bluuebunny/crossref_metadata_2025_split huggingface dataset:
Redundant Roles for Histone H3 N-Terminal Lysine Residues in Subtelomeric Gene Repression in Saccharomyces cerevisiae
Authors: Martin Amy M , Pouchnik Derek J , Walker Jennifer L , Wyrick John J 
Published: August 2004

Abstract
The transcription of genes located in subtelomeric regions of yeast chromosomes is repressed relative to the rest of the genome. This repression requires wild-type nucleosome levels but not the telomere silencing factors Sir2, Sir3, Sir4, and Rap1. Subtelomeric heterochromatin is characterized by the absence of acetylation or methylation of histone H3 lysine residues, but it is not known whether histone H3 hypoacetylation or hypomethylation is a prerequisite for the establishment of subtelomeric heterochromatin. We have systematically mutated the N-terminal tails of histone H3 and H4 in Saccharomyces cerevisiae and characterized the effects each mutant has on genome-wide expression. Our results show that subtelomeric transcriptional repression is dependent on the histone H3 N-terminal domain, but not the histone H4 N-terminal domain. Mutating lysine-4, lysine-9, lysine-14, lysine-18, lysine-23, and lysine-27 to glycine in histone H3 is also sufficient to significantly reduce subtelomeric gene repression. Individual histone H3 lysine mutations, however, have little effect on subtelomeric gene repression or genome-wide expression, indicating that these six lysine residues have redundant functions. We propose that acetylation and methylation of histone H3 N-terminal lysine residues act as redundant mechanisms to demarcate regions of euchromatin from heterochromatin.
Comparative Evolutionary Histories of Chitinase Genes in the Genus Zea and Family PoaceaeSequence data from this article have been deposited with the EMBL/GenBank Data Libraries under accession nos. AY532721, AY532722, AY532723, AY532724, AY532725, AY532726, AY532727, AY532728, AY532729, AY532730, AY532731, AY532732, AY532733, AY532734, AY532735, AY532736, AY532737, AY532738, AY532739, AY532740, AY532741, AY532742, AY532743, AY532744, AY532745, AY532746, AY532747, AY532748, AY532749, AY532750, AY532751, AY532752, AY532753, AY532754, AY532755, AY532756, AY532757, AY532758, AY532759, AY532760, AY532761, AY532762, AY532763, AY532764, AY532765, AY532766, AY532767, AY532768, AY532769, AY532770, AY532771, AY532772, AY532773, AY532774, AY532775, AY532776, AY532777, AY532778, AY532779, AY532780, AY532781, AY532782, AY532783, AY532784, AY532785, AY532786, AY532787, AY532788.
Authors: Tiffin Peter 
Published: August 2004

Abstract
Patterns of DNA sequence diversity vary widely among genes encoding proteins that protect plants against pathogens and herbivores. Comparative studies may help determine whether these differences are due to the strength of selection acting on different types of defense, in different evolutionary lineages, or both. I analyzed sequence diversity at three chitinases, a well-studied component of defense, in two species of Zea and several Poaceae taxa. Although the Zea species are closely related and these genes code for proteins with similar biochemical function, patterns of diversity vary widely within and among species. Intraspecific diversity at chiB, chiI, and Z. mays ssp. parviglumis chiA are consistent with a neutral-equilibrium model whereas chiA had no segregating sites within Z. diploperennis—consistent with a recent and strong selective sweep. Codons identified as having diverged among Poaceae taxa in response to positive selection were significantly overrepresented among targets of selection in Arabis, suggesting common responses to selection in distantly related plant taxa. Divergence of the recent duplicates chiA and chiB is consistent with positive selection but relaxed constraint cannot be rejected. Weak evidence for adaptive divergence of these duplicated downstream components of defense contrasts with strong evidence for adaptive divergence of genes involved in pathogen recognition.
The Mod(mdg4) Component of the Su(Hw) Insulator Inserted in the P Transposon Can Repress Its Mobility in Drosophila melanogaster
Authors: Karakozova Marina , Savitskaya Ekaterina , Melnikova Larisa , Parshikov Aleksandr , Georgiev Pavel 
Published: August 2004

Abstract
Transposable element P of Drosophila melanogaster is one of the best-characterized eukaryotic transposons. Successful transposition requires the interaction between transposase complexes at both termini of the P element. Here we found that insertion of one or two copies of the Su(Hw) insulator in the P transposon reduces the frequency of its transposition. Inactivation of a Mod(mdg4) component of the Su(Hw) insulator suppresses the insulator effect. Thus, the Su(Hw) insulator can modulate interactions between transposase complexes bound to the ends of the P transposon in germ cells.
Requirement for Sex Comb on Midleg Protein Interactions in Drosophila Polycomb Group Repression
Authors: Peterson Aidan J , Mallin Daniel R , Francis Nicole J , Ketel Carrie S , Stamm Joyce , Voeller Rochus K , Kingston Robert E , Simon Jeffrey A 
Published: August 2004

Abstract
The Drosophila Sex Comb on Midleg (SCM) protein is a transcriptional repressor of the Polycomb group (PcG). Although genetic studies establish SCM as a crucial PcG member, its molecular role is not known. To investigate how SCM might link to PcG complexes, we analyzed the in vivo role of a conserved protein interaction module, the SPM domain. This domain is found in SCM and in another PcG protein, Polyhomeotic (PH), which is a core component of Polycomb repressive complex 1 (PRC1). SCM-PH interactions in vitro are mediated by their respective SPM domains. Yeast two-hybrid and in vitro binding assays were used to isolate and characterize &gt;30 missense mutations in the SPM domain of SCM. Genetic rescue assays showed that SCM repressor function in vivo is disrupted by mutations that impair SPM domain interactions in vitro. Furthermore, overexpression of an isolated, wild-type SPM domain produced PcG loss-of-function phenotypes in flies. Coassembly of SCM with a reconstituted PRC1 core complex shows that SCM can partner with PRC1. However, gel filtration chromatography showed that the bulk of SCM is biochemically separable from PH in embryo nuclear extracts. These results suggest that SCM, although not a core component of PRC1, interacts and functions with PRC1 in gene silencing.
Isolation and Gene Expression Analysis of Arabidopsis thaliana Mutants With Constitutive Expression of ATL2, an Early Elicitor-Response RING-H2 Zinc-Finger GeneThis article is dedicated to the memory of the late Gilberto Mosqueda Cano.
Authors: Serrano Mario , Guzmán Plinio 
Published: August 2004

Abstract
Genes with unstable transcripts often encode proteins that play important regulatory roles. ATL2 is a member of a multigene family coding highly related RING-H2 zinc-finger proteins that may function as E3 ubiquitin ligases. ATL2 mRNA accumulation occurs rapidly and transiently after incubation with elicitors of pathogen response. We screened 50,000 M2 families from a line that carries a fusion of pATL2 to the GUS reporter gene and isolated five mutants, which we named eca (expresión constitutiva de ATL2), that showed constitutive expression of the reporter gene. One mutant exhibits a drastic stunted phenotype while the other four grow similarly to wild type. Two early chitin-induced genes and known pathogenesis-related genes such as NPR1, PAL, and CHS are activated in all the mutants whereas members of the ATL family and PR-1 and PDF2.1, which are markers of the salicylic acid (SA) jasmonate (JA) defense-response pathways, display differential expression between the mutants. These observations indicate that the ECA gene products may function in the early steps of an elicitor-response pathway, although some of them may function at other stages on the SA or JA defense-response pathways. Likewise, the fact that ATL2 and other members of the ATL family are activated in eca mutants links the induction of this putative class of ubiquitin ligases to plant defense signaling pathways.
Defects Arising From Whole-Genome Duplications in Saccharomyces cerevisiae
Authors: Andalis Alex A , Storchova Zuzana , Styles Cora , Galitski Timothy , Pellman David , Fink Gerald R 
Published: August 2004

Abstract
Comparisons among closely related species have led to the proposal that the duplications found in many extant genomes are the remnants of an ancient polyploidization event, rather than a result of successive duplications of individual chromosomal segments. If this interpretation is correct, it would support Ohno's proposal that polyploidization drives evolution by generating the genetic material necessary for the creation of new genes. Paradoxically, analysis of contemporary polyploids suggests that increased ploidy is an inherently unstable state. To shed light on this apparent contradiction and to determine the effects of nascent duplications of the entire genome, we generated isogenic polyploid strains of the budding yeast Saccharomyces cerevisiae. Our data show that an increase in ploidy results in a marked decrease in a cell's ability to survive during stationary phase in growth medium. Tetraploid cells die rapidly, whereas isogenic haploids remain viable for weeks. Unlike haploid cells, which arrest growth as unbudded cells, tetraploid cells continue to bud and form mitotic spindles in stationary phase. The stationary-phase death of tetraploids can be prevented by mutations or conditions that result in growth arrest. These data show that whole-genome duplications are accompanied by defects that affect viability and subsequent survival of the new organism.
Does Random X-Inactivation in Mammals Reflect a Random Choice Between Two X Chromosomes?
Authors: Williams Benjamin R , Wu Chao-ting 
Published: August 2004

Abstract
Inactivation of the maternal or paternal X chromosome in a mammalian embryonic XX cell is believed to involve random choice between the two X's. We propose two alternative models. One suggests that choice is not random, while the other is consistent with random choice, but not one between two X's.
Introducing Student Inquiry in Large Introductory Genetics Classes
Authors: Pukkila Patricia J 
Published: August 2004

Abstract
An appreciation of genetic principles depends upon understanding the individual curiosity that sparked particular investigations, the creativity involved in imagining alternative outcomes and designing experiments to eliminate these outcomes, and the clarity of thought necessary to convince one's scientific peers of the validity of the conclusions. At large research universities, students usually begin their study of genetics in large lecture classes. It is widely assumed that the lecture format, coupled with the pressures to be certain that students become familiar with the principal conclusions of genetics investigations, constrains most if not all departures from the formats textbooks used to explain these conclusions. Here I present several examples of mechanisms to introduce meaningful student inquiry in an introductory genetics course and to evaluate student creative effort. Most of the examples involve altered student preparation prior to class and additional in-class activities, while a few depend upon a smaller recitation section, which accompanies the course from which the examples have been drawn. I conclude that large introductory classes are suitable venues to teach students how to identify scientific claims, determine the evidence that is essential to eliminate alternative conclusions, and convince their peers of the validity of their arguments.
The Podospora rmp1 Gene Implicated in Nucleus-Mitochondria Cross-Talk Encodes an Essential Protein Whose Subcellular Location Is Developmentally Regulated
Authors: Contamine Véronique , Zickler Denise , Picard Marguerite 
Published: August 2004

Abstract
It has been previously reported that, at the time of death, the Podospora anserina AS1-4 mutant strains accumulate specific deleted forms of the mitochondrial genome and that their life spans depend on two natural alleles (variants) of the rmp1 gene: AS1-4 rmp1-2 strains exhibit life spans strikingly longer than those of AS1-4 rmp1-1. Here, we show that rmp1 is an essential gene. In silico analyses of eight rmp1 natural alleles present in Podospora isolates and of the putative homologs of this orphan gene in other filamentous fungi suggest that rmp1 evolves rapidly. The RMP1 protein is localized in the mitochondrial and/or the cytosolic compartment, depending on cell type and developmental stage. Strains producing RMP1 without its mitochondrial targeting peptide are viable but exhibit vegetative and sexual defects.
sel-7, a Positive Regulator of lin-12 Activity, Encodes a Novel Nuclear Protein in Caenorhabditis elegans
Authors: Chen Jiabin , Li Xiajun , Greenwald Iva 
Published: August 2004

Abstract
Suppressor genetics in C. elegans has identified key components of the LIN-12/Notch signaling pathway. Here, we describe a genetic and molecular characterization of the suppressor gene sel-7. We show that reducing or eliminating sel-7 activity suppresses the effects of constitutive lin-12 activity, enhances the effects of partially reduced lin-12 activity, and causes a synthetic Lin-12(0) phenotype when combined with a null mutation in the sel-12 presenilin gene. These observations suggest that sel-7 is a positive regulator of lin-12 activity. We also show that SEL-7 encodes a novel nuclear protein. Through yeast two-hybrid screening, we identified an apparent interaction partner, K08E3.8, that also interacts with SEL-8, a known component of the nuclear complex that forms upon LIN-12 activation. Our data suggest potential roles for SEL-7 in the assembly or function of this nuclear complex.
eat-2 and eat-18 Are Required for Nicotinic Neurotransmission in the Caenorhabditis elegans Pharynx
Authors: McKay James P , Raizen David M , Gottschalk Alexander , Schafer William R , Avery Leon 
Published: August 2004

Abstract
Mutations in eat-2 and eat-18 cause the same defect in C. elegans feeding behavior: the pharynx is unable to pump rapidly in the presence of food. EAT-2 is a nicotinic acetylcholine receptor subunit that functions in the pharyngeal muscle. It is localized to the synapse between pharyngeal muscle and the main pharyngeal excitatory motor neuron MC, and it is required for MC stimulation of pharyngeal muscle. eat-18 encodes a small protein that has no homology to previously characterized proteins. It has a single transmembrane domain and a short extracellular region. Allele-specific genetic interactions between eat-2 and eat-18 suggest that EAT-18 interacts physically with the EAT-2 receptor. While eat-2 appears to be required specifically for MC neurotransmission, eat-18 also appears to be required for the function of other nicotinic receptors in the pharynx. In eat-18 mutants, the gross localization of EAT-2 at the MC synapse is normal, suggesting that it is not required for trafficking. These data indicate that eat-18 could be a novel component of the pharyngeal nicotinic receptor.
The sys-1 and sys-3 Genes Cooperate With Wnt Signaling to Establish the Proximal-Distal Axis of the Caenorhabditis elegans Gonad
Authors: Siegfried Kellee R , Kidd Ambrose R , Chesney Michael A , Kimble Judith 
Published: August 2004

Abstract
To form the proximal-distal axis of the C. elegans gonad, two somatic gonadal precursor cells, Z1 and Z4, divide asymmetrically to generate one daughter with a proximal fate and one with a distal fate. Genes governing this process include the lin-17 frizzled receptor, wrm-1/β-catenin, the pop-1/TCF transcription factor, lit-1/nemo-like kinase, and the sys-1 gene. Normally, all of these regulators promote the distal fate. Here we show that nuclear levels of a pop-1 GFP fusion protein are less abundant in the distal than in the proximal Z1/Z4 daughters. This POP-1 asymmetry is lost in mutants disrupting Wnt/MAPK regulation, but retained in sys-1 mutants. We find that sys-1 is haplo-insufficient for gonadogenesis defects and that sys-1 and pop-1 mutants display a strong genetic interaction in double heterozygotes. Therefore, sys-1 is a dose-sensitive locus and may function together with pop-1 to control Z1/Z4 asymmetry. To identify other regulatory genes in this process, we screened for mutants resembling sys-1. Four such genes were identified (gon-14, -15, -16, and sys-3) and shown to interact genetically with sys-1. However, only sys-3 promotes the distal fate at the expense of the proximal fate. We suggest that sys-3 is a new key gene in this pathway and that gon-14, gon-15, and gon-16 may cooperate with POP-1 and SYS-1 at multiple stages of gonad development.
A Mosaic Genetic Screen Reveals Distinct Roles for trithorax and Polycomb Group Genes in Drosophila Eye Development
Authors: Janody Florence , Lee Jeffrey D , Jahren Neal , Hazelett Dennis J , Benlali Aude , Miura Grant I , Draskovic Irena , Treisman Jessica E 
Published: August 2004

Abstract
The wave of differentiation that traverses the Drosophila eye disc requires rapid transitions in gene expression that are controlled by a number of signaling molecules also required in other developmental processes. We have used a mosaic genetic screen to systematically identify autosomal genes required for the normal pattern of photoreceptor differentiation, independent of their requirements for viability. In addition to genes known to be important for eye development and to known and novel components of the Hedgehog, Decapentaplegic, Wingless, Epidermal growth factor receptor, and Notch signaling pathways, we identified several members of the Polycomb and trithorax classes of genes encoding general transcriptional regulators. Mutations in these genes disrupt the transitions between zones along the anterior-posterior axis of the eye disc that express different combinations of transcription factors. Different trithorax group genes have very different mutant phenotypes, indicating that target genes differ in their requirements for chromatin remodeling, histone modification, and coactivation factors.
Knockouts of Kekkon1 Define Sequence Elements Essential for Drosophila Epidermal Growth Factor Receptor Inhibition
Authors: Alvarado Diego , Rice Amy H , Duffy Joseph B 
Published: August 2004

AbstractThroughout development, cells utilize feedback inhibition of receptor tyrosine kinase (RTK) signaling as an important means to direct cellular fates. In Drosophila, epidermal growth factor receptor (EGFR) activity is tightly regulated by a complex array of autoregulatory loops, involving an assortment of inhibitory proteins. One inhibitor, the transmembrane protein Kekkon1 (Kek1) functions during oogenesis in a negative feedback loop to directly attenuate EGFR activity. Kek1 contains both leucine-rich repeats (LRRs) and an immunoglobulin (Ig) domain, two of the most prevalent motifs found within metazoan genomes. Here we demonstrate that Kek1 inhibits EGFR activity during eye development and use this role to identify kek1 loss-of-function mutations that implicate the LRRs in directing receptor inhibition. Using a GMR-GAL4, UAS kek1-GFP misexpression phenotype we isolated missense mutations in the kek1 transgene affecting its ability to inhibit EGFR signaling. Genetic, molecular, and biochemical characterization of these alleles indicated that they represent two functionally distinct classes. Class I alleles directly diminish Kek1's affinity for EGFR, while class II alleles disrupt Kek1's subcellular localization, thereby indirectly affecting its ability to associate with and inhibit the receptor. All class I alleles map to the first and second LRRs of Kek1, suggesting a primary role for these two repeats in specifying association with and inhibition of EGFR. Last, our analysis implicates glycine 160 of the second LRR in regulating EGFR binding.
The P Cytotype in Drosophila melanogaster: A Maternally Transmitted Regulatory State of the Germ Line Associated With Telomeric P Elements
Authors: Simmons Michael J , Raymond John D , Niemi Jarad B , Stuart Jeremy R , Merriman Peter J 
Published: August 2004

Abstract
The incomplete P elements TP5 and TP6 are inserted in the TAS repeats near the left telomere of the Drosophila melanogaster X chromosome. These telomeric P elements repress P-induced gonadal dysgenesis and germ-line hypermutability in both sexes. However, their capacity to repress hypermutability is lost when they are transmitted patroclinously in a cross. TP5 and TP6 do not repress P-element activity in somatic cells, nor do they alter the somatic or germ-line phenotypes of P-insertion alleles. In the germ line, these elements suppress the phenotype of a P-insertion allele of the singed gene that is evoked by other P elements, presumably because these other elements encode repressor polypeptides. This suppression is more effective when the telomeric P elements are inherited maternally. Regulation by telomeric P elements parallels that of the P cytotype, a state that represses P-element activity in some strains of Drosophila. This state exists only in the germ line and is maternally transmitted along with the P elements themselves. Regulation by known repressor P polypeptides is not restricted to the germ line and does not require maternal transmission of the relevant P elements. Regulation by telomeric P elements appears to be epistatic to regulation by repressor P polypeptides.
Strong Positive Selection and Recombination Drive the Antigenic Variation of the PilE Protein of the Human Pathogen Neisseria meningitidis
Authors: Andrews T Daniel , Gojobori Takashi 
Published: August 2004

Abstract
The PilE protein is the major component of the Neisseria meningitidis pilus, which is encoded by the pilE/pilS locus that includes an expressed gene and eight homologous silent fragments. The silent gene fragments have been shown to recombine through gene conversion with the expressed gene and thereby provide a means by which novel antigenic variants of the PilE protein can be generated. We have analyzed the evolutionary rate of the pilE gene using the nucleotide sequence of two complete pilE/pilS loci. The very high rate of evolution displayed by the PilE protein appears driven by both recombination and positive selection. Within the semivariable region of the pilE and pilS genes, recombination appears to occur within multiple small sequence blocks that lie between conserved sequence elements. Within the hypervariable region, positive selection was identified from comparison of the silent and expressed genes. The unusual gene conversion mechanism that operates at the pilE/pilS locus is a strategy employed by N. meningitidis to enhance mutation of certain regions of the PilE protein. The silent copies of the gene effectively allow “parallelized” evolution of pilE, thus enabling the encoded protein to rapidly explore a large area of sequence space in an effort to find novel antigenic variants.