bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selection in ContextSequence data from this article have been deposited with the EMBL/GenBank Data Libraries under accession nos. AF016760, AF016761, AF016762, AF016763, AF016764, AF016765, AF016766, AF016767, AF016768, AF016769, AF016770, AF016771, AF016772, AF016773, AF016774, AF016775, AF016776, AF016777, AF016778, AF016779, AF016780, AF016781, AF016782, AF016783, AF016784, AF016785, AF016786, AF016787, AF016788, AF016789, AF016790, AF016791, AF016792, AF016793, AF016794, AF016795, AF016796, AF016797, AF016798, AF016799, AF016800, AF016801, AF016802, AF016803, AF016804, AF016805, AF016806, AF016807, AF016808, AF016809, AF016810, AF016811, AF016812, AF016813, AF016814, AF016815, AF016816, AF016817, AF016818, AF016819, AF016820, AF016821, AF016822, AF016823, AF016824, AF016825 and AF089109, AF089708.
Authors: Templeton Alan R , Reichert Rebecca A , Weisstein Anton E , Yu Xiao-Fang , Markham Richard B 
Published: September 2004

Abstract
Evolution of the HIV-1 V3 loop was monitored in 15 subjects over a period of 5 years at ∼6-month intervals. Putative recombination was detected in many of the sequences. Evolutionary trees were estimated from the nonrecombinant viral sequences found in each individual. Selection and altered demographic regimes were detected with logit and other contingency analyses in a highly context-dependent fashion. Mutations leading to amino acid substitutions are subject to positive selection over a broad range of clinical conditions in the nonsyncytium-inducing (NSI) form, and the growth rates of the NSI strains and their level of genetic subdivision change little in going from a healthy immune system to a severely compromised immune system. In contrast, the SI form has a significant increase in growth rate as the immune system goes from healthy to compromised, particularly in those subjects who did not receive any antiviral drug therapy. This increase in SI growth rate results in a significant growth advantage of SI over NSI when the immune system is compromised. The SI strains also show more demographic subdivision when the immune system is healthy than when the immune system is compromised, and the SI form has greater demographic subdivision than NSI in subjects with healthy immune systems who also are not receiving antiviral drug therapy. Positive selection on amino-acid-changing mutations weakens and then intensifies again in the SI strains in going from healthy to compromised immune systems. These patterns are consistent with other studies that suggest that NSI strains inhibit replication of SI strains, that the V3 loop is more hidden from the immune system in the NSI form, that evolution in the V3 loop influences cell tropism and coreceptor usage, that substrate for replication of SI forms increases as the disease progresses, and that death of CD8 cells is influenced by the type of coreceptor usage typically found in SI but not in NSI strains. Finally, the transition between NSI and SI forms is associated with a burst of evolutionary change due to strong positive selection at sites other than those that define the NSI/SI phenotypes.
The Aspergillus nidulans npkA Gene Encodes a Cdc2-Related Kinase That Genetically Interacts With the UvsBATR KinaseSequence data from this article have been deposited with the NCBI under accession no. AY166593.
Authors: Fagundes Marcia R V Z Kress , Lima Joel Fernandes , Savoldi Marcela , Malavazi Iran , Larson Roy E , Goldman Maria H S , Goldman Gustavo H 
Published: September 2004

Abstract
The DNA damage response is a protective mechanism that ensures the maintenance of genomic integrity. We have used Aspergillus nidulans as a model system to characterize the DNA damage response caused by the antitopoisomerase I drug, camptothecin. We report the molecular characterization of a p34Cdc2-related gene, npkA, from A. nidulans. The npkA gene is transcriptionally induced by camptothecin and other DNA-damaging agents, and its induction in the presence of camptothecin is dependent on the uvsBATR gene. There were no growth defects, changes in developmental patterns, increased sensitivity to DNA-damaging agents, or effects on septation or growth rate in the A. nidulans npkA deletion strain. However, the ΔnpkA mutation can partially suppress HU sensitivity caused by the ΔuvsBATR and uvsD153ATRIP checkpoint mutations. We demonstrated that the A. nidulans uvsBATR gene is involved in DNA replication and the intra-S-phase checkpoints and that the ΔnpkA mutation can suppress its intra-S-phase checkpoint deficiency. There is a defect in both the intra-S-phase and DNA replication checkpoints due to the npkA inactivation when DNA replication is slowed at 6 mm HU. Our results suggest that the npkA gene plays a role in cell cycle progression during S-phase as well as in a DNA damage signal transduction pathway in A. nidulans.
Translating Available Food Into the Number of Eggs Laid by Drosophila melanogaster
Authors: Terashima Jun , Bownes Mary 
Published: September 2004

AbstractIn Drosophila and other insects egg production is related to the nutrients available. Somehow the nutritional status of the environment is translated into hormonal signs that can be “read” by each individual egg chamber, influencing the decision to either develop into an egg or die. We have shown that BR-C is a control gene during oogenesis and that the differential expression of BR-C isoforms plays a key role in controlling whether the fate of the egg chamber is to develop or undergo apoptosis.
Intralocus Sexual Conflict Can Drive the Evolution of Genomic Imprinting
Authors: Day Troy , Bonduriansky Russell 
Published: September 2004

AbstractGenomic imprinting is a phenomenon whereby the expression of an allele differs depending upon its parent of origin. There is an increasing number of examples of this form of epigenetic inheritance across a wide range of taxa, and imprinting errors have also been implicated in several human diseases. Various hypotheses have been put forward to explain the evolution of genomic imprinting, but there is not yet a widely accepted general hypothesis for the variety of imprinting patterns observed. Here a new evolutionary hypothesis, based on intralocus sexual conflict, is proposed. This hypothesis provides a potential explanation for much of the currently available empirical data, and it also makes new predictions about patterns of genomic imprinting that are expected to evolve but that have not, as of yet, been looked for in nature. This theory also provides a potential mechanism for the resolution of intralocus sexual conflict in sexually selected traits and a novel pathway for the evolution of sexual dimorphism.
Transposition of Reversed Ac Element Ends Generates Chromosome Rearrangements in Maize
Authors: Zhang Jianbo , Peterson Thomas 
Published: September 2004

Abstract
In classical “cut-and-paste” transposition, transposons are excised from donor sites and inserted at new locations. We have identified an alternative pathway in which transposition involves the 5′ end of an intact Ac element and the 3′ end of a nearby terminally deleted fAc (fractured Ac). The Ac and fAc elements are inserted at the maize p1 locus on chromosome 1s in the same orientation; the adjacent ends of the separate elements are thus in reversed orientation with respect to each other and are separated by a distance of ∼13 kb. Transposition involving the two ends in reversed orientation generates inversions, deletions, and a novel type of local rearrangement. The rearrangement breakpoints are bounded by the characteristic footprint or target site duplications typical of Ac transposition reactions. These results demonstrate a new intramolecular transposition mechanism by which transposons can greatly impact genome evolution.
Mapping of Multiple Quantitative Trait Loci Affecting Bovine Spongiform Encephalopathy
Authors: Zhang Chi , de Koning Dirk-Jan , Hernández-Sánchez Jules , Haley Chris S , Williams John L , Wiener Pamela 
Published: September 2004

AbstractA whole-genome scan was conducted to map quantitative trait loci (QTL) for BSE resistance or susceptibility. Cows from four half-sib families were included and 173 microsatellite markers were used to construct a 2835-cM (Kosambi) linkage map covering 29 autosomes and the pseudoautosomal region of the sex chromosome. Interval mapping by linear regression was applied and extended to a multiple-QTL analysis approach that used identified QTL on other chromosomes as cofactors to increase mapping power. In the multiple-QTL analysis, two genome-wide significant QTL (BTA17 and X/Yps) and four genome-wide suggestive QTL (BTA1, 6, 13, and 19) were revealed. The QTL identified here using linkage analysis do not overlap with regions previously identified using TDT analysis. One factor that may explain the disparity between the results is that a more extensive data set was used in the present study. Furthermore, methodological differences between TDT and linkage analyses may affect the power of these approaches.
Extensive Sex-Specific Nonadditivity of Gene Expression in Drosophila melanogaster
Authors: Gibson Greg , Riley-Berger Rebecca , Harshman Larry , Kopp Artyom , Vacha Scott , Nuzhdin Sergey , Wayne Marta 
Published: September 2004

Abstract
Assessment of the degree to which gene expression is additive and heritable has important implications for understanding the maintenance of variation, adaptation, phenotypic divergence, and the mapping of genotype onto phenotype. We used whole-genome transcript profiling using Agilent long-oligonucleotide microarrays representing 12,017 genes to demonstrate that gene transcription is pervasively nonadditive in Drosophila melanogaster. Comparison of adults of two isogenic lines and their reciprocal F1 hybrids revealed 5820 genes as significantly different between at least two of the four genotypes in either males or females or across both sexes. Strikingly, while 25% of all genes differ between the two parents, 33% differ between both F1's and the parents, averaged across sexes. However, only 5% of genes show overdominance, suggesting that heterosis for expression is rare.
Enhancer Choice in Cis and in Trans in Drosophila melanogaster
Authors: Morris James R , Petrov Dmitri A , Lee Anne M , Wu Chao-ting 
Published: September 2004

Abstract
Eukaryotic enhancers act over very long distances, yet still show remarkable specificity for their own promoter. To better understand mechanisms underlying this enhancer-promoter specificity, we used transvection to analyze enhancer choice between two promoters, one located in cis to the enhancer and the other in trans to the enhancer, at the yellow gene of Drosophila melanogaster. Previously, we demonstrated that enhancers at yellow prefer to act on the cis-linked promoter, but that mutation of core promoter elements in the cis-linked promoter releases enhancers to act in trans. Here, we address the mechanism by which these elements affect enhancer choice. We consider and explicitly test three models that are based on promoter competency, promoter pairing, and promoter identity. Through targeted gene replacement of the endogenous yellow gene, we show that competency of the cis-linked promoter is a key parameter in the cis-trans choice of an enhancer. In fact, complete replacement of the yellow promoter with both TATA-containing and TATA-less heterologous promoters maintains enhancer action in cis.
A Single-Amino-Acid Change of the Gustatory Receptor Gene, Gr5a, Has a Major Effect on Trehalose Sensitivity in a Natural Population of Drosophila melanogaster
Authors: Inomata Nobuyuki , Goto Hiroki , Itoh Masanobu , Isono Kunio 
Published: September 2004

Abstract
Variation in trehalose sensitivity and nucleotide sequence polymorphism of the Gr5a gene encoding the gustatory receptor to sugar trehalose were investigated in 152 male lines of Drosophila melanogaster collected from a natural population. Among the observed 59 segregating sites, some pairs of sites showed significant linkage disequilibrium. A single SNP, which results in the Ala218Thr amino acid change, was significantly associated with trehalose sensitivity, as previously suggested. Threonine at amino acid position 218 was found to be the ancestral form in D. melanogaster, suggesting that low trehalose sensitivity was an ancestral form with respect to the receptor function. There was large genetic variation in trehalose sensitivity. It was continuously distributed, indicating that trehalose sensitivity measured by the behavioral assay is a quantitative trait. These results suggest that apart from the Gr5a gene, other genetic factors contribute to variation in trehalose sensitivity. Nucleotide diversity (π) and nucleotide variation (θ) per site were 0.00874 and 0.00590, respectively. Fu and Li's test and the MK test showed no significant departure from the expectation of selective neutrality in the Gr5a gene. However, we rejected selective neutrality by Tajima's test and Fay and Wu's test with the observed level of recombination. We discuss possible causes of the observed pattern of nucleotide variation in the gustatory receptor Gr5a gene.
The Speed of Adaptation in Large Asexual Populations
Authors: Wilke Claus O 
Published: September 2004

Abstract
In large asexual populations, beneficial mutations have to compete with each other for fixation. Here, I derive explicit analytic expressions for the rate of substitution and the mean beneficial effect of fixed mutations, under the assumptions that the population size N is large, that the mean effect of new beneficial mutations is smaller than the mean effect of new deleterious mutations, and that new beneficial mutations are exponentially distributed. As N increases, the rate of substitution approaches a constant, which is equal to the mean effect of new beneficial mutations. The mean effect of fixed mutations continues to grow logarithmically with N. The speed of adaptation, measured as the change of log fitness over time, also grows logarithmically with N for moderately large N, and it grows double-logarithmically for extremely large N. Moreover, I derive a simple formula that determines whether at given N beneficial mutations are expected to compete with each other or go to fixation independently. Finally, I verify all results with numerical simulations.
Dynamical Analysis of Regulatory Interactions in the Gap Gene System of Drosophila melanogaster
Authors: Jaeger Johannes , Blagov Maxim , Kosman David , Kozlov Konstantin N ,   Manu, Myasnikova Ekaterina , Surkova Svetlana , Vanario-Alonso Carlos E , Samsonova Maria , Sharp David H , Reinitz John 
Published: September 2004

Abstract
Genetic studies have revealed that segment determination in Drosophila melanogaster is based on hierarchical regulatory interactions among maternal coordinate and zygotic segmentation genes. The gap gene system constitutes the most upstream zygotic layer of this regulatory hierarchy, responsible for the initial interpretation of positional information encoded by maternal gradients. We present a detailed analysis of regulatory interactions involved in gap gene regulation based on gap gene circuits, which are mathematical gene network models used to infer regulatory interactions from quantitative gene expression data. Our models reproduce gap gene expression at high accuracy and temporal resolution. Regulatory interactions found in gap gene circuits provide consistent and sufficient mechanisms for gap gene expression, which largely agree with mechanisms previously inferred from qualitative studies of mutant gene expression patterns. Our models predict activation of Kr by Cad and clarify several other regulatory interactions. Our analysis suggests a central role for repressive feedback loops between complementary gap genes. We observe that repressive interactions among overlapping gap genes show anteroposterior asymmetry with posterior dominance. Finally, our models suggest a correlation between timing of gap domain boundary formation and regulatory contributions from the terminal maternal system.
A piggyBac Transposon Gene Trap for the Analysis of Gene Expression and Function in Drosophila
Authors: Bonin Christopher P , Mann Richard S 
Published: September 2004

Abstract
P-element-based gene and enhancer trap strategies have provided a wealth of information on the expression and function of genes in Drosophila melanogaster. Here we present a new vector that utilizes the simple insertion requirements of the piggyBac transposon, coupled to a splice acceptor (SA) site fused to the sequence encoding enhanced green fluorescent protein (EGFP) and a transcriptional terminator. Mobilization of the piggyBac splice site gene trap vector (PBss) was accomplished by heat-shock-induced expression of piggyBac transposase (PBase). We show that insertion of PBss into genes leads to fusions between the gene's mRNA and the PBss-encoded EGFP transcripts. As heterozygotes, these fusions report the normal pattern of expression of the trapped gene. As homozygotes, these fusions can inactivate the gene and lead to lethality. Molecular characterization of PBss insertion events shows that they are single copy, that they always occur at TTAA sequences, and that splicing utilizes the engineered splice site in PBss. In those instances where protein-EGFP fusions are predicted to occur, the subcellular localization of the wild-type protein can be inferred from the localization of the EGFP fusion protein. These experiments highlight the utility of the PBss system for expanding the functional genomics tools that are available in Drosophila.
Genetic Suppression of Intronic +1G Mutations by Compensatory U1 snRNA Changes in Caenorhabditis elegans
Authors: Zahler Alan M , Tuttle John D , Chisholm Andrew D 
Published: September 2004

Abstract
Mutations to the canonical +1G of introns, which are commonly found in many human inherited disease alleles, invariably result in aberrant splicing. Here we report genetic findings in C. elegans that aberrant splicing due to +1G mutations can be suppressed by U1 snRNA mutations. An intronic +1G-to-U mutation, e936, in the C. elegans unc-73 gene causes aberrant splicing and loss of gene function. We previously showed that mutation of the sup-39 gene promotes splicing at the mutant splice donor in e936 mutants. We demonstrate here that sup-39 is a U1 snRNA gene; suppressor mutations in sup-39 are compensatory substitutions in the 5′ end, which enhance recognition of the mutant splice donor. sup-6(st19) is an allele-specific suppressor of unc-13(e309), which contains an intronic +1G-to-A transition. The e309 mutation activates a cryptic splice site, and sup-6(st19) restores splicing to the mutant splice donor. sup-6 also encodes a U1 snRNA and the mutant contains a compensatory substitution at its 5′ end. This is the first demonstration that U1 snRNAs can act to suppress the effects of mutations to the invariant +1G of introns. These findings are suggestive of a potential treatment of certain alleles of inherited human genetic diseases.
The ULTRAPETALA1 Gene Functions Early in Arabidopsis Development to Restrict Shoot Apical Meristem Activity and Acts Through WUSCHEL to Regulate Floral Meristem Determinacy
Authors: Carles Cristel C , Lertpiriyapong Kvin , Reville Keira , Fletcher Jennifer C 
Published: September 2004

Abstract
Shoot and floral meristem activity in higher plants is controlled by complex signaling networks consisting of positive and negative regulators. The Arabidopsis ULTRAPETALA1 (ULT1) gene has been shown to act as a negative regulator of meristem cell accumulation in inflorescence and floral meristems, as loss-of-function ult1 mutations cause inflorescence meristem enlargement, the production of extra flowers and floral organs, and a decrease in floral meristem determinacy. To investigate whether ULT1 functions in known meristem regulatory pathways, we generated double mutants between ult1 alleles and null alleles of the meristem-promoting genes SHOOTMERISTEMLESS (STM) and WUSCHEL (WUS). We found that, although the ult1 alleles have no detectable embryonic or vegetative phenotypes, ult1 mutations restored extensive organ-forming capability to stm null mutants after germination and increased leaf and floral organ production in stm partial loss-of-function mutants. Mutations in ULT1 also partially suppressed the wus shoot and floral meristem phenotypes. However, wus was epistatic to ult1 in the center of the flower, and WUS transcriptional repression was delayed in ult1 floral meristems. Our results show that during the majority of the Arabidopsis life cycle, ULT1 acts oppositely to STM and WUS in maintaining meristem activity and functions in a separate genetic pathway. However, ULT1 negatively regulates WUS to establish floral meristem determinacy, acting through the WUS-AG temporal feedback loop.
A Genomic Basis for the Evolution of Vertebrate Transcription Factors Containing Amino Acid Runs
Authors: Caburet Sandrine , Vaiman Daniel , Veitia Reiner A 
Published: September 2004

Abstract
We have previously shown that polyAla (A) tract-containing proteins frequently present runs of glycine (G), proline (P), and histidine (H) and that, in their ORFs, GC content at all codon positions is higher than that in the rest of the genome. In this study, we present new analyses of these human proteins/ORFs. We detected striking differences in codon usage for A, G, and P in and out of runs. After dividing the ORFs, we found that 5′ halves were richer in runs than 3′ halves. Afterward, when removing the runs, we observed that the run-rich halves (grouped irrespectively of their 5′ or 3′ position) had a marked statistical tendency to have more homo- and hetero-dicodons for A, G, P, and H than the run-poor halves. This suggests that, in addition to the necessary GC-rich genomic background, a specific codon organization is probably required to generate these coding repeats. Homo-dicodons may indeed provide primers for run formation through polymerase slippage. The compositional analysis of human HOX genes, the most polyAla-rich family, and their comparison with their zebrafish homologs, support these hypotheses and suggest possible effects of genomic environment on ORF evolution and organismal diversification.
The High-Mobility Group A-Type Protein CarD of the Bacterium Myxococcus xanthus as a Transcription Factor for Several Distinct Vegetative GenesSequence data from this article have been deposited with the EMBL/GenBank Data Libraries under accession nos. AJ505751, AJ505752, AJ505753, and AJ505849.
Authors: Galbis-Martínez Marisa , Fontes Marta , Murillo Francisco J 
Published: September 2004

AbstractCarD is the only reported prokaryotic protein showing structural and functional features typical of eukaryotic high-mobility group A transcription factors. In prokaryotes, proteins similar to CarD appear to be confined primarily to myxobacteria. In Myxococcus xanthus, CarD has been previously shown to act as a positive element in two different regulatory networks: one for light-induced synthesis of carotenoids and the other for starvation-induced fruiting body formation. We have now tested the effect of a loss-of-function mutation in the carD gene (carD1) on the expression of a random collection of lacZ-tagged genes, which are normally expressed in the dark during vegetative growth in rich medium. Our results indicate that CarD plays a significant role in the transcriptional regulation of various indicated genes. The carD1 mutation downregulates some genes and upregulates others. Also reported here is the isolation of several mutations that suppress the strong effect of carD1 on the expression of a particular vegetative gene. One of them (sud-2) also suppresses the effect of carD1 on other vegetative genes and on fruiting-body formation. Thus, CarD and the sud-2 gene product appear to participate in a single mechanism, which underlies various apparently diverse regulatory phenomena ascribed to CarD.