a dysgenic cross. The data are largely consistent with the superposition of at least three different systems of hybrid dysgenesis, each repressing a different transposable element, which break down following the hybrid cross, possibly because they share a common pathway in the host. The data are also consistent with a mechanism in which mobilization of a single element triggers that of others, perhaps through chromosome breakage. The mobilization of multiple, unrelated elements in hybrid dysgenesis is reminiscent of McClintock's evidence [McClintock, B. (1955) Brookhaven Symp. Biol. 8, 58-74] for simultaneous mobilization of different transposable elements in maize.
Transposable elements are a major source of genetic change, including the creation of novel genes, the alteration of gene expression in development, and the genesis of major genomic rearrangements. They are ubiquitous among contemporary organisms and probably as old as life itself. The long coexistence of transposable elements in the genome would be expected to be accompanied by host-element coevolution. Indeed, the important role of host factors in the regulation of transposable elements has been illuminated by recent studies of several systems in Drosophila. These include host factors that regulate the P element, a host mutation that renders the genome permissive for gypsy mobilization and infection, and newly induced mutations that affect the expression of transposon insertion mutations. The finding of a type of hybrid dysgenesis in D. virilis, in which multiple unrelated transposable elements are mobilized simultaneously, may also be relevant to host-factor regulation of transposition.
The baseline rate of spontaneous integration of the autonomous mariner element Mos1 into the germline of Drosophila melanogaster is estimated as 16 +/- 5% (mean +/- SE) among fertile G0 flies. However, the transformation rate is reduced approximately 20-fold in Mos1 constructs with exogenous DNA in the size range 5-12 kb inserted into the SacI site. To provide alternative Mos1 helper plasmids for transformation experiments, two types of Mos1-promoter fusions were constructed: hsp-70:Mos1 and hsp26-Sgs3:Mos1. The former has the Mos1 coding region driven by the hsp70 heat-shock promoter; the latter has it driven by the basal Sgs3 promoter under the control of the hsp26 female-germline specific transcriptional regulator. When introduced into D. melanogaster by P-element-mediated germline transformation, these elements are unable to transpose or excise in the presence of autonomous Mos1-related elements (they are "marooned") because the 5' inverted repeat of Mos1 is missing. As expected, the hsp26-Sgs3:Mos1 fusions exhibit a significantly greater rate of germline excision of a target mariner element than do the hsp70:Mos1 fusions. Unexpectedly, the rate of excision of target mariner elements induced by hsp26-Sgs3:Mos1 is the same in the male germline as in the female germline. Both hsp:Mos1 fusions show strong germline expression and a maternal effect of the mariner transposase. A significant grand-maternal effect of the hsp:Mos1 fusions was also detected as a result of a maternal effect on the germline of the F1 progeny. Among flies carrying the promoter fusions inherited maternally, about three-quarters of the overall rate of germline excision derives from the direct genotypic effect and about one-quarter results from the grand-maternal effect. Despite the strong somatic expression of the hsp:Mos1 fusions, mariner transformants carrying a white+ reporter gene at the SacI site remained stable in the soma.
Horizontal transmission has been well documented as a major mechanism for the dissemination of mariner-like elements (MLEs) among species. Less well understood are mechanisms that limit vertical transmission of MLEs resulting in the "spotty" or discontinuous distribution observed in closely related species. In this article we present evidence that the genome of the common ancestor of the melanogaster species subgroup of Drosophila contained an MLE related to the mellifera (honey bee) subfamily. Horizontal transmission, approximately 3-10 MYA, is strongly suggested by the observation that the sequence of the MLE in Drosophila erecta is 97% identical in nucleotide sequence with that of an MLE in the cat flea, Ctenocephalides felis. The D. erecta MLE has a spotty distribution among species in the melanogaster subgroup. The element has a high copy number in D. erecta and D. orena, a moderate copy number in D. teissieri and D. yakuba, and was apparently lost ("stochastic loss") in the lineage leading to D. melanogaster, D. simulans, D. mauritiana, and D. sechellia. In D. erecta, most copies are concentrated in the heterochromatin. Two copies from D. erecta, denoted De12 and De19, were cloned and sequenced, and they appear to be nonfunctional ("vertical inactivation"). It therefore appears that the predominant mode of MLE evolution is vertical inactivation and stochastic loss balanced against occasional reinvasion of lineages by horizontal transmission.
The vast diversity in spectral sensitivities in the vision of many organisms is mediated mostly (although not entirely) through variation in the photosensitive visual pigments (opsins) of the eye. Specifically, shifts in absorption maxima of visual pigments are thought to be a result of interactions within the binding pocket of the opsin, between amino acid side chains and the retinal chromophore, However, it has proven difficult to identify specific amino acid residues important in determining wavelength absorption maxima, especially for some of the short wavelength (blue) opsins. In this paper, a comparative phylogenetic approach was applied to opsin protein sequence data to identify residues important in opsin wavelength regulation. In essence, this approach consisted of interpreting evolutionary history as a series of experiments in which natural selection has repeatedly favored amino acid replacements of certain residues to shift the opsin absorption spectra to either shorter or longer wavelengths. Opsin protein sequences were obtained from GenBank, aligned, and used to reconstruct a phylogenetic tree. Amino acid replacements were traced along the branches of this opsin tree, focusing only on residues likely to reside within the chromophore-binding pocket. A number of functionally convergent, nonconservative amino acid replacements in independently evolved opsins with similar shifts in spectral properties were identified. In short, reconstruction of the phylogeny of the opsin molecule allowed us to track amino acid substitutions in specific sites within the opsin and to target those particular substitutions that are repeatedly associated with marked changes in peak absorbance, shifting the spectral sensitivity of the opsin toward shorter or longer wavelengths. Based on these results, we propose a model for blue shifts of opsin absorption spectra. Amino acid replacements of four polar and charged residues near the protonated Schiff base (SBH+) end of the chromophore are proposed to result in blue shifts of the opsin absorption spectra. This model may explain some of the diversity of blue opsins apparent in both vertebrates and invertebrates.