bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Influence of Genes on the Aging Process of Mice
Authors: de Magalhães João Pedro , Cabral José A S , Magalhães Domingos 
Published: October 2004

AbstractGenetic interventions that accelerate or retard aging in mice are crucial in advancing our knowledge over mammalian aging. Yet determining if a given intervention affects the aging process is not straightforward since, for instance, many disease-causing mutations may decrease life span without affecting aging. In this work, we employed the Gompertz model to determine whether several published interventions previously claimed to affect aging in mice do indeed alter the aging process. First, we constructed age-specific mortality tables for a number of mouse cohorts used in longevity experiments and calculated the rate at which mortality increases with age. Estimates of age-independent mortality were also calculated. We found no statistical evidence that GHRHR, IGF1R, INSR, PROP1, or TRX delay or that ATM + TERC, BubR1, klotho, LMNA, PRDX1, p53, WRN + TERC, or TOP3B accelerate mouse aging. Often, changes in the expression of these genes affected age-independent mortality and so they may prove useful to other aspects of medicine. We found statistical evidence that C/EBP, MSRA, SHC1, growth hormone, GHR, PIT1, and PolgA may influence aging in mice. These results were interpreted together with age-related physiological and pathological changes and provide novel insights regarding the role of several genes in the mammalian aging process.
Mutations That Rescue the Paralysis of Caenorhabditis elegans ric-8 (Synembryn) Mutants Activate the Gαs Pathway and Define a Third Major Branch of the Synaptic Signaling Network
Authors: Schade Michael A , Reynolds Nicole K , Dollins Claudia M , Miller Kenneth G 
Published: October 2004

Abstract
To identify hypothesized missing components of the synaptic Gαo-Gαq signaling network, which tightly regulates neurotransmitter release, we undertook two large forward genetic screens in the model organism C. elegans and focused first on mutations that strongly rescue the paralysis of ric-8(md303) reduction-of-function mutants, previously shown to be defective in Gαq pathway activation. Through high-resolution mapping followed by sequence analysis, we show that these mutations affect four genes. Two activate the Gαq pathway through gain-of-function mutations in Gαq; however, all of the remaining mutations activate components of the Gαs pathway, including Gαs, adenylyl cyclase, and protein kinase A. Pharmacological assays suggest that the Gαs pathway-activating mutations increase steady-state neurotransmitter release, and the strongly impaired neurotransmitter release of ric-8(md303) mutants is rescued to greater than wild-type levels by the strongest Gαs pathway activating mutations. Using transgene induction studies, we show that activating the Gαs pathway in adult animals rapidly induces hyperactive locomotion and rapidly rescues the paralysis of the ric-8 mutant. Using cell-specific promoters we show that neuronal, but not muscle, Gαs pathway activation is sufficient to rescue ric-8(md303)'s paralysis. Our results appear to link RIC-8 (synembryn) and a third major Gα pathway, the Gαs pathway, with the previously discovered Gαo and Gαq pathways of the synaptic signaling network.
Characterization of AFLP Sequences From Regions of Maize B Chromosome Defined by 12 B-10L TranslocationsSequence data from this article have been deposited with the GenBank Data Libraries under accession nos. CL603055, CL603056, CL603057, CL603058, CL603059, CL603060, CL603061, CL603062, CL603063, CL603064, CL603065, CL603066, CL603067, CL603068, CL603069, CL603070.
Authors: Peng Shu-Fen , Lin Yao-Pin , Lin Bor-yaw 
Published: October 2004

Abstract
Maize B chromosome sequences have been previously cloned by microdissection, and all are proven to be highly repetitive, to be homologous to the normal complement, and to show no similarity to any published gene other than mobile elements. In this study, we isolated sequences from defined B regions. The strategy involved identification and then mapping of AFLP-derived B fragments before cloning. Of 14 B AFLPs, 13 were mapped by 12 B-10L translocations: 3 around the centromeric knob region, 3 in the proximal euchromatic, 1 around the border of proximal euchromatic and distal heterochromatic, and 6 in the distal heterochromatic region of the B long arm. The AFLP fragments were cloned and sequenced. Analogous to the microdissected sequences, all sequences were repetitive, and all but two were highly homologous to the A chromosomes. FISH signals of all but three clones appeared in pachytene B as well as in somatic A and B chromosomes. None of these clones exhibits identity to any published gene. Six clones displayed homology to two centromeric BACs, four to sequences of chromosomes 3, 4, 7, and 10, four to retrotransposons, and three to no sequence deposited in GenBank. Furthermore, flanking regions of two highly B-specific clones were characterized, showing extension of a B-exclusive nature. The possibility of the presence of novel B repeat(s) is discussed.
High-Resolution Mapping of the Drosophila Fourth Chromosome Using Site-Directed Terminal Deficiencies
Authors: Sousa-Neves Rui , Lukacsovich Tamas , Mizutani Claudia Mieko , Locke John , Podemski Lynn , Marsh J Lawrence 
Published: October 2004

Abstract
For more than 80 years, the euchromatic right arm of the Drosophila fourth chromosome (101F-102F) has been one of the least genetically accessible regions of the fly genome despite the fact that many important genes reside there. To improve the mapping of genes on the fourth chromosome, we describe a strategy to generate targeted deficiencies and we describe 13 deficiencies that subdivide the 300 kb between the cytological coordinates 102A6 and 102C1 into five discrete regions plus a 200-kb region from 102C1 to 102D6. Together these deficiencies substantially improve the mapping capabilities for mutant loci on the fourth chromosome.
Sperm Competitive Ability in Drosophila melanogaster Associated With Variation in Male Reproductive Proteins
Authors: Fiumera Anthony C , Dumont Bethany L , Clark Andrew G 
Published: October 2004

Abstract
Multiple mating by females establishes the opportunity for postcopulatory sexual selection favoring males whose sperm is preferentially employed in fertilizations. Here we use natural variation in a wild population of Drosophila melanogaster to investigate the genetic basis of sperm competitive ability. Approximately 101 chromosome 2 substitution lines were scored for components of sperm competitive ability (P1′, P2′, fecundity, remating rate, and refractoriness), genotyped at 70 polymorphic markers in 10 male reproductive genes, and measured for transcript abundance of those genes. Permutation tests were applied to quantify the statistical significance of associations between genotype and phenotype. Nine significant associations were identified between polymorphisms in the male reproductive genes and sperm competitive ability and 13 were identified between genotype and transcript abundance, but no significant associations were found between transcript abundance and sperm competitive ability. Pleiotropy was evident in two genes: a polymorphism in Acp33A associated with both P1′ and P2′ and a polymorphism in CG17331 associated with both elevated P2′ and reduced refractoriness. The latter case is consistent with antagonistic pleiotropy and may serve as a mechanism maintaining genetic variation.
Nonadditive Gene Expression in Diploid and Triploid Hybrids of Maize
Authors: Auger Donald L , Gray Anjali Dogra , Ream Thomas S , Kato Akio , Coe Edward H , Birchler James A 
Published: October 2004

Abstract
The molecular basis of hybrid vigor (heterosis) has remained unknown despite the importance of this phenomenon in evolution and in practical breeding programs. To formulate a molecular basis of heterosis, an understanding of gene expression in inbred and hybrid states is needed. In this study, we examined the amount of various transcripts in hybrid and inbred individuals (B73 and Mo17) to determine whether the quantities of specific messenger RNAs were additive or nonadditive in the hybrids. Further, we examined the levels of the same transcripts in hybrid triploid individuals that had received unequal genomic contributions, one haploid genome from one parent and two from the other. If allelic expression were merely the additive value in hybrids from the two parents, the midparent values would be observed. Our study revealed that a substantial number of genes do not exhibit the midparent value of expression in hybrids. Instead, transcript levels in the diploid hybrids correlate negatively with the levels in diploid inbreds. Although transcript levels were clearly nonadditive, transcript levels in triploid hybrids were affected by genomic dosage.
A Mutation With Major Effects on Drosophila melanogaster Sex Pheromones
Authors: Marcillac Fabrice , Bousquet François , Alabouvette Josiane , Savarit Fabrice , Ferveur Jean-François 
Published: October 2004

Abstract
Sex pheromones are intraspecific chemical signals that are crucial for mate attraction and discrimination. In Drosophila melanogaster, the predominant hydrocarbons on the cuticle of mature female and male flies are radically different and tend to stimulate or inhibit male courtship, respectively. This sexual difference depends largely upon the number of double bonds (one in males and two in females) added by desaturase enzymes. A mutation was caused by a PGal4 transposon inserted in the desat1 gene that codes for the desaturase crucial for setting these double bonds. Homozygous mutant flies produced 70–90% fewer sex pheromones than control flies, and the pheromonal difference between the sexes was almost abolished. A total of 134 excision alleles were induced by pulling out all or a part of the transposon. The pheromonal profile was generally rescued in excision alleles with a completely or largely removed transposon whereas it remained mutant in alleles with a larger piece of the transposon. Five desat1 transcripts were detected during larval-to-adult development. Their levels were precisely quantified in 24-hr-old adults, a critical period for the production of sex pheromones. Three transcripts significantly varied between control females and males; however, the predominant transcript showed no difference. In mutant flies, the predominant transcript was highly decreased with the two sexually dimorphic transcripts.These two transcripts were also absent in the sibling species D. simulans, which shows no sexually dimorphic hydrocarbons. We also induced a larval-lethal allele that lacked all transcripts and failed to complement the defective hydrocarbon phenotype of mutant alleles.
The Meiotic Recombination Hot Spot ura4A in Schizosaccharomyces pombe
Authors: Baur Michel , Hartsuiker Edgar , Lehmann Elisabeth , Ludin Katja , Munz Peter , Kohli Juerg 
Published: October 2004

Abstract
The meiotic recombination hot spot ura4A (formerly ura4-aim) of Schizosaccharomyces pombe was observed at the insertion of the ura4+ gene 15 kb centromere-proximal to ade6 on chromosome III. Crosses heterozygous for the insertion showed frequent conversion at the heterology with preferential loss of the insertion. This report concerns the characterization of 12 spontaneous ura4A mutants. A gradient of conversion ranging from 18% at the 5′ end to 6% at the 3′ end was detected. A novel phenomenon also was discovered: a mating-type-related bias of conversion. The allele entering with the h+ parent acts preferentially as the acceptor for conversion (ratio of 3:2). Tetrad analysis of two-factor crosses showed that heteroduplex DNA is predominantly asymmetrical, enters from the 5′ end, and more often than not covers the entire gene. Restoration repair of markers at the 5′ end was inferred. Random spore analyses of two-factor crosses and normalization of prototroph-recombinant frequencies to physical distance led to the demonstration of map expansion: Crosses involving distant markers yielded recombinant frequencies higher than the sum of the frequencies measured in the subintervals. Finally, marker effects on recombination were defined for two of the ura4A mutations.
Mss11p Is a Central Element of the Regulatory Network That Controls FLO11 Expression and Invasive Growth in Saccharomyces cerevisiae
Authors: van Dyk Dewald , Pretorius Isak S , Bauer Florian F 
Published: October 2004

Abstract
The invasive and filamentous growth forms of Saccharomyces cerevisiae are adaptations to specific environmental conditions, under particular conditions of limited nutrient availability. Both growth forms are dependent on the expression of the FLO11 gene, which encodes a cell-wall-associated glycoprotein involved in cellular adhesion. A complex regulatory network consisting of signaling pathways and transcription factors has been associated with the regulation of FLO11. Mss11p has been identified as a transcriptional activator of this gene, and here we present an extensive genetic analysis to identify functional relationships between Mss11p and other FLO11 regulators. The data show that Mss11p is absolutely required for the activation of FLO11 by most proteins that have previously been shown to affect FLO11 expression, including the signaling proteins Ras2p, Kss1p, and Tpk2p, the activators Tec1p, Flo8p, and Phd1p, and the repressors Nrg1p, Nrg2p, Sok2p, and Sfl1p. The genetic evidence furthermore suggests that Mss11p activity is not dependent on the presence of any of the above-mentioned factors and that the protein also regulates other genes involved in cellular adhesion phenotypes. Taken together, the data strongly suggest a central role for Mss11p in the regulatory network controlling FLO11 expression, invasive growth, and pseudohyphal differentiation.
Genetic Evidence for a Regulatory Pathway Controlling Alternative Oxidase Production in Neurospora crassa
Authors: Descheneau Andrea T , Cleary Ian A , Nargang Frank E 
Published: October 2004

Abstract
When the cytochrome-mediated mitochondrial electron transport chain of Neurospora crassa is disrupted, an alternative oxidase encoded by the nuclear aod-1 gene is induced. The alternative oxidase donates electrons directly to oxygen from the ubiquininol pool and is insensitive to chemicals such as antimycin A and KCN that affect the standard electron transport chain. To facilitate isolation of mutants affecting regulation of aod-1, a reporter system containing the region upstream of the aod-1 coding sequence fused to the coding sequence of the N. crassa tyrosinase gene (T) was transformed into a strain carrying a null allele of the endogenous T gene. In the resulting reporter strain, growth in the presence of chloramphenicol, an inhibitor of mitochondrial translation whose action decreases the level of mitochondrial translation products resulting in impaired cytochrome-mediated respiration, caused induction of both alternative oxidase and tyrosinase. Conidia from the reporter strain were mutagenized, plated on medium containing chloramphenicol, and colonies that did not express tyrosinase were identified as potential regulatory mutants. After further characterization, 15 strains were found that were unable to induce both the reporter and the alternative oxidase. Complementation analysis revealed that four novel loci involved in aod-1 regulation had been isolated. The discovery that several genes are required for regulation of aod-1 suggests the existence of a complex pathway for signaling from the mitochondria to the nucleus and/or for expression of the gene.
Mapping a Syntenic Modifier on Mouse Chromosome 1 Influencing the Expressivity of the Compact Phenotype in the Myostatin Mutant (MstnCmpt-dl1Abc) Compact Mouse
Authors: Varga László , Pinke Orsolya , Müller Géza , Kovács Balázs , Korom Edit , Szabó Gyula , Soller Morris 
Published: October 2004

Abstract
A novel method for mapping a modifier gene that is syntenic to its major gene was used to map a male-sex-limited modifier of the expressivity of the Compact phenotype in the myostatin mutant (MstnCmpt-dl1Abc) Compact mouse. The modifier was mapped to the general region of D1Mit262, 40 cM distal to Mstn on chromosome 1. Myogenin, a postulated downstream target of myostatin, maps to the same region.
A Screen for Schizosaccharomyces pombe Mutants Defective in Rereplication Identifies New Alleles of rad4+, cut9+ and psf2+
Authors: Gómez Eliana B , Angeles Vanessa T , Forsburg Susan L 
Published: October 2004

Abstract
Fission yeast mutants defective in DNA replication have widely varying morphological phenotypes. We designed a screen for temperature-sensitive mutants defective in the process of replication regardless of morphology by isolating strains unable to rereplicate their DNA in the absence of cyclin B (Cdc13). Of the 42 rereplication-defective mutants analyzed, we were able to clone complementing plasmids for 10. This screen identified new alleles of the APC subunit cut9+, the initiation/checkpoint factor rad4+/cut5+, and the first mutant allele of psf2+, a subunit of the novel GINS replication complex. Other genes identified are likely to play general roles in gene expression and protein localization.
How the Rgt1 Transcription Factor of Saccharomyces cerevisiae Is Regulated by Glucose
Authors: Polish Jeffrey A , Kim Jeong-Ho , Johnston Mark 
Published: October 2004

Abstract
Rgt1 is a transcription factor that regulates expression of HXT genes encoding glucose transporters in the yeast Saccharomyces cerevisiae. Rgt1 represses HXT gene expression in the absence of glucose; high levels of glucose cause Rgt1 to activate expression of HXT1. We identified four functional domains of Rgt1. A domain required for transcriptional repression (amino acids 210–250) is required for interaction of Rgt1 with the Ssn6 corepressor. Another region of Rgt1 (320–380) is required for normal transcriptional activation, and sequences flanking this region (310–320 and 400–410) regulate this function. A central region (520–830) and a short sequence adjacent to the zinc cluster DNA-binding domain (80–90) inhibit transcriptional repression when glucose is present. We found that this middle region of Rgt1 physically interacts with the N-terminal portion of the protein that includes the DNA-binding domain. This interaction is inhibited by the Rgt1 regulator Mth1, which binds to Rgt1. Our results suggest that Mth1 promotes transcriptional repression by Rgt1 by binding to it and preventing the intramolecular interaction, probably by preventing phosphorylation of Rgt1, thereby enabling Rgt1 to bind to DNA. Glucose induces HXT1 gene expression by causing Mth1 degradation, allowing Rgt1 phosphorylation, and leading to the intramolecular interaction that inhibits DNA binding of Rgt1.
Structure and Evolution of the r/b Chromosomal Regions in Rice, Maize and SorghumSequence data from this article have been deposited with the EMBL/GenBank Data Libraries under accession nos. AY542311, AF466202, AF466203, and AY542310.
Authors: Swigoňová Zuzana , Bennetzen Jeffrey L , Messing Joachim 
Published: October 2004

Abstract
The r1 and b1 genes of maize, each derived from the chromosomes of two progenitors that hybridized &gt;4.8 million years ago (MYA), have been a rich source for studying transposition, recombination, genomic imprinting, and paramutation. To provide a phylogenetic context to the genetic studies, we sequenced orthologous regions from maize and sorghum (&gt;600 kb) surrounding these genes and compared them with the rice genome. This comparison showed that the homeologous regions underwent complete or partial gene deletions, selective retention of orthologous genes, and insertion of nonorthologous genes. Phylogenetic analyses of the r/b genes revealed that the ancestral gene was amplified independently in different grass lineages, that rice experienced an intragenomic gene movement and parallel duplication, that the maize r1 and b1 genes are descendants of two divergent progenitors, and that the two paralogous r genes of sorghum are almost as old as the sorghum lineage. Such sequence mobility also extends to linked genes. The cisZOG genes are characterized by gene amplification in an ancestral grass, parallel duplications and deletions in different grass lineages, and movement to a nonorthologous position in maize. In addition to gene mobility, both maize and rice regions experienced recent transposition (&lt;3 MYA).
A Genetic Linkage Map of the Mimetic ButterflyHeliconius melpomene
Authors: Jiggins Chris D , Mavarez Jesus , Beltrán Margarita , McMillan W Owen , Johnston J Spencer , Bermingham Eldredge 
Published: October 2004

AbstractHeliconius melpomene is a mimetic butterfly that exhibits great geographic variation in color pattern. We present here a genetic linkage map based on analysis of genetic markers in 73 individuals from a single F2 family, offspring of a cross between H. m. cythera from western Ecuador and H. m. melpomene from French Guiana. A novel “three-step method” is described for the analysis of dominant markers in an F2 cross, using outbred parental strains and taking advantage of the lack of crossing over in female Lepidoptera. This method is likely to prove useful for future mapping studies in outbred species with crossing over restricted to one sex, such as the Lepidoptera and Drosophila. The resulting linkage map has 21 linkage groups corresponding to the 21 chromosomes of H. melpomene and includes 219 AFLP markers, 23 microsatellites, 19 single-copy nuclear genes, and the color pattern switch genes Yb and Sb. The marker density is high, averaging &gt;1/7 cM. The total map length is 1616 cM and the average chromosome length is 77 cM. The genome size of H. melpomene was estimated to be 292 Mb, giving a relationship of physical-to-map distance of 180 kb/cM. This map forms the basis for future comparative linkage analysis of color pattern evolution in Heliconius.
On the Evolution of Codon Volatility
Authors: Zhang Jianzhi 
Published: October 2004

Abstract
Volatility of a codon is defined as the probability that a random point mutation in the codon generates a nonsynonymous change. It has been proposed that higher-than-expected mean codon volatility of a gene indicates that positive selection for nonsynonymous changes has acted on the gene in the recent past. I show that strong frequency-dependent selection (minority advantage) in large populations can increase codon volatility slightly, whereas directional positive selection has no effect on volatility. Factors unrelated to positive selection, such as expression-related or GC-content-related codon usage bias, also affect volatility. These and other considerations suggest that codon volatility has only limited utility for detecting positive selection at the DNA sequence level.