bluuebunny/crossref_metadata_2025_split huggingface dataset:
ON THE THEORY OF SPECIATION INDUCED BY TRANSPOSABLE ELEMENTS
Authors: Ginzburg Lev R , Bingham Paul M , Yoo Sinjae 
Published: January 2021

ABSTRACT
A simple methematical model describes the invasion of panmictic, sexually reproducing populations by a newly introduced transposon. The model places important constraints on the properties that transposons must have to successfully invade a population and describes the kinetics with which such an invasion will occur. Invasibility conditions serve as a basis for new, detailed scenarios whereby transposon-mediated depression in fitness produces reproductive isolation of populations. These scenarios, in turn, lead to several speculations concerning the role of transposons in evolution.
ON THE COMPONENTS OF SEGREGATION DISTORTION IN DROSOPHILA MELANOGASTER. III. NATURE OF ENHANCER OF SD
Authors: Brittnacher John G , Ganetzky Barry 
Published: January 2021

ABSTRACT
Analysis of X-ray-induced deletions in the Segregation Distorter (SD) chromosome, SD-5, revealed that this chromosome had a gene proximal to lt in the centric heterochromatin of 2L that strongly enhanced the meiotic drive caused by the SD chromosome. This Enhancer of Segregation Distortion [E(SD)] locus had not been characterized in earlier studies of SD chromosomes because it cannot be readily separated by recombination from the Responder (Rsp) locus in the proximal heterochromatin of 2R.—To determine whether E(SD) is a general component of all SD chromosomes and to examine further its effects on distortion, we produced deletions of E(SD) in three additional SD chromosomes. Analysis of these deletions leads to the following conclusions: (1) along with Sd and Rsp, E(SD) is common to all SD chromosomes; (2) the E(SD) allele on each SD chromosome enhances distortion by the same amount, which indicates that allelic variation at the E(SD) locus is not responsible for the different drive strengths seen among SD chromosomes; (3) E(SD) causes very little or no distortion by itself in the absence of Sd; (4) E(SD), like Sd, acts in a dosage-dependent manner; (5) E(SD) exerts its effect in cis or trans to Sd; and (6) if E(SD) + exists, its function is not related to SD.
MEASUREMENT OF FITNESS AND ITS COMPONENTS IN SIX LABORATORY STRAINS OF DROSOPHILA MELANOGASTER
Authors: Yamazaki Tsuneyuki 
Published: January 2021

ABSTRACT
Six laboratory strains of Drosophila melanogaster were used to measure "net fitness" and its components by interspecific competition with D. hydei using 100 experimental populations. The "total competitive ability," an estimate of net fitness measured in these competition experiments, was tightly correlated with another measure of net fitness, the population size, in single-species experiments (phenotypic correlation rp = 0.675 and genotypic correlation rg = 0.997). Other components of fitness were also measured simultaneously, and the correlation with the net fitness was calculated. The very high correlation between two measurements of net fitness and lower correlations between net fitness and components of fitness suggests that these net fitness measures are more reliable estimates of the "real net fitness" than the components of fitness.
THE GENETIC STRUCTURE OF NATURAL POPULATIONS OF DROSOPHILA MELANOGASTER. XVIII. CLINAL AND UNIFORM GENETIC VARIATION OVER POPULATIONS
Authors: Kusakabe Shinichi , Mukai Terumi 
Published: January 2021

ABSTRACT
It has been reported in the previous papers of this series that in the eastern United States and Japan there is a north-to-south cline of additive genetic variance of viability and that the amount of the additive genetic variance in the northern population can be explained by mutation-selection balance. To determine whether or not the difference in the genetic variation in northern and southern populations can be explained by the differences in mutation rate and/or effective population size, numerical calculations were made using population genetic parameters. In addition, the average heterozygosities of the northern and southern populations at ten of 19 polymorphic structural loci surveyed were estimated in relation to the cline of additive genetic variance of viability, and the following findings were obtained. (1) The changes in mutation rate and population size cannot simultaneously explain the difference in additive genetic variance and inbreeding decline between the northern and southern populations. Thus, the operation of some kind of balancing selection, most likely diversifying selection, was suggested to explain the observed excess of additive genetic variance. (2) Estimates of the average heterozygosities of the southern population were not significantly different from those of the northern population. Thus, it was strongly suggested that the excess of additive genetic variance in the southern population cannot be caused by structural loci, but by factors outside the structural loci, and that protein polymorphisms are selectively neutral or nearly neutral.
RECOMBINATION AND ASSORTMENT IN THE MACRONUCLEUS OF TETRAHYMENA THERMOPHILA: A THEORETICAL STUDY BY COMPUTER SIMULATION
Authors: Doerder F P , Diblasi S L 
Published: January 2021

ABSTRACT
The compound nature of the macronucleus of Tetrahymena thermophila presents multiple opportunities for recombination between genes on the same macronuclear chromosome. Such recombinants should be detectable through their assortment at subsequent amitotic macronuclear divisions. Thus, a macronucleus that is initially AB/ab should produce recombinant assortees of the genotypes Ab/aB. Computer simulation shows that, when the recombination frequency is two or fewer times per cell cycle, recombinant assortees are produced at experimentally measurable frequencies of less than 40%. At higher recombination frequencies, linked genes appear to assort independently. The simulations also show that recombination during macronuclear development can be distinguished from recombination in subsequent cell cycles only if the first appearance of recombinant assortees is 100 or more fissions after conjugation. The use of macronuclear recombination and assortment as a means of mapping macronuclear genes is severely constrained by the large variances in assortment outcomes; with experimentally small sample sizes, such mapping is impossible.
GENETIC STUDIES OF MEMBRANE EXCITABILITY IN DROSOPHILA: LETHAL INTERACTION BETWEEN TWO TEMPERATURE-SENSITIVE PARALYTIC MUTATIONS
Authors: Ganetzky Barry 
Published: January 2021

ABSTRACT
Two mutants of Drosophila melanogaster, parats 1 (1-53.9) and napts (2-56.2) both display similar temperature-sensitive paralysis associated with blockage in the conduction of nerve action potentials, suggesting that the two gene products have a similar function. This idea is supported by the observation that the double mutant is unconditionally lethal. Genetic analysis of this synergistic interaction has revealed the following: 1) it specifically involves the para and nap loci; (2) all para alleles interact with napts, but the strength of the interaction varies in an allele-dependent fashion; (3) lethality of the double mutant occurs during the first larval instar with parats 1 but differs with other para alleles; (4) hypodosage of para + causes lethality in a napts background. These results together with previous electrophysiological, behavioral and pharmacological studies of these mutants suggest that both para and nap affect sodium channels and possibly encode different subunits.
A GENETIC AND CYTOGENETIC ANALYSIS OF THE REGION SURROUNDING THE LSP-1 β-GENE IN DROSOPHILA MELANOGASTER
Authors: Roberts David B , Brock Hugh W , Rudden Nancy C , Evans-Roberts Susan 
Published: January 2021

ABSTRACT
The region surrounding the gene coding for the β-polypeptide (21D-22C) of the major Drosophila melanogaster larval serum protein, LSP-1, has been studied in detail. Seven new γ-ray-induced deficiencies of the region have been used, together with the two extant deficiencies, to map the position of the β-gene and of the 55 newly induced ethyl methanesulfonate mutants uncovered by one of the largest deficiencies. No lethal mutation of the β-gene was found.
TRANSLOCATIONS IN DICTYOSTELIUM DISCOIDEUM
Authors: Welker D L , Williams K L 
Published: January 2021

ABSTRACT
Fourteen translocations of independent origin were identified in Dictyostelium discoideum on the basis of segregation anomalies of diploids heterozygous for these chromosome rearrangements, all of which led to the cosegregation of unlinked markers. Many of these translocations were discovered in strains mutagenized with MNNG or in strains carrying mutations affecting DNA repair; however, spontaneous translocations were also obtained. Haploid mitotic recombinants of the rearranged linkage groups were produced from diploids heterozygous for the translocations at frequencies of up to 5% of viable haploid segregants; this is at least a ten-fold higher frequency than that seen with diploids not heterozygous for translocations (∼0.1%). These haploid recombinants included both translocated and nontranslocated strains. The T354(II,VII) translocation and possibly the T357(IV,VII) translocation reduce the chromosome number to n = 6; haploids carrying 11 other translocations all have karyotypes with n = 7. Genetic characterization of the T357(IV,VII) translocation showed that the bwnA and whiC loci normally found on linkage group IV were physically linked to the linkage group VII loci couA, phgA, bsgB and cobA.
EVOLUTION AND EXTINCTION OF TRANSPOSABLE ELEMENTS IN MENDELIAN POPULATIONS
Authors: Kaplan Norman , Darden Tom , Langley Charles H 
Published: January 2021

ABSTRACT
A model of the evolution of a transposable element family in a Mendelian host population is proposed that incorporates heritable phenotypic mutations in the elements. The temporal behavior of the numbers of mutant and wild-type elements is studied, and the expected extinction time of the transposable element family is examined. Our results indicate that, if the mutant can be transposed equally well in the presence of the wild type, then it can be expected to be found in preponderance, whereas elements, such as retroviruses, where the transposing genome and its phenotypic expression are coupled, may be characterized by a low mutant frequency.
SON-KILLER: A THIRD EXTRACHROMOSOMAL FACTOR AFFECTING THE SEX RATIO IN THE PARASITOID WASP, NASONIA (=MORMONIELLA) VITRIPENNIS
Authors: Skinner Samuel Way 
Published: January 2021

ABSTRACT
An extrachromosomal factor, termed son-killer (sk), affects the sex ratio in a parasitoid wasp, Nasonia (=Mormoniella) vitripennis. The factor is maternally transmitted and alters the secondary sex ratio of an infected female through mortality of approximately 80% of the male embryos. No effect on the primary (zygotic) sex ratio is observed. Ninety-five percent of the daughters of an infected female inherit son-killer. The factor can also be transmitted contagiously when the progeny of infected and uninfected females develop simultaneously on a single host. In newly infected strains, the sex ratio effects are equivalent to those in the original.
THE ROLE OF THE SPO11 GENE IN MEIOTIC RECOMBINATION IN YEAST
Authors: Klapholz Sue , Waddell Candace S , Esposito Rochelle Easton 
Published: January 2021

ABSTRACT
Several complementary experimental approaches were used to demonstrate that the SPO11 gene is specifically required for meiotic recombination. First, sporulating cultures of spo11-1 mutant diploids were examined for landmark biochemical, cytological and genetic events of meiosis and ascosporogenesis. Cells entered sporulation with high efficiency and showed a near-doubling of DNA content. Synaptonemal complexes, hallmarks of intimate homologous pairing, and polycomplex structures appeared during meiotic prophase. Although spontaneous mitotic intra- and intergenic recombination occurred at normal levels, no meiotic recombination was observed. Whereas greater than 50% of cells completed both meiotic divisions, packaging of the four meiotic products into mature ascospores took place in only a small subset of asci. Haploidization occurred in less than 1% of viable colony-forming units. Second, the Rec- meiotic defect conferred by spo11-1 was confirmed by dyad analysis of spores derived from spo13-1 single-division meiosis in which recombination is not a requirement for viable ascospore production. Diploids homozygous for the spo13-1 mutation undergo meiotic levels of exchange followed by a single predominantly equational division and form asci containing two near-diploid spores. With the introduction of the spo11-1 mutation, high spore viability was retained, whereas intergenic recombination was reduced by more than 100-fold.
MICROGEOGRAPHIC AND TEMPORAL GENETIC DIFFERENTIATION IN NATURAL POPULATIONS OF DROSOPHILA SUBOBSCURA
Authors: Cabrera V M , González A M , Hernández M , Larruga J M , Martell M 
Published: January 2021

ABSTRACT
Evidence of microgeographic and temporal genetic differentiation in natural populations of Drosophila subobscura is presented. The alcohol dehydrogenease locus was used as a genetic marker. Behavioral differences among the sexes and genotypes may explain these observations, although the molecular basis remains obscure.
APPARENT GENETIC COMPLEXITY GENERATED BY DEVELOPMENTAL THRESHOLDS: THE APTEROUS LOCUS IN DROSOPHILA MELANOGASTER
Authors: Stevens Mary E , Bryant Peter J 
Published: January 2021

ABSTRACT
Mutations at the apterous (ap) locus in Drosophila melanogaster give rise to three distinct phenotypes: aberrant wings, female sterility and precocious adult death. The wing phenotype includes five types of abnormality: blistering, deficiencies, duplications, high-order repetitions and transformation of structures. The mildest phenotype is seen with homozygous apblt animals which have either normal or slightly blistered wings. Most alleles produce, in the homozygote, a deficient wing in which part or all of the wing margin and wing blade is missing, but wing hinge and notum regions are normal. Animals hemizygous for each of 20 ap alleles, as well as apID/apXa heterozygotes, show duplication of parts of the notum associated with complete wing deficiency. Animals heterozygous for apc and the other tested ap alleles show repetitions of parts of the anterior wing margin, an engrailed-like transformation of posterior wing margin into anterior margin or both. Both apblt and apc show similar phenotypes in homozygotes and hemizygotes, yet both produce a less extreme phenotype than that of the other hemizygotes, suggesting that neither mutation causes loss of the entire ap + function. The 15 alleles that cause precocious death and female sterility occur in six complementation groups based on complementation for these phenotypes. This supports the previous conclusion that the effects of apterous mutations on the wing do not correlate with their effects on viability and fertility. We propose an explanation for the effects of apterous mutations on the wing in which quantitative reductions in the activity of gene product give rise to qualitatively different phenotypes because of different threshold requirements of the ap + function for critical events in wing disc development.
MOLECULAR CLONING OF α-AMYLASE GENES FROM DROSOPHILA MELANOGASTER. I. CLONE ISOLATION BY USE OF A MOUSE PROBE
Authors: Gemmill Robert M , Levy Jack N , Doane Winifred W 
Published: January 2021

ABSTRACT
A cloned ä-amylase cDNA sequence from the mouse is homologous to a small set of DNA sequences from Drosophila melanogaster under appropriate conditions of hybridization. A number of recombinant lambda phage that carry homologous Drosophila genomic DNA sequences were isolated using the mouse clone as a hybridization probe. Putative amylase clones hybridized in situ to one or the other of two distinct sites in polytene chromosome 2R and were assigned to one of two classes, A and B. Clone λDm32, representing class A, hybridizes within chromosome section 53CD. Clone λDm65 of class B hybridizes within section 54A1-B1. Clone λDm65 is homologous to a 1450- to 1500-nucleotide RNA species, which is sufficiently long to code for α-amylase. No RNA homologous to λDm32 was detected. We suggest that the class B clone, λDm65, contains the functional Amy structural gene(s) and that class A clones contain an amylase pseudogene.
GENE GENEALOGY AND VARIANCE OF INTERPOPULATIONAL NUCLEOTIDE DIFFERENCES
Authors: Takahata Naoyuki , Nei Masatoshi 
Published: January 2021

ABSTRACT
A mathematical theory is developed for computing the probability that m genes sampled from one population (species) and n genes sampled from another are derived from l genes that existed at the time of population splitting. The expected time of divergence between the two most closely related genes sampled from two different populations and the time of divergence (coalescence) of all genes sampled are studied by using this theory. It is shown that the time of divergence between the two most closely related genes can be used as an approximate estimate of the time of population splitting (T) only when T ≡ t/(2 N) is small, where t and N are the number of generations and the effective population size, respectively. The variance of Nei and Li's estimate (d) of the number of net nucleotide differences between two populations is also studied. It is shown that the standard error (sd) of d is larger than the mean when T is small (T &lt;&lt; 1). In this case, sd is reduced considerably by increasing sample size. When T is large (T &gt; 1), however, a large proportion of the variance of d is caused by stochastic factors, and increase in the sample size does not help to reduce sd. To reduce the stochastic variance of d, one must use data from many independent unlinked gene loci.
ALTERED FIDELITY OF MITOTIC CHROMOSOME TRANSMISSION IN CELL CYCLE MUTANTS OF S. CEREVISIAE
Authors: Hartwell Leland H , Smith David 
Published: January 2021

ABSTRACT
Thirteen of 14 temperature-sensitive mutants deficient in successive steps of mitotic chromosome transmission (cdc2, 4, 5, 6, 7, 8, 9, 13, 14, 15, 16, 17 and 20) from spindle pole body separation to a late stage of nuclear division exhibited a dramatic increase in the frequency of chromosome loss and/or mitotic recombination when they were grown at their maximum permissive temperatures. The increase in chromosome loss and/or recombination is likely to be due to the deficiency of functional gene product rather than to an aberrant function of the mutant gene product since the mutant alleles are, with one exception, recessive to the wild-type allele for this phenotype. The generality of this result suggests that a delay in almost any stage of chromosome replication or segregation leads to a decrease in the fidelity of mitotic chromosome transmission. In contrast, temperature-sensitive mutants defective in the control step of the cell cycle (cdc28), in cytokinesis (cdc3) or in protein synthesis (ils1) did not exhibit increased recombination or chromosome loss.—Based upon previous results with mutants and DNA-damaging agents in a variety of organisms, we suggest that the induction of mitotic recombination in certain mutants is due to the action of a repair pathway upon nicks or gaps left in the DNA. This interpretation is supported by the fact that the induced recombination is dependent upon the RAD52 gene product, an essential component in the recombinogenic DNA repair pathway. Gene products whose deficiency leads to induced recombination are, therefore, strong candidates for proteins that function in DNA metabolism. Among the mutants that induce recombination are those known to be defective in some aspect of DNA replication (cdc2, 6, 8, 9) as well as some mutants defective in the G2 (cdc13 and 17) and M (cdc5 and 14) phases of the mitotic cycle. We suggest that special aspects of DNA metabolism may be occurring in G2 and M in order to prepare the chromosomes for proper segregation.
MUTATIONS IN GENES ENCODING ESSENTIAL MITOTIC FUNCTIONS IN DROSOPHILA MELANOGASTER
Authors: Smith David A , Baker Bruce S , Gatti Maurizio 
Published: January 2021

ABSTRACT
Temperature-sensitive mutations at 15 loci that affect the fidelity of mitotic chromosome behavior have been isolated in Drosophila melanogaster. These mitotic mutants were detected in a collection of 168 EMS-induced X-linked temperature-sensitive (ts) lethal and semilethal mutants. Our screen for mutations with mitotic effects was based upon the reasoning that under semirestrictive conditions such mutations could cause an elevated frequency of mitotic chromosome misbehavior and that such events would be detectable with somatic cell genetic techniques. Males hemizygous for each ts lethal and heterozygous for the recessive autosomal cell marker mwh were reared under semirestrictive conditions, and the wings of those individuals surviving to adulthood were examined for an increased frequency of mwh clones. Those mutations producing elevated levels of chromosome instability during growth of the wing imaginal disc were also examined for their effects on chromosome behavior in the cell lineages producing the abdominal cuticle. Fifteen mutations affect chromosome behavior in both wing and abdominal cells and thus identify loci generally required for the fidelity of mitotic chromosome transmission. Mapping and complementation tests show that these mutations represent 15 loci. One mutant is an allele of a locus (mus-101) previously identified by mutagensensitive mutants and a second mutant is an allele of the lethal locus zw10.—The 15 mutants were also examined cytologically for their effects on chromosomes in larval neuroblasts. Taken together, the results of our cytological and genetical studies show that these mutants identify loci with wild-type functions necessary for either (1) maintenance of chromosome integrity or (2) regular disjunction of chromosomes or (3) chromosome condensation. Thus, these mutations define a broad spectrum of genes required for the normal execution of the mitotic chromosome cycle.
A MOUSE β-GLOBIN MUTANT THAT IS AN EXACT MODEL OF HEMOGLOBIN RAINIER IN MAN
Authors: Peters J , Andrews S J , Loutit J F , Clegg J B 
Published: January 2021

ABSTRACT
A mutation induced by ethylnitrosourea in a spermatogonial stem cell of a 101/H mouse has resulted in a structurally altered β-diffuse major globin in one of his offspring. The mutant hemoglobin is associated with polycythemia, rubor, increased oxygen affinity and decreased hem-hem interaction. The mutant haplotype has been designated Hbbd 4, polycythemia. Amino acid analysis of the mutant globin has shown that a single substitution β145 Tyr → Cys has occurred, and it is proposed that ethylnitrosourea induced an A → G transition in the tyrosine codon (TAC → TGC). This murine polycythemia is homologous with hemoglobin Rainier in man, in which the amino acid substitution is also β145 Tyr → Cys and which is associated with similar physiological consequences.
THE LOCUS ENCODING αA-CRYSTALLIN IS CLOSELY LINKED TO H-2K ON MOUSE CHROMOSOME 17
Authors: Skow Loren C , Donner Maria E 
Published: January 2021

ABSTRACT
We have used a complementary DNA (cDNA) for mouse αA-crystallin to probe genomic DNA for restriction fragment length polymorphisms which could be used to map the αA-crystallin gene locus (Acry-1) in the mouse genome. Ten of 12 restriction endonucleases produced fragment polymorphism among various inbred strains of mice. A comprehensive strain survey conducted with six endonucleases resulted in the discovery of six allelic forms of Acry-1. Linkage analysis was conducted on DNA from three sets of recombinant inbred strains of mice and demonstrated close linkage of Acry-1 with the major histocompatibility complex (H-2) on chromosome 17. Analysis of congenic and recombinant congenic strains of mice confirmed the linkage of Acry-1 and H-2 and located the αA gene to the region between glyoxylase (Glo-1) and H-2K.