bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mutations in CEN3 cause aberrant chromosome segregation during meiosis in Saccharomyces cerevisiae.
Authors: Gaudet A , Fitzgerald-Hayes M 
Published: January 2021

Abstract
We investigated the structural requirements of the centromere from chromosome III (CEN3) of Saccharomyces cerevisiae by analyzing the ability of chromosomes with CEN3 mutations to segregate properly during meiosis. We analyzed diploid cells in which one or both copies of chromosome III carry a mutant centromere in place of the wild-type centromere and found that some alterations in the length, base composition and primary sequence characteristics of the central A+T-rich region (CDE II) of the centromere had a significant effect on the ability of the chromosome to segregate properly through meiosis. Chromosomes containing mutations which delete a portion of CDE II showed a high rate of premature disjunction at meiosis I. Chromosomes containing point mutations in CDE I or lacking CDE I appeared to segregate properly through meiosis; however, plasmids carrying centromeres with CDE I completely deleted showed an increased frequency of segregation to nonsister spores.
Molecular genetics of the Caenorhabditis elegans heterochronic gene lin-14.
Authors: Ruvkun G , Ambros V , Coulson A , Waterston R , Sulston J , Horvitz H R 
Published: January 2021

Abstract
We describe a general strategy for the genetic mapping in parallel of multiple restriction fragment length polymorphism (RFLP) loci. This approach allows the systematic identification for cloning of physical genetic loci within about 100 kb of any gene in Caenorhabditis elegans. We have used this strategy of parallel RFLP mapping to clone the heterochronic gene lin-14, which controls the timing and sequence of many C. elegans postembryonic developmental events. We found that of about 400 polymorphic loci in the C. elegans genome associated with the Tc1 family of repetitive elements, six are within 0.3 map unit of lin-14. The three closest lin-14-linked Tc1-containing restriction fragments were cloned and used to identify by hybridization an 830-kb region of contiguous cloned DNA fragments assembled from cosmid and yeast artificial chromosome libraries. A lin-14 intragenic recombinant that separated a previously cryptic lin-14 semidominant mutation from a cis-acting lin-14 suppressor mutation was used to map the location of the lin-14 gene to a 25-kb region of this 830-kb contig. DNA probes from this region detected lin-14 allele-specific DNA alterations and a lin-14 mRNA. Two lin-14 semi-dominant alleles, which cause temporally inappropriate lin-14 gene activity and lead to the reiterated expression of specific early developmental events, were shown to delete sequences from the lin-14 gene and mRNA. These deletions may define cis-acting sequences responsible for the temporal regulation of lin-14.
A repeated segment on the mouse Y chromosome is composed of retroviral-related, Y-enriched and Y-specific sequences.
Authors: Eicher E M , Hutchison K W , Phillips S J , Tucker P K , Lee B K 
Published: January 2021

Abstract
We report the isolation and characterization of two recombinant clones containing DNA derived from the Y chromosome of the C57BL/10 inbred mouse strain. Both clones were isolated from a lambda phage library derived from a partial EcoRI digest of C57BL/10 male DNA using the murine retrovirus M720. Characterization of these clones showed they were derived from a repeated segment present on the C57BL/10J Y chromosome that contains sequences found elsewhere in the genome. In addition, one clone contained a sequence, designated YB10, that is unique to the Y chromosome and present in approximately 500 copies on the C57BL/10J Y chromosome. Analysis of Southern blots containing DNAs prepared from females and males of representative species from four subgenera of Mus probed with pYB10 and the 3'LTR from one of the Y-associated retroviruses (MuRVY) revealed that, with the exception of a single fragment observed in both female and male DNA of Mus saxicola, hybridization to pYB10 was observed only to male DNA of the species Mus spretus, Mus hortulanus, Mus musculus, Mus domesticus and Mus abbotti. In addition, the pattern and intensity of hybridization to YB10 and the MuRVY-LTR indicated that sequence of divergence was followed by amplification of Y chromosome sequences containing YB10 and MuRVY. The divergence and amplification occurred separately in each of the ancestral lineages leading to M. spretus, M. hortulanus, M. abbotti, M. musculus and M. domesticus. We suggest that acquisition and amplification of DNA sequences by the mammalian Y chromosome has contributed to its evolution and may imply that the mammalian Y chromosome is evolving at a faster rate than the rest of the genome.
Chromosome breakage undetectable in active Mu lines of maize.
Authors: Rowland L J , Robertson D S , Strommer J 
Published: January 2021

Abstract
We have used a set of Mutator-induced mutants of Bz1 to test whether members of the Mutator (Mu) family of maize transposable elements produce broken chromosomes. From our inability to demonstrate the simultaneous loss of two dominant endosperm markers distal to Mu insertions at Bz1 we conclude that either Mu, unlike many elements of the Ds family, does not induce such breaks, or it does so at a very low frequency.
Nucleotide variation and divergence in the histone multigene family in Drosophila melanogaster.
Authors: Matsuo Y , Yamazaki T 
Published: January 2021

Abstract
Nucleotide differences in the histone H3 gene family in Drosophila melanogaster were studied on three levels: (1) within a chromosome, (2) within a population and (3) between species (D. melanogaster and Drosophila simulans). The average difference within the H3 gene within a chromosome was 0.0040 per nucleotide site, about 52% of that within a population (0.0077). The proportion of divergent sites between the two species was 0.0575, which is about 8.5 times the difference within a species. The distribution of divergence between species was similar to that of variation within a species. Divergence and variation were noted to be greatest in the 3' noncoding region and least in the coding region. Values intermediate between these were found for the 5' noncoding region. Divergence and variation in silent sites exceeded those in the total coding region, thus indicating possible purifying selection for amino-acid-altering change. Phylogenetic relations among H3 genes and genetic differences on these three levels are evidence for the concerted evolution of the histone gene family. The molecular mechanism by which variation is produced and maintained is discussed.
Genetic and physical mapping of the mcrA (rglA) and mcrB (rglB) loci of Escherichia coli K-12.
Authors: Raleigh E A , Trimarchi R , Revel H 
Published: January 2021

Abstract
We have genetically analyzed, cloned and physically mapped the modified cytosine-specific restriction determinants mcrA (rglA) and mcrB (rglB) of Escherichia coli K-12. The independently discovered Rgl and Mcr restriction systems are shown to be identical by three criteria: 1) mutants with the RglA- or RglB- phenotypes display the corresponding McrA- or McrB- phenotypes, and vice versa; 2) the gene(s) for RglA and McrA reside together at one locus, while gene(s) for RglB and McrB are coincident at a different locus; and 3) RglA+ and RglB+ recombinant clones complement for the corresponding Mcr-deficient lesions. The mcrA (rglA) gene(s) is on the excisable element e14, just clockwise of purB at 25 min. The mcrB (rglB) gene(s), at 99 min, is in a cluster of restriction functions that includes hsd and mrr, determinants of host-specific restriction (EcoK) and methyladenine-specific restriction respectively. Gene order is mcrB-hsdS-hsdM-hsdR-mrr-serB. Possible models for the acqusition of these restriction determinants by enteric bacteria are discussed.
Mutations in the Saccharomyces cerevisiae opi3 gene: effects on phospholipid methylation, growth and cross-pathway regulation of inositol synthesis.
Authors: McGraw P , Henry S A 
Published: January 2021

Abstract
We report the isolation of two new opi3 mutants by EMS mutagenesis, and construction of an insertion allele in vitro using the cloned gene. We have demonstrated that the opi3 mutations cause a deficiency in the two terminal phospholipid N-methyltransferase (PLMT) activities required for the de novo synthesis of PC (phosphatidylcholine). The opi3 mutants, under certain growth conditions, produce membrane virtually devoid of PC although, surprisingly, none of the mutants displays a strict auxotrophic requirement for choline. Although the opi3 mutants grow without supplements, we have shown that the atypical membrane affects the ability of the mutant strains to initiate log phase growth and to sustain viability at stationary phase. The commencement of log phase growth is enhanced by addition of choline or to a lesser extent DME (dimethylethanolamine), and retarded by addition of MME (monomethylethanolamine). The mutant cells lose viability at the stationary phase of the cell cycle in the absence of DME or choline, and are also temperature sensitive for growth at 37 degrees especially in media containing MME. These growth defects have been correlated to the presence of specific phospholipids in the membrane. The opi3 growth defects are suppressed by an unusual mutation in the phospholipid methylation pathway that perturbs the N-methyltransferase (PEMT) activity immediately preceding the reactions affected by the opi3 lesion. We believe this mutation, cho2-S, alters the substrate specificity of the PEMT. A secondary effect of opi3 mutations is disruption of the cross pathway regulation of the synthesis of the PI (phosphatidylinositol) precursor inositol. Synthesis of inositol is controlled through regulation of the INO1 gene which encodes inositol-1-phosphate synthase. This highly regulated gene is expressed constitutively in opi3 mutants. We have used the opi3 strains to demonstrate that synthesis of either PC or PD (phosphatidyldimethylethanolamine) will restore normal regulation of the INO1 gene.
gcd12 mutations are gcn3-dependent alleles of GCD2, a negative regulator of GCN4 in the general amino acid control of Saccharomyces cerevisiae.
Authors: Paddon C J , Hinnebusch A G 
Published: January 2021

Abstract
GCD12 encodes a translational repressor of the GCN4 protein, a transcriptional activator of amino acid biosynthetic genes in the yeast Saccharomyces cerevisiae. gcd12 mutations override the requirement for the GCN2 and GCN3 gene products for derepression of GCN4 expression, suggesting that GCN2 and GCN3 function indirectly as positive regulators by negative regulation of GCD12. In addition to their regulatory phenotype, gcd12 mutants are temperature-sensitive for growth (Tsm-) and, as shown here, deletion of the GCD12 gene is unconditionally lethal. Both the regulatory and the Tsm- phenotypes associated with gcd12 point mutations are completely overcome by wild-type GCN3, implying that GCN3 can promote or partially substitute for the functions of GCD12 in normal growth conditions even though it antagonizes GCD12 regulatory function in starvation conditions. The GCD12 gene has been cloned and mapped to the right arm of chromosome VII, very close to the map position reported for GCD2. We demonstrate that GCD12 and GCD2 are the same genes; however, unlike gcd12 mutations, the growth defect and constitutive derepression phenotypes associated with the gcd2-1 mutation are expressed in the presence of the wild-type GCN3 gene. These findings can be explained by either of two alternative hypotheses: (1) gcd12 mutations affect a domain of the GCD2 protein that directly interacts with GCN3, and complex formation stabilizes mutant gcd12 (but not gcd2-1) gene products; (2) gcd12 mutations selectively impair one function of GCD2 that is replaceable by GCN3, whereas gcd2-1 inactivates a different GCD2 function for which GCN3 cannot substitute. Both models imply a close interaction between these two positive and negative regulators in general amino acid control.
Extrachromosomal elements cause a reduced division potential in nib 1 strains of Saccharomyces cerevisiae.
Authors: Sweeney R , Zakian V A 
Published: January 2021

Abstract
The nib 1 allele of yeast confers a sensitivity to an endogenous plasmid, 2 mu DNA, in that nib 1 strains bearing 2 mu DNA (cir+) exhibit a reduction in division potential. In the present study, the reduction in division potential characteristic of nib 1 cir+ strains is shown to be dependent on the simultaneous presence of both the A and the D open reading frames of 2 mu DNA as well as on the presence of an unidentified extrachromosomal element other than 2 mu DNA. Furthermore, in nib 1 strains, an uncharacterized extrachromosomal element can cause a less severe reduction of division potential in the absence of intact 2 mu DNA. Thus, the nib 1 allele may confer a generalized sensitivity to extrachromosomal elements.
cdc2 and the regulation of mitosis: six interacting mcs genes.
Authors: Molz L , Booher R , Young P , Beach D 
Published: January 2021

Abstract
A cdc2-3w weel-50 double mutant of fission yeast displays a temperature-sensitive lethal phenotype that is associated with gross abnormalities of chromosome segregation and has been termed mitotic catastrophe. In order to identify new genetic elements that might interact with the cdc2 protein kinase in the regulation of mitosis, we have isolated revertants of the lethal double mutant. The suppressor mutations define six mcs genes (mcs: mitotic catastrophe suppressor) that are not allelic to any of the following mitotic control genes: cdc2, wee 1, cdc13, cdc25, suc1 or nim1. Each mcs mutation is recessive with respect to wild-type in its ability to suppress mitotic catastrophe. None confer a lethal phenotype as a single mutant but few of the mutants are expected to be nulls. A diverse range of genetic interactions between the mcs mutants and other mitotic regulators were uncovered, including the following examples. First, mcs2 cdc2w or mcs6 cdc2w double mutants display a cell cycle defect dependent on the specific wee allele of cdc2. Second, both mcs1 cdc25-22 or mcs4 cdc25-22 double mutants are nonconditionally lethal, even at a temperature normally permissive for cdc25-22. Finally, the characteristic suppression of the cdc25 phenotype by a loss-of-function wee1 mutation is reversed in a mcs3 mutant background. The mcs genes define new mitotic elements that might be activators or substrates of the cdc2 protein kinase.
Position effect variegation in Drosophila melanogaster: relationship between suppression effect and the amount of Y chromosome.
Authors: Dimitri P , Pisano C 
Published: January 2021

Abstract
Position effect variegation results from chromosome rearrangements which translocate euchromatic genes close to the heterochromatin. The euchromatin-heterochromatin association is responsible for the inactivation of these genes in some cell clones. In Drosophila melanogaster the Y chromosome, which is entirely heterochromatic, is known to suppress variegation of euchromatic genes. In the present work we have investigated the genetic nature of the variegation suppressing property of the D. melanogaster Y chromosome. We have determined the extent to which different cytologically characterized Y chromosome deficiencies and Y fragments suppress three V-type position effects: the Y-suppressed lethality, the white mottled and the brown dominant variegated phenotypes. We find that: (1) chromosomes which are cytologically different and yet retain similar amounts of heterochromatin are equally effective suppressors, and (2) suppression effect is positively related to the size of the Y chromosome deficiencies and fragments that we tested. It increases with increasing amounts of Y heterochromatin up to 60-80% of the entire Y, after which the effect reaches a plateau. These findings suggest suppression is a function of the amount of Y heterochromatin present in the genome and is not attributable to any discrete Y region.
The cloning of the Bar region and the B breakpoint in Drosophila melanogaster: evidence for a transposon-induced rearrangement.
Authors: Tsubota S I , Rosenberg D , Szostak H , Rubin D , Schedl P 
Published: January 2021

Abstract
We have cloned the B breakpoint in Drosophila melanogaster using DNA from a P-M-induced revertant of B, which has a P element inserted at the B breakpoint. The analysis of the B DNA reveals that there is a transposable element, B104, right at the breakpoint. This suggests that this element may have been involved in the generation of the B breakpoint and the associated tandem duplication. One possible mechanism to generate the B duplication is a recombination event between two B104 elements, one at 16A1 and the other at 16A7. DNA sequencing data of the junctions of the B104 element support this model. Four partial revertants of B are the result of insertions of transposable elements very close to the B breakpoint. This supports the hypothesis that the breakpoint is the cause of the B mutation. The clones from B were used to isolate wild-type clones from 16A1, the location of the Bar gene. Four rearrangement breakpoints associated with various Bar mutations map within a 37-kb region, suggesting that the Bar gene is very large.
Effects of mutation on selection limits in finite populations with multiple alleles.
Authors: Zeng Z B , Tachida H , Cockerham C C 
Published: January 2021

Abstract
The ultimate response to directional selection (i.e., the selection limit) under recurrent mutation is analyzed by a diffusion approximation for a population in which there are k possible alleles at a locus. The limit mainly depends on two scaled parameters S (= 4Ns sigma a) and theta (= 4Nu) and k, the number of alleles, where N is the effective population size, u is the mutation rate, s is the selection coefficient, and sigma 2a is the variance of allelic effects. When the selection pressure is weak (S less than or equal to 0.5), the limit is given approximately by 2S sigma a[1 - (1 + c2)/k]/(theta + 1) for additive effects of alleles, where c is the coefficient of variation of the mutation rates among alleles. For strong selection, other approximations are devised to analyze the limit in different parameter regions. The effect of mutation on selection limits largely relies on the potential of mutation to introduce new and better alleles into the population. This effect is, however, bounded under the present model. Unequal mutation rates among alleles tend to reduce the selection limit, and can have a substantial effect only for small numbers of alleles and weak selection. The selection limit decreases as the mutation rate increases.
Sexual transmission of transposed activator elements in transgenic tomatoes.
Authors: Belzile F , Lassner M W , Tong Y , Khush R , Yoder J I 
Published: January 2021

Abstract
The transmission of transposed Ac elements in progeny derived by self-pollination of ten transformed tomato plants has been examined by Southern hybridization analysis. We show that six of these primary transformants have transmitted a transposed Ac to at least one progeny. One of the families was segregating for at least two different insertion events. In five of ten families, progeny were detected that contained a transposed Ac but no donor T-DNA sequences, indicating that a recombination event occurred between the original and new Ac insertion site. Somatic transposition of Ac as late as the R2 generation is evidenced. One family contained an empty donor site fragment but Ac was not detected in either the parent or progeny, indicating Ac was lost in this population early in regeneration. While four of ten families were segregating for aberrant phenotypes, there was no evidence that the mutated gene was linked to a transposed Ac.
Pachytene arrest and other meiotic effects of the start mutations in Saccharomyces cerevisiae.
Authors: Shuster E O , Byers B 
Published: January 2021

Abstract
Mutations in the Start class of cell division cycle genes (CDC28, CDC36 and CDC39) define the point in the G1 phase of the vegetative cycle at which the cell becomes committed to completing another round of cell division. Genetic, cytological and biochemical data demonstrate that these mutations cause meiotic cells to become arrested at pachytene following completion of both chromosomal DNA replication and spindle pole body (SPB) duplication. In contrast these mutations have previously been found to cause arrest of the mitotic cell cycle prior to either of these landmark events, so the role of the Start genes in these events during vegetative growth must be indirect. Our observations are consistent with the hypothesis that CDC28, CDC36 and CDC39 are required for irreversible commitment to nuclear division in both the mitotic and meiotic pathways. CDC28 was additionally found to be required for the SPB separation that precedes spindle formation in preparation for the second meiotic division. Cytological and genetic analyses of this requirement revealed both that such separation may fail independently at either SPB and that ascospore formation can proceed independently of SPB separation.
Distribution of Chi-stimulated recombinational exchanges and heteroduplex endpoints in phage lambda.
Authors: Cheng K C , Smith G R 
Published: January 2021

Abstract
The recombination hotspot Chi, 5' G-C-T-G-G-T-G-G 3', stimulates the RecBCD recombination pathway of Escherichia coli. We have determined, with precision greater than previously reported, the distribution of Chi-stimulated exchanges around a Chi site in phage lambda. Crosses of lambda phages with single base-pair mutations surrounding a Chi site were conducted in and analyzed on mismatch correction-impaired hosts to preserve heteroduplex mismatches for analysis. Among phages recombinant for flanking markers, Chi stimulated exchanges most intensely in the intervals immediately adjacent to the Chi site, both to its right and to its left. Stimulation fell off abruptly to the right but gradually to the left (with respect to the orientation of the Chi sequence written above). We have also determined that Chi stimulated the formation of heteroduplex DNA, which frequently had one endpoint to the right of Chi and the other endpoint to the left. These data support a model of Chi-stimulated recombination in which RecBCD enzyme cuts DNA immediately to the right of Chi and unwinds DNA to the left of Chi; segments of unwound single-stranded DNA are sometimes, but not always, degraded before synapsis with homologous DNA.
A general screen for mutant of Saccharomyces cerevisiae deficient in tRNA biosynthesis.
Authors: van Zyl W H , Wills N , Broach J R 
Published: January 2021

Abstract
We have devised a general screen for isolating conditional lethal mutants defective in synthesis of mature tRNA in Saccharomyces cerevisiae. Using this screen, we have identified several new genes in yeast that are required for production of mature tRNA. These genes most likely encode essential functions, since the mutations we isolated are recessive and cause temperature-sensitive growth. One of the mutants, tpd3, is defective in de novo transcription of 4S RNA at the nonpermissive temperature. A second mutant, tpd1, is specifically defective in excision of intervening sequence from a variety of tRNA species. Finally, two other mutants are defective in production of tRNA from a suppressor tRNA locus, as measured by an in vitro suppression assay. The specific lesion in these strains, though, is not known. These data confirm that the screen does, in fact, yield a broad spectrum of mutants defective in tRNA maturation.
Interaction between the sbcC gene of Escherichia coli and the gam gene of phage lambda.
Authors: Kulkarni S K , Stahl F W 
Published: January 2021

Abstract
gam mutants of phage lambda carrying long palindromes fail to form plaques on wild-type Escherichia coli but do grow on strains that are mutant in the sbcC gene. gam + lambda carrying the same palindrome grow on both hosts and on a host deleted for the recB, C and D genes. These results suggest that the Gam protein of lambda, known to interact also with E. coli's recBCD protein, can interact with the product of the sbcC gene.