We present the complete nucleotide and deduced amino acid sequence for the gene encoding Drosophila sn-glycerol-3-phosphate dehydrogenase. A transcription unit of 5kb was identified which is composed of eight protein encoding exons. Three classes of transcripts were shown to differ only in the 3'-end and to code for three protein isoforms each with a different C-terminal amino acid sequence. Each transcript is shown to arise through the differential expression of three isotype-specific exons at the 3'-end of the gene by a developmentally regulated process of 3'-end formation and alternate splicing pathways of the pre-mRNA. In contrast, the 5'-end of the gene is simple in structure and each mRNA is transcribed from the same promoter sequence. A comparison of the organization of the Drosophila and murine genes and the primary amino acid sequence between a total of four species indicates that the GPDH gene-enzyme system is highly conserved and is evolving slowly.
A 26-kilobase-pair region encompassing the sn-glycerol-3-phosphate dehydrogenase (sn-glycerol-3-phosphate:NAD+ 2-oxidoreductase, EC 1.1.1.8) locus in Drosophila melanogaster from two natural populations in Japan was surveyed by restriction mapping. Both tandem duplications and triplications in this region were found in both populations.
Using the 602 second chromosome lines extracted from the Ishigakijima population of Drosophila melanogaster in Japan, partial diallel cross experiments (Design II of Comstock & Robinson, 1952) were carried out, and the additive genetic variance and the dominance variance of viability were estimated. The estimated value of the additive genetic variance is 001754 + 000608, and the dominance variance 000151 ±000114, using a logarithmic scale. Since the value of the additive genetic variance is much larger than expected under mutation-selection balance although the dominance variance is compatible with it, we speculate that in the Ishigakijima population some type of balancing selection must be operating to maintain the genetic variability with respect to viability at a minority of loci. As candidates for such selection, overdominance, frequency-dependent selection, and diversifying selection are considered, and it is suggested that diversifying selection is the most probable candidate for increasing the additive genetic variance.
The lethal and detrimental loads per second chromosome rapidly increased from 1968 to 1970 in a local population of Drosophila melanogaster in Japan (lethal load, from about 0.16 to 0.38; detrimental load, from 0.125 to 0.231 [Watanabe, T. K., Watanabe, T. & Oshima, C. (1976) Evolution 30,[109][110][111][112][113][114][115][116][117][118]). When the homozygous loads were measured in 1983, the lethal load had decreased to approximately the original amount (0.19) but the detrimental load had stayed high (0.241). The rise and fall of the lethal load can be accounted for by a P-type element that invaded a population with M cytotype, producing a high mutation rate. The mutation rate fell back to the earlier value after the cytotype became P. That the detrimental load did not decrease can be explained by assuming a longer persistence for detrimental mutations in the population. Evidence for a P-type mutator factor is that the mutation rate of the wild-type chromosomes differs between the different cytoplasmic and chromosomal backgrounds, being lower in the background from which the chromosomes were taken.Since the P element was detected in Drosophila melanogaster (1, 2) the studies on this factor have advanced a great deal, and now it is clear that this element and its derivatives are ubiquitous. Two hypotheses have been proposed to explain the relationship between strain distribution and laboratory age of the P factors or, more generally, of transposons-i.e., the rapid-invasion hypothesis (3)(4)(5) and the recent-loss (or stochastic-loss) hypothesis (6). The former assumes that the invasion of the P elements into natural populations occurred recently and their frequencies rapidly increased. Thus, the frequency of the P element-carrying strains is lower in the old laboratory strains than in the recently established ones. The latter hypothesis assumes the reverse order, namely, the natural populations had been invaded by the P elements or transposons and they became ubiquitous many years ago, and the lower fraction of the P element-carrying old laboratory strains is caused by the stochastic loss due to small population sizes in the laboratory after their establishment.The P type transposable elements cause the induction of mutations in the M type cytoplasm as a component of the syndrome of hybrid dysgenesis (7,8). To investigate the presence of P type elements in a local population of D. melanogaster that had been investigated over a 10-year period by C. Oshima and his associates (9), we have estimated inbreeding depression per second chromosome in both the M type (foreign) and P type (native) cytoplasms. Com (0) virgin females and the remainder were individually crossed with C160(K). In addition, 175 isofemale lines were established by using females captured at the same time. From each isofemale line, two males were chosen at random and one of them was crossed with C160 (0) Estimation of Viability. The Cy method of Wallace (10) was employed. Homozygous and heterozygous viabilities were estimated by the cros...
For the elucidation of the phylogenetic position of insectivora in eutheria, we have sequenced the cytochrome c oxidase subunit II (COII) gene of mitochondria for three insectivoran species [musk screw (Suncus murinus), shrew mole (Urotrichus talpoides), Japanese mole (Mogera wogura)] and analyzed these amino acid sequences with neighbor-joining (NJ) method and maximum likelihood (ML) method. NJ analysis shows polyphyly of Insectivora and Chiroptera. Assuming that each of Primates, Ferungulata, Chiroptera, Insectivora and Rodentia is a monophyletic group, ML analysis suggests that Chiroptera is a sister group of Insectivora and that Ferungulata is the closest outgroup to the (Insectivora and Chiroptera) clade.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.