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At least 703 records · Page 39Linked to original sources
PubMed2003

The Rtf1 component of the Paf1 transcriptional elongation complex is required for ubiquitination of histone H2B.

In yeast cells, the Rtf1 and Paf1 components of the Paf1 transcriptional elongation complex are important for recruitment of Set1, the histone H3-lysine 4 (H3-Lys4) methylase, to a highly localized domain at the 5' portion of active mRNA coding regions. Here, we show that Rtf1 is essential for global methylation of H3-Lys4 and H3-Lys79, but not H3-Lys36. This role of Rtf1 resembles that of Rad6, which mediates ubiquitination of histone H2B at lysine 123. Indeed, Rtf1 is required for H2B ubiquitination, suggesting that its effects on H3-Lys4 and H3-Lys79 methylation are an indirect consequence of its effect on H2B ubiquitination. Rtf1 is important for telomeric silencing, with loss of H3-Lys4 and H3-Lys79 methylation synergistically reducing Sir2 association with telomeric DNA. Dot1, the H3-Lys79 methylase, associates with transcriptionally active genes, but unlike the association of Set1 and Set2 (the H3-Lys36 methylase), this association is largely independent of Rtf1. We suggest that Rtf1 affects genome-wide ubiquitination of H2B by a mechanism that is distinct from its function as a transcriptional elongation factor.

Blotting, Western↗
PubMed2026

A GWAS-derived histone H4 variant linked to ear row number reveals functional insights into the maize ZmHistone gene family.

Ear row number (ERN) is a major yield determinant in maize and a key target for breeding of high-yielding varieties. This study utilized a multi-parent population (MPP) of 780 recombinant inbred lines (RILs) derived from seven inbred lines across three environments. Genotyping-by-sequencing (GBS) of the MPP yielded 638,646 high-quality SNPs. Using genome-wide association study (GWAS), we detected 80 significant SNPs including S2-15316355 and S4-224453431, which were consistently detected in all environments and best linear unbiased prediction (BLUP) analysis. A linkage disequilibrium-defined ±20 kb window around these two lead SNPs contained three positional candidate genes: Zm00001eb072840, Zm00001eb072850 and Zm00001eb202890. Zm00001eb072850 (ZmHistone12), a histone H4 variant, was prioritized for hypothesis-driven follow-up because the lead SNP lies within its coding sequence and the gene is expressed in ear-related tissues. Additionally, we identified 91 ZmHistone genes in the maize genome and described their phylogeny, promoter motif and expression patterns. Public transcriptome and qRT-PCR analysis in seven parental lines provide descriptive evidence of Histone variant genes in maize ear development. These results suggest a potential involvement of chromatin-associated regulation of ERN in maize and provide a foundation for future functional validation.

Ear development↗
PubMed2006

The nucleosome: a little variation goes a long way.

Changes in the overall structure of chromatin are essential for the proper regulation of cellular processes, including gene activation and silencing, DNA repair, chromosome segregation during mitosis and meiosis, X chromosome inactivation in female mammals, and chromatin compaction during apoptosis. Such alterations of the chromatin template occur through at least 3 interrelated mechanisms: post-translational modifications of histones, ATP-dependent chromatin remodeling, and the incorporation (or replacement) of specialized histone variants into chromatin. Of these mechanisms, the exchange of variants into and out of chromatin is the least well understood. However, the exchange of conventional histones for variant histones has distinct and profound consequences within the cell. This review focuses on the growing number of mammalian histone variants, their particular biological functions and unique features, and how they may affect the structure of the nucleosome. We propose that a given nucleosome might not consist of heterotypic variants, but rather, that only specific histone variants come together to form a homotypic nucleosome, a hypothesis that we refer to as the nucleosome code. Such nucleosomes might in turn participate in marking specific chromatin domains that may contribute to epigenetic inheritance.

Animals↗
PubMed1989

Nucleotide sequence of the Stp-1 gene coding for rat spermatid nuclear transition protein 1 (TP1): homology with protamine P1 and assignment of the mouse Stp-1 gene to chromosome 1.

Spermatid transition protein 1 (TP1) is a 54 amino acid (aa), highly basic chromosomal protein found in mammals during the brief period when histones are being replaced by protamines in the haploid phase of spermatogenesis. Using a cDNA clone as probe, we have isolated the gene (Stp-1) coding for rat TP1 from a population of recombinant bacteriophage lambda. The nucleotide (nt) sequence was established from a point 126 nt upstream from the mRNA cap site to a point about 30 nt downstream from the predicted site of polyadenylation. The gene contains a single intron separating the codon for aa 45 of the mature protein. Comparison of the nucleotide sequences for Stp-1 and the mouse gene coding for protamine P1 suggests a possible evolutionary relationship. Southern blot hybridization to genomic DNA isolated from a panel of mouse-hamster somatic cell hybrids unambiguously mapped Stp-1 to mouse chromosome 1.

Amino Acid Sequence↗
PubMed2000

Spermatogenesis in mice is not affected by histone H1.1 deficiency.

The linker histone subtype H1.1 belongs to the group of main-type histones and is synthesized in somatic tissues as well as in germ cells during the S phase of the cell cycle. In adult mice the histone gene H1.1 is expressed mainly in thymus, spleen, and testis. The single-copy gene coding for the H1.1 protein was eliminated by homologous recombination in mouse embryonic stem cells. Mice homozygous for the deficient H1.1 gene developed normally until the adult stage without H1.1 mRNA and H1.1 protein. No anatomic abnormalities could be detected. In addition, mice lacking the H1.1 gene were fertile and they showed normal spermatogenesis and testicular morphology.

Animals↗
PubMed2006

Cross-species clues of an epigenetic imprinting regulatory code for the IGF2R gene.

The epigenetic marks on the IGF2R gene that encodes a receptor responsible for IGF-II degradation consist of differentially methylated DNA in association with multiple modifications on the associated histones. We review these epigenetic marks across various species during the evolution of IGF2R imprinting. Both IGF2 and IGF2R genesare imprinted in the mammal lineage that diverged from Monotremata approximately 150 million years ago. While IGF2 is consistently imprinted in all mammals following its divergence, IGF2R imprinting disappears in the Euarchonta lineage, including human species, approximately 75 million years ago. Differential DNA methylation marks on the two parental alleles correlate with imprinting in all imprinted genes including IGF2R. While the DNA methylation marks in the IGF2R promoter region 1 (DMR1) correlate with IGF2R allelic expression, the DNA methylation marks in the intron region 2 (DMR2) fail to correlate with IGF2R imprinting status in a number of species. Human IGF2R and mouse neuronal Igf2r are not imprinted despite the presence of DMR2. We have noted that human IGF2R is not imprinted in more than 100 informative samples including various tumor tissues. Furthermore, opossum (Marsupialia) IGF2R is consistently imprinted despite the absence of DMR2. These lines of evidence indicate that DNA methylation marks in DMR2 are neither necessary nor sufficient for consistent imprinting of IGF2R across species. Histone modification marks, however, correlate more consistently with the tissue-specific and species-specific imprinting status of IGF2R in human and mouse. Acetylated histone H3 and H4 and methylated lysine 4 of H3 (H3-K4Me) associate with transcriptionally active alleles while tri-methylated lysine 9 of H3 (H3-K9Me3) marks the silenced alleles. In the mouse, an antisense non-coding transcript called Air is transcribed from DMR2 on the paternal allele, and this imprinted transcript plays a central role in Igf2r imprinting. Mouse Igf2r imprinting depends on an Air RNA while the existence of AIR in other species is unknown. Overall, DNA methylation, histone acetylation, and histone methylation play a vital role in coordinating IGF2R allelic expression across all species. Rare monoallelic or skewed allelic expression of human IGF2R and their biological importance warrants further rigorous study.

Animals↗
PubMed1990

Chromosomal localization of the human protamine genes, PRM1 and PRM2, to 16p13.3 by in situ hybridization.

Protamines are sperm-specific proteins that replace histones in the nuclear chromatin of mature spermatozoa. A chromosomal localization of the genes coding for human protamines has been achieved by in situ hybridization. Two cDNA probes of 423 bp and 397 bp containing the entire coding sequence for human protamine 1 (HP1) and human protamine 2 (HP2), respectively, have been used. The genes, called PRM1 and PRM2, have been found, tightly linked, on band 16p13.3. Arguments are given for the existence of these two genes as single copies, PRM1 coding for the unique HP1 protamine and PRM2 coding for a precursor of several proteins belonging to the HP2 family.

Chromosome Banding↗
PubMed1991

Systematic characterization of curved DNA segments randomly cloned from Escherichia coli and their functional significance.

In addition to the set of curved DNA segments isolated previously from Escherichia coli, another set of curved DNA segments has now been isolated. To gain an insight into the functional significance of these curved DNA sequences, systematic analyses were carried out, which included not only mapping of the precise locations of the segments on the E. coli chromosome but also clarification of the gene organization in the chromosomal regions surrounding the curved DNA sequences. It was demonstrated that most of the curved DNA sequences, which have been characterized so far, appear to be located immediately upstream of the coding sequences of adjacent genes. It was also demonstrated that an E. coli histone-like protein, named H-NS (or H1a), exhibits a strong affinity for naturally occurring curved DNA sequences in regions upstream promoters.

Bacterial Proteins↗
PubMed2006

Combinatorial epigenetics, "junk DNA", and the evolution of complex organisms.

At certain evolutionary junctures, two or more mutations participating in the build-up of a new complex function may be required to become available simultaneously in the same individuals. How could this happen in higher organisms whose populations are small compared to those of microbes, and in which chances of combined nearly simultaneous highly specific favorable mutations are correspondingly low? The question can in principle be answered for regulatory evolution, one of the basic processes of evolutionary change. A combined resetting of transcription rates in several genes could occur in the same individual. It is proposed that, in eukaryotes, changes in epigenetic trends and epigenetically transforming encounters between alternative chromatin structures could arise frequently enough so as to render probable particular conjunctions of changed transcription rates. Such conjunctions could involve mutational changes with low specificity requirements in gene-associated regions of non-protein-coding sequences. The effects of such mutations, notably when they determine the use of histone variants and covalent modifications of histones, can be among those that migrate along chromatin. Changes in chromatin structure are often cellularly inheritable over at least a limited number of generations of cells, and of individuals when the germ line is involved. SINEs and LINEs, which have been considered "junk DNA", are among the repeat sequences that would appear liable to have teleregulatory effects on the function of a nearby promoter, through changes in their numbers and distribution. There may also be present preexisting unstably inheritable epigenetic trends leading to cellular variegation, trends endemic in a cell population based on DNA sequences previously established in the neighborhood. Either way, epigenetically conditioned teleregulatory trends may display only limited penetrance. The imposition at a distance of new chromatin structures with regulatory impact can occur in cis as well as in trans, and is examined as intrachromosomally spreading teleregulation and interchromosomal "gene kissing". The chances for two or more particular epigenetically determined regulatory trends to occur together in a cell are increased thanks to the proposed low specificity requirements for most of the pertinent sequence changes in intergenic and intronic DNA or in the distribution of middle repetitive sequences that have teleregulatory impact. Inheritable epigenetic changes ("epimutations") with effects at a distance would then perdure over the number of generations required for "assimilation" of the several regulatory novelties through the occurrence and selection, gene by gene, of specific classical mutations. These mutations would have effects similar to the epigenetic effects, yet would provide stability and penetrance. The described epigenetic/genetic partnership may well at times have opened the way toward certain complex new functions. Thus, the presence of "junk DNA", through co-determining the (higher or lower) order and the variants of chromatin structure with regulatory effects at a distance, might make an important contribution to the evolution of complex organisms.

Animals↗
PubMed2002

Genes coding structural proteins in the Leishmania braziliensis complex.

Acidic ribosomal P1 and P2b proteins, referred to as P proteins, and histone H3 are reported for first time in the Leishmania braziliensis complex. Deoxyribonucleic acid analysis and multiple sequence alignment suggest that both P proteins may maintain their structural function in the ribosomal stalk, in spite of the high rate of mutations detected. The deduced amino acid sequence of protein P1 showed 51% identity with Trypanosoma cruzi protein P1 and protein P2b showed 61% identity with T. cruzi protein P2b. Another conserved protein, L. (Viannia) braziliensis histone H3, showed 82% and 70% identity with histone H3 of L. (Leishmania) infantum and T. cruzi, respectively. The N-terminal end of this histone is divergent in comparison with the consensus eukaryotic sequence. Their predicted tridimensional structure was designed.

Amino Acid Sequence↗
PubMed1993

Characterization of HIV replication complexes early after cell-to-cell infection.

In this study, we have characterized the HIV DNA-containing replication complexes present in cells early after cell-to-cell infection, using sucrose gradient sedimentation and immunoprecipitation. Six hours after cell-to-cell infection, a cytoplasmic HIV replication complex sedimented as a large structure (320S). This replication complex was precipitated by antisera to three virus-coded enzymes (reverse transcriptase, integrase, protease), to the matrix protein (p17), and to cellular histones but not to the major capsid protein (p24). This replication complex was not associated with cell membranes and could not be dissociated into smaller discrete subunits, using detergents. Nuclear extracts from the same cell-to-cell infection contained a smaller (80S) complex that lacked reverse transcriptase and matrix protein (p17). Cytoplasmic replication complexes from a cell-free virus infection sedimented as 160S structures under identical conditions, as previously reported. Our results indicate that, following cell-to-cell transmission of HIV, all the HIV pol gene products, the matrix protein p17, and cellular histones are present in cytoplasmic replication complexes that are taking part in or have completed reverse transcription. Transportation of the cytoplasmic replication complex to the nucleus is associated with structural changes, including a reduction in size and altered protein composition.

Base Sequence↗
PubMed2005

Imprinted X inactivation and reprogramming in the preimplantation mouse embryo.

X chromosome inactivation is a developmentally regulated process that causes one of the two X chromosomes in normal female mammals to become transcriptionally silenced, thus equalizing the expression of X-linked genes between the sexes. Such dosage compensation depends upon dynamic genetic and epigenetic events occurring very early in development. X inactivation is controlled by an X inactivation centre that is associated with the expression of non-coding RNAs required for the silencing. Also associated with the inactive X are repressive histone modifications and polycomb protein-mediated states, which are progressively acquired during the inactivation process. In mouse, two forms of X inactivation have been described. Random X inactivation happens in the derivatives of the inner cell mass (ICM) giving rise to embryos where the maternally inherited X(Xm) is inactive in some cells and the paternally derived X (Xp) is inactive in others. Random X inactivation occurs around the time of implantation. Imprinted X inactivation, the preferential inactivation of the Xp chromosome, occurs earlier and, although there has been some debate as to the precise timing of initiation of this event, is apparent in all cells early in preimplantation development, then is subsequently confined to the cells of the extraembryonic lineages. A picture is emerging whereby initial epigenetic asymmetry between the two parental X chromosomes is reprogrammed in a lineage specific manner resulting in a switch from imprinted to random inactivation in embryonic derivatives. Neither the underlying reason nor the full extent of these early lineage specific epigenetic changes is known, but they may be correlated with more genome-wide reprogramming events essential for normal development.

Alleles↗
PubMed1994

Disturbances of nuclear condensation in human spermatozoa: search for mutations in the genes for protamine 1, protamine 2 and transition protein 1.

During spermiogenesis, the successive replacement of the somatic histones by basic proteins, the transition proteins and protamines, allows normal sperm nuclear condensation. It was suggested that disturbances in nuclear condensation may result in male infertility. Here we report the first molecular analysis of the structure of three genes which code for germ cell-specific nuclear proteins, namely protamine 1 (PRM1), protamine 2 (PRM2) and transition protein 1 (TNP1) in infertile men with disturbed sperm chromatin condensation. In 36 infertile men whose spermatozoa showed a positive reaction with aniline blue, which is an indication for the presence of histones in the nuclei, the complete nucleotide sequences of the coding regions and 5' and 3' untranslated regions of the three genes were evaluated. In addition, 10 infertile patients with oligoasthenoteratozoospermia were studied in the same way, as well as nine infertile patients whose spermatozoa showed a reduction of the protamine 2 content. We did not detect any mutation in the three genes in any of the patients. We assume that the disturbances in the sperm chromatin condensation of our patients, and those described in the literature, are not primarily due to mutations in the genes for PRM1, PRM2 and TNP1.

Base Sequence↗
PubMed2025

Constructing epigenetic regulatory landscapes of plant lncRNAs-an exploration utilizing the novel specialized platform PERlncDB.

Long non-coding RNAs (lncRNAs), once overlooked as transcriptional byproducts, are now recognized for their crucial roles in plant growth, development, and stress responses, with increasing focus on their epigenetic regulation. However, studies investigating epigenomic signals to explore the functions of lncRNAs in plants remain relatively limited. This study collected a comprehensive dataset of over 160 000 high-quality lncRNAs from 19 representative plant species and integrated 6715 ChIP-seq, BS-seq, and RNA-seq datasets to analyze epigenomic patterns at lncRNA loci. Results showed elevated DNA methylation in lncRNA regions. The highest levels occurred in transposable element-associated lncRNAs. Additionally, activating histone modifications at lncRNA loci showed tissue specificity, with epigenetic preferences differed from those at protein-coding gene (PCG) loci. Differential site analysis in epigenetic mutants further highlighted the selective regulation of lncRNA loci by specific epigenetic factors. To facilitate research, we developed PERlncDB, a platform that provides species-specific lncRNA browsing, epigenetic annotation, cross-species conservation analysis, and visualization of epigenomic landscapes. Case studies on MARS and LINC-AP2 emphasized the platform's utility. Conserved epigenetic mechanisms regulating lncRNAs across species, exemplified by a syntenic conserved MET1-regulated lncRNA pair in Arabidopsis and tomato, suggested the stability of regulatory mechanisms underlying lncRNA functions. This work provides critical insights and resources for understanding plant lncRNA epigenetic regulation.

RNA, Long Noncoding↗
PubMed1991

Frequencies of codons in histones, tubulins and fibrinogen: bias due to interference between transcription signals and protein function.

The distribution of codons was studied in 65 proteins: 48 histones, 14 tubulins, and three fibrinogens, With the methodology used, (1) we confirmed that the preterminator state of a codon has no detectable effect on codon bias. (2) The well-known effect of CG suppression was visible. We also found that (3) some codons which are very rare, are equal to parts of known transcription signals. Thus, we advanced that to avoid signal interference, the use of these codons is suppressed when a synonymous codon is available. In addition we found that in the whole series of codons, transcription signals are less frequent than in a random sequence of equal composition. Finally we observed (4) that tryptophan is absent in histones. This absence was related not to the TGG codon itself, but to characteristics of the amino acid. We conclude that the functional constraints of a protein can influence, at least for synonymous codon usage, the evolution of its own coding sequence.

Animals↗
PubMed1999

Guilt by association: non-coding RNAs, chromosome-specific proteins and dosage compensation in Drosophila.

Dosage compensation is a striking example of the interplay between gene-specific regulation and chromosomal architecture. This process has evolved to make X-linked gene expression equivalent in males with one X chromosome and females with two. Examining species at the molecular level has shown that dosage compensation is mediated by sex-specific factors that decorate the X chromosomes to regulate chromatin structure and gene expression. In Drosophila, dosage compensation is achieved, at least in part, through site-specific histone H4 acetylation, which is modulated by a male- and X-specific protein complex. The discovery of non-coding RNAs that 'paint' dosage-compensated X chromosomes in mammals and in Drosophila suggests that RNAs play an intriguing, unexpected role in the regulation of chromatin structure and gene expression.

Animals↗
PubMed1993

Association of a human H1 histone gene with an H2A pseudogene and genes encoding H2B.1 and H3.1 histones.

A cluster of human histone genes was found on three overlapping clones isolated from cosmid and bacteriophage libraries. These three overlapping segments of the human genome comprise genes coding for H3.1, an H2A pseudogene, and an H2B.1 gene downstream of the previously characterized H1.2 gene. The cosmid clone covers 30 kb upstream of the H1.2 gene and overlaps with two phage clones covering the core histone genes and the pseudogene. The same arrangement of an H3 gene, an H2A pseudogene and an H2B gene downstream of an H1 gene has been described within a mouse histone gene cluster [Yang et al.:J Biol Chem 262:17118-17125, 1987; Gruber et al.:Gene 95:303-304, 1990].

Amino Acid Sequence↗
PubMed1993

Synthesis of the Bacillus subtilis histone-like DNA-binding protein HBsu in Escherichia coli and secretion into the periplasm.

A synthetic gene encoding the histone-like DNA-binding protein, HBsu, of Bacillus subtilis was cloned in-frame behind the coding region of the OmpA signal peptide of Escherichia coli. The gene encoding the fusion protein is under control of both the lpp promoter and the lac promoter-operator. Upon induction of gene expression, mature HBsu is secreted into the periplasm. The OmpA signal peptide is correctly removed, resulting in the production of authentic-length HBsu protein. The observed in vitro DNA-binding ability is taken as evidence for the correct folding and assembly of homodimeric HBsu protein. A normally intracellular protein can thus be secreted from E. coli in high yield and with full functionality. By analogy, every histone-like protein or mutant forms thereof may be produced heterologously in E. coli and may be purified without being contaminated by the homologous E. coli HU protein.

Bacillus subtilis↗