bluuebunny/crossref_metadata_2025_split huggingface dataset:
GENETIC DISSECTION OF SEGREGATION DISTORTION. III. UNEQUAL RECOVERY OF RECIPROCAL RECOMBINANTS
Authors: Hartl Daniel L 
Published: April 2021

ABSTRACT
The genetic structure of a segregation distorter chromosome (a derivative of SD-36) has been analyzed in a system in which recombination in the second chromosome is blocked by inversions except for the critical region around the centromeric heterochromatin. The results confirm the map order and characteristics of four loci known to be involved in segregation distortion, namely Sd, E(SD), Rspins, M(SD). However, SD-36 carries a fifth major locus involved in distortion. This locus is near pr in 2L and has the effect of enhancing the degree of distortion. In addition, reciprocal recombinant products from SD-36 are recovered unequally. All recombinants carrying the pr region from SD-36 seem also to carry Sd, although Sd has previously been mapped 1.6 units to the left of pr. Both the enhancement of distortion and the unequal recovery of reciprocal products can be explained if it is assumed that the new locus near pr in SD-36 is actually a duplication of Sd.
GENETIC CHANGES IN FLUCTUATING VOLE POPULATIONS: SELECTIVE VS. NONSELECTIVE FORCES
Authors: Gaines Michael S , Whittam Thomas S 
Published: April 2021

ABSTRACT
The Lewontin-Krakauer test for selective neutrality of polymorphisms was applied to temporal variation in gene frequency at five electrophoretic loci in each of four fluctuating vole populations over a three-year period. The results indicate that changes in gene frequencies were primarily due to nonselective forces.
ON THE EVOLUTION OF NEW METABOLIC FUNCTIONS IN DIPLOID ORGANISMS
Authors: Hall Barry G 
Published: April 2021

ABSTRACT
Evolution of lactose utilization via the ebg system of Escherichia coli requires both structural gene (ebgA) and regulatory gene (ebgR) mutations. Because evolution of new metabolic functions in diploids might be subject to constraints not present in haploid organisms, merodiploid strains carrying a wild-type and an evolved ebgA allele, or a wild-type and an evolved ebgR allele were constructed. I show that heterozygosity at ebgA does not significantly affect the selective advantage of the evolved ebgA allele; whereas heterozygosity at ebgR eliminates the selective advantage of the evolved ebgR allele. It is suggested that, in diploid organisms, evolution of new functions for systems under negative control would be very difficult.
THE ROLE OF DOSAGE OF THE REGION 7D1–7D5-6 OF THE X CHROMOSOME IN THE PRODUCTION OF HOMEOTIC TRANSFORMATIONS IN DROSOPHILA MELANOGASTER
Authors: Gans M , Forquignon F , Masson M 
Published: April 2021

ABSTRACT
A high frequency of homeotic transformations appears in Df(3)red/+ progeny of Df(1)snC128 /+ females. Generally, the metathoracic appendages are partially transformed into mesothoracic ones. Df(1)snC128 includes a small region of the X chromosome: 7D1 to 7D5-6. Hypodosage of this region is mainly effective at the level of the maternal genotype, and the effect is probably due to hypodosage of the wild-type allele of the gene fs(1)h. Df(3)red has an effect that is mainly, if not exclusively, zygotic, probably due to hypodosage of the wild-type allele of Rg-bx. The frequencies of transformed flies resulting from the interaction between Df(1)snC128 and Df(3)red are not very sensitive to external conditions and genetic background. Studies of the interactions between Df(1)snC128 and other mutations or deficiencies of chromosome 3 [Rg-pbx, bx, pbx, Ubx1, Ubx130, Ubx80, Df(3)P9] reveal an analogy between the hypodosage effect of region 7D1–7D5-6 and the effects of ether treatment of blastoderm stage eggs. The role of the gene fs(1)h in the process of segment determination is discussed in the light of these results.
VARIATION IN BIOCHEMICAL PROPERTIES OF ALLOZYMES OF XANTHINE DEHYDROGENASE IN DROSOPHILA PSEUDOOBSCURA
Authors: Wilcox David R , Prakash Satya 
Published: April 2021

ABSTRACT
Twenty-six D. pseudoobscura strains isogenic for xanthine dehydrogenase alleles from Mesa Verde, Colorado, were tested for differences in the biochemical properties of different allelic forms of xanthine dehydrogenase. No significant differences in binding affinity (Km) or substrate specificity of the enzyme were found. Significant variation among strains, in activity (V max) and among electromorphs, as well as among strains, in thermolability was found. For the few strains tested, the activity and thermolability differences were shown to co-segregate with the electrophoretic mobility of the variant allele.
CRYPTIC OPERON FOR β-GLUCOSIDE METABOLISM IN ESCHERICHIA COLI K12: GENETIC EVIDENCE FOR A REGULATORY PROTEIN
Authors: Defez Roberto , De Felice Maurilio 
Published: April 2021

ABSTRACT
Escherichia coli K12 does not metabolize β-glucosides such as arbutin and salicin because of lack of expression of the bglBSRC operon, which contains structural genes for transport (bglC) and hydrolysis (bglB) of phospho-β-glucosides. Mutants carrying lesions in the cis-acting regulatory site bglR metabolize β-glucosides as a consequence of expression of this cryptic operon (Prasad and Schaefler 1974). We isolated mutations promoting β-glucoside metabolism that were unlinked to bglR; some of these mutations were shown to be amber. All of them were mapped at 27 min on the E. coli K12 linkage map and appeared to define a single gene, for which we propose the designation bglY. Utilization of β-glucosides in bglY mutants appeared to be a consequence of expression of the bglBSRC operon, since bglB bglR and bglB bglY double mutants had the same phenotype. All bglY mutations analyzed were recessive to the wild-type bglY + allele. Phospho-β-glucosidase B and β-glucoside transport activities are inducible in bglY mutants, as they are in bglR mutants. Metabolism of β-glucosides in both bglR and bglY mutants required cyclic AMP. We propose that bglY encodes a protein acting as a repressor of the bglBSRC operon, active in both the presence and absence of β-glucosides, whose recognition site would be within the bglR locus.
THE MUTATION SK(ad-3A) CANCELS THE DOMINANCE OF ad-3A
+ OVER ad-3A IN THE ASCUS OF NEUROSPORA
Authors: Delange A M 
Published: April 2021

ABSTRACT
A newly induced mutant of Neurospora, when crossed with an ad-3A mutant, produces asci with four viable black and four inviable white ascospores. The survivors always contain the new mutant allele, never ad-3A. The new allele, which is called SK(ad-3A) (for spore killer of ad-3A), is located at or very near the ad-3A locus. —In crosses homozygous for ad-3A, each ascus contains only inviable white ascospores. This defect in ascospore maturation is complemented by the wild-type allele, ad-3A + (crosses heterozygous for ad-3A and ad-3A + produce mainly viable ascospores), but it is not complemented by the new SK(ad-3A) allele (all ad-3A ascospores from crosses heterozygous for SK(ad-3A) and ad-3A are white and inviable). In crosses homozygous for SK(ad-3A) or heterozygous for SK(ad-3A) and ad-3A +, each ascus contains only viable black ascospores. SK(ad-3A) does not require adenine for growth, and forced heterokaryons between SK(ad-3A) and ad-3A grow at wild-type rates and produce conidia of both genotypes with approximately equal frequency. Thus, the action of SK(ad-3A) is apparently restricted to ascospore formation. Possible mechanisms of the action of this new allele are discussed.
CLUSTERING OF GENES FOR 20 kd ZEIN SUBUNITS IN THE SHORT ARM OF MAIZE CHROMOSOME 7
Authors: Soave Carlo , Reggiani Remo , Di Fonzo Natale , Salamini Francesco 
Published: April 2021

ABSTRACT
Zein is the major storage protein of the endosperm of maize kernels. When this alcohol-soluble protein is subjected to SDS polyacrylamide gel electrophoresis, it is resolved into four fractions of different molecular weight: 10, 14, 20 and 22 kilodaltons (kd). Each fraction is heterogeneous with respect to isoelectric pH. For example, the 20 kd fraction contains at least seven subfractions as revealed by isoelectric focusing in polyacrylamide gels. In this report, we present evidence that the structural genes coding for the 20 kd proteins are clustered on the short arm of chromosome 7, a region that also bears loci regulating endosperm zein biosynthesis [opaque-2 (02) and defective endosperm-B30 (De*-B30)]. The organization of these zein genes suggests that the evolution of at least some of the maize genome has occurred as the result of repeated duplication and divergence of chromosome segments.
THE GENETICS OF DROSOPHILA SUBOBSCURA POPULATIONS. XVII. FURTHER GENIC HETEROGENEITY WITHIN ELECTROMORPHS BY UREA DENATURATION AND THE EFFECT OF THE INCREASED GENIC VARIABILITY ON LINKAGE DISEQUILIBRIUM STUDIES
Authors: Loukas M , Vergini Y , Krimbas C B 
Published: April 2021

ABSTRACT
Urea denaturation of allozymes was used to provide finer resolution of allelic states within classes of different electrophoretic mobility. This method gives perfectly repeatable results. About 170 isogenic strains for the O chromosome of Drosophila subobscura, derived from two natural populations, were constructed. Their gene arrangements were studied, as well as eight polymorphic genes located on the O chromosome (Est-5, Odh, Ao, ME, Xdh, Lap, Pept-1 and Acph). Crosses performed indicate that differences in urea sensitivity are genetically controlled by the same genes that control electrophoretic mobility. Twice as many alleles have been detected in comparison to the usual electrophoretic method. However, the effective number of alleles did not increase considerably.
Studies of linkage disequilibria, by taking into account the finer resolution of allelic states, gave results nearly identical with those obtained in studies where the usual electrophoretic method was used. Although the power of the test is diminished, the absence of genic associations seems to indicate that there are no hidden linkage disequilibria in electrophoretic studies (because of consolidation effects of real alleles into few electromorph classes). The paucity of linkage disequilibria would indicate that there are no epistatic interactions such as those suggested in the model of Franklin and Lewontin (1970).
MATING-TYPE DIFFERENTIATION BY TRANSPOSITION OF CONTROLLING ELEMENTS IN SACCHAROMYCES CEREVISIAE
Authors: Oshima Takehiro , Takano Isamu 
Published: April 2021

ABSTRACT
The nonfunctional mutation of the homothallic gene HMLα, designated hmlα, produced two mutant alleles, hmlα-1 and hmlα-2. Both mutant clones were mixed cultures consisting of a mating-type cells and nonmating haploid cells. The frequencies of the two cell types were different, and a few diploid cells able to sporulate were found in the hmlα-2 mutant. Conversions of an a mating-type cell to nonmater, and uice uersa, were observed in both mutants. The conversion of an a mating phenotype to nonmating is postulated to occur by alteration of the a mating type to the sterile mating-type allele in the hmlα-1 mutant. In tetrad dissection of prototrophic diploids that were obtained by rare-mating of hmlα-1 mutants with a heterothallic strain having the MATa ho HMRa HMLa genotype, many mating-deficient haploid segregants were found, while α mating-type segregants were observed in a similar diploid using an hmlα-2 mutant. The mating-type-deficient haploid segregants were supposed to have the sterile a mating-type allele because the nonmating genetic trait always segregated with the mating-type locus. Sporogenous diploid cells obtained in the hmlα-2 mutant clone had the MATa/MAT,α HO/HO HMRa/ HMRa hmlα-2/hmlα-2 genotype. These observations suggested that the hmla-I allele produces a transposable element that gives rise to the sterile su mating type by transposition into the mating-type locus, and that the hmlα-2 allele produces an element that provides,α mating-type information, but is defective in the structure for transposition.
GENETIC VARIATION AND GENETIC LOAD DUE TO THE MALE REPRODUCTIVE COMPONENT OF FITNESS IN DROSOPHILA
Authors: Brittnacher John G 
Published: April 2021

ABSTRACT
The genetic variation and genetic load due to virility, the male reproductive component of fitness, was measured in Drosophila melanogaster and D. pseudoobscura using males homozygous and heterozygous for the second chromosome of each species. Virility was determined in a female-choice, male mating competition experiment where both mating propensity and fertility were taken into account.——The mean virility of the homozygous D. melanogaster males relative to the heterozygous males was 0.50; the relative mean virility of the quasinormal homozygotes was 0.56. The mean virility of the homozygous D. pseudoobscura males relative to the heterozygous males was 0.70; the relative mean virility of the nonsterile homozygotes was 0.72, and of the quasinormal homozygotes, 0.68.——Depending on the species and chromosome sampled, fertile homozygous males had a mean virility 15 to 50% lower than the mean viability of individuals homozygous for a chromosome with quasinormal viability. The genetic load due to virility was also greater than that due to the female reproductive component. This higher level of hidden genetic variation (or genetic load) indicates that the results of PROUT(1971a, b) and BUNDGAARD and CHRISTIANSEN(1972), where the virility component of fitness dominated the dynamics of an artificial polymorphism, may be more general and that virility may dominate the dynamics of natural polymorphisms as well.
THE INBREEDING EFFECTIVE POPULATION NUMBER AND THE EXPECTED HOMOZYGOSITY FOR AN X-LINKED LOCUS
Authors: Nagylaki Thomas 
Published: April 2021

ABSTRACT
Assuming random mating and discrete nonoverlapping generations, the inbreeding effective population number, N(i) e, is calculated for an X-linked locus. For large populations, the result agrees with the variance effective population number. As an application, the maintenance of genetic variability by the joint action of mutation and random drift is investigated. It is shown that, if every allele mutates at rate u to new types, then the probabilities of identity in state (and hence the expected homozygosity of females) converge to the approximate value (1 + 4N(i) eu)-1 at the approximate asymptotic rate exp{—[2u + (2N(i)e)-1]t}.
DIFFERENTIAL MITOTIC STABILITY OF YEAST DISOMES DERIVED FROM TRIPLOID MEIOSIS
Authors: Campbell Douglas , Doctor John S , Feuersanger Jeane H , Doolittle Mark M 
Published: April 2021

ABSTRACT
The frequencies of recovered disomy among the meiotic segregants of yeast (Saccharomyces cerevisiae) triploids were assessed under conditions in which all 17 yeast chromosomes were monitored simultaneously. The studies employed inbred triploids, in which all homologous centromeres were identical by descent, and single haploid testers carrying genetic markers for all 17 linkage groups. The principal results include: (1) Ascospores from triploid meiosis germinate at frequencies comparable to those from normal diploids, but most fail to produce visible colonies due to the growth-retarding effects of high multiple disomy. (2) The probability of disome formation during triploid meiosis is the same for all chromosomes; disomy for any given chromosome does not exclude simultaneous disomy for any other chromosome. (3) The 17 yeast chromosomes fall into three frequency classes in terms of disome recovery. The results support the idea that multiply disomic meiotic segregants of the triploid experience repeated, nonrandom, post-germination mitotic chromosome losses (N+1→N) and that the observed variations in individual disome recovery are wholly attributable to inherent differences in disome mitotic stability.
HYBRID DYSGENESIS IN DROSOPHILA MELANOGASTER: THE GENETICS OF CYTOTYPE DETERMINATION IN A NEUTRAL STRAIN
Authors: Kidwell Margaret G 
Published: April 2021

ABSTRACT
The genetic determination of resistance to the sterility-producing genetic elements called P factors was studied in a strain characterized as neutral (Q) in the P-M system of hybrid dysgenesis. Sixteen lines were synthesized, representing all possible homozygous combinations of the three major chromosomes and differing maternal cytoplasms of an original resistant (Q) and susceptible (M) strain.—The results provide a detailed genetic analysis of the determination of cytotype (which mediates resistance or susceptibility to P factors) in the absence of the P-M dysgenic interaction. They extend the findings of Engels (1979) by providing specific information on both the location and relative magnitude of effect of cytotype-determining chromosomal factors and their interaction over time with maternally transmitted cytoplasm.—Cytotype was found to be primarily controlled by the genotype, but the maternal cytoplasm, under some circumstances, has an important short-term effect. Major cytotype-determining chromosomal factors are localized to the distal half of the X chromosome. However, there was also evidence for minor factors located on the major autosomes, particularly chromosome 3. Under certain circumstances, cytotypic switches in either direction can be produced in a single generation by the substitution of an X chromosome carrying a major cytotype determinant. This may provide an explanation of why reciprocal differences have sometimes been interpreted as direct effects of X-chromosome suppressors. However, slow but systematic changes of M to P cytotype were observed in five synthesized lines of mixed origin over twenty generations with no chromosomal substitution. Alternative explanations of these changes in terms of delayed effects of minor autosomal factors or of the transposability of cytotype determinants are discussed.
AN INCREASE IN THE X-LINKED LETHAL MUTATION RATE ASSOCIATED WITH AN UNSTABLE LOCUS IN DROSOPHILA MELANOGASTER
Authors: Raymond John D , Simmons Michael J 
Published: April 2021

ABSTRACT
The behavior of an unstable allele of the singed-bristle locus on the X chromosome was studied in connection with the occurrence of lethal mutations on that same chromosome. The unstable allele, weak singed (snw), is under the control of the P-M system of hybrid dysgenesis and, in the M cytotype, mutates secondarily to extreme singed (sne) and to wild type (sn +) at high rates. Chromosomes whose snw allele had mutated in this fashion sustained lethal mutations at a rate of 3%; whereas, those whose snw allele had apparently remained unchanged, acquired lethals at a lower rate, 1.3%. The significant difference between these values indicates a statistical coincidence between the phenomena of snw instability and X-linked lethal mutation induction. This coincidence can be explained by postulating that mutations at the singed locus sometimes release a genetic element capable of reinserting elsewhere in the chromosome. Alternately, snw instability and lethal induction might be associated because they are the effects of a common cause, perhaps some mutation-inducing substance present in various amounts in the germ cells of dysgenic flies.—The lethals that occurred on chromosomes whose snw allele had mutated to sne mapped preferentially close to singed. The lethals on the snw and sn + chromosomes did not show this concentration on the map. Cytological analysis of samples of all three types of lethal chromosomes indicated that, with one exception, there was no detectable breakage at the singed locus itself. The single instance of breakage at singed was not associated with any change in the singed phenotype. Thus, the instability of snw apparently does not involve detectable breakage of the singed locus, or if it does, this breakage is not a common event.
THE CHROMOSOMES OF TURKEY EMBRYOS DURING EARLY STAGES OF PARTHENOGENETIC DEVELOPMENT
Authors: Harada Ko , Buss Edward G 
Published: April 2021

ABSTRACT
In the early stages of parthenogenetic development in turkey eggs, many blastoderms are mosaics of haploid, diploid and polyploid cells. The genome composition of these blastoderms can be identified by C-banding. They may be generally described as either A-Z/2A-ZZ/nA-nZ or A-W/2A-WW/nA-nW and are found in a nearly 1:1 ratio. The blastoderms showing the W body (W +) become lethal within two days of incubation. The haploid cell proportion decreases rapidly during the early stage of development, and, as haploid cells decrease, the proportion of polyploid cells appears to increase. At six days of incubation, various kinds of parthenogenetic development can be observed. Their genome compositions are either diploid (2A-ZZ) or mosaic (A-Z/2A-ZZ). These findings suggest that diploid parthenogenesis occurs by either suppression of meiosis II or chromosome doubling some time after the first cleavage division. The frequent occurrence of mosaic blastoderms indicates that the majority, if not all, of the parthenogenetic embryos initiate their development in haploid ova.
AN APPROXIMATION OF THE MINIMUM-VARIANCE ESTIMATOR OF HERITABILITY BASED ON VARIANCE COMPONENT ANALYSIS
Authors: Grossman M , Norton H W 
Published: April 2021

ABSTRACT
An approximate minimum-variance estimate of heritability (h 2) is proposed, using the sire and dam components of variance from a hierarchical analysis of variance. The minimum sampling variance is derived for unbalanced data. Optimum structures for the estimation of h 2 are given for the balanced case. The degree to which ĥ 2 is more precise than the equally weighted estimate ĥ 2 S+D is a function of the size and structure of the sample used. However, computer simulation reveals that ĥ 2 has less desirable behavior than ĥ 2 S+D. An iterative procedure improved the estimation of h 2, especially in small populations, when those values of ĥ 2 S or ĥ 2 D outside the range of the parameter were constrained to zero or unity.
INOSITOL MUTANTS OF SACCHAROMYCES CEREVISIAE: MAPPING THE ino1 LOCUS AND CHARACTERIZING ALLELES OF THE ino1, ino2 AND ino4 LOCI
Authors: Donahue Thomas F , Henry Susan A 
Published: April 2021

ABSTRACT
An extensive genetic analysis of inositol auxotrophic mutants of yeast is reported. The analysis includes newly isolated mutants, as well as those previously reported (Culbertson and Henry 1975). Approximately 70% of all inositol auxotrophs isolated are shown to be alleles of the ino1 locus, the structural gene for inositol-1-phosphate synthase, the major enzyme involved in inositol biosynthesis. Alleles of two other loci, ino2 and ino4, comprise 9% of total mutants, with the remainder representing unique loci or complementation groups. The ino1 locus was mapped by trisomic analysis with an n + 1 disomic strain constructed with complementing alleles at this locus. The ino1 locus is shown to be located between ura2 (11.1 cm) and cdc6 (21.8 cm) on chromosome X. An extended map of chromosome X of yeast is presented. Unlike most yeast loci, but similar to the his1 locus, the ino1 locus lacks allelic representatives that are suppressible by known suppressors. This finding suggests that premature termination of translation of the ino1 gene product may be incompatible with cell viability.