scholarly journals Heterochromatin-dependent transcription of satellite DNAs in the Drosophila melanogaster female germline

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Xiaolu Wei ◽  
Danna G Eickbush ◽  
Iain Speece ◽  
Amanda M Larracuente
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Segregation ◽  
Genome Stability ◽  
Satellite Dnas ◽  
Heterochromatin Formation ◽  
Repeat Units ◽  
Repeated Dnas ◽  
Female Germline ◽  
Insight Into

Large blocks of tandemly repeated DNAs-satellite DNAs (satDNAs)-play important roles in heterochromatin formation and chromosome segregation. We know little about how satDNAs are regulated, however their misregulation is associated with genomic instability and human diseases. We use the Drosophila melanogaster germline as a model to study the regulation of satDNA transcription and chromatin. Here we show that complex satDNAs (>100-bp repeat units) are transcribed into long noncoding RNAs and processed into piRNAs (PIWI interacting RNAs). This satDNA piRNA production depends on the Rhino-Deadlock-Cutoff complex and the transcription factor Moonshiner—a previously-described non-canonical pathway that licenses heterochromatin-dependent transcription of dual-strand piRNA clusters. We show that this pathway is important for establishing heterochromatin at satDNAs. Therefore, satDNAs are regulated by piRNAs originating from their own genomic loci. This novel mechanism of satDNA regulation provides insight into the role of piRNA pathways in heterochromatin formation and genome stability.

scholarly journals Heterochromatin-dependent transcription of satellite DNAs in the Drosophila melanogaster female germline

2020 ◽  
Author(s):  
Xiaolu Wei ◽  
Danna G. Eickbush ◽  
Iain Speece ◽  
Amanda M. Larracuente
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Segregation ◽  
Genome Stability ◽  
Satellite Dnas ◽  
Heterochromatin Formation ◽  
Repeat Units ◽  
Repeated Dnas ◽  
Female Germline ◽  
Insight Into

ABSTRACTLarge blocks of tandemly repeated DNAs—satellite DNAs (satDNAs)—play important roles in heterochromatin formation and chromosome segregation. We know little about how satDNAs are regulated, however their misregulation is associated with genomic instability and human diseases. We use the Drosophila melanogaster germline as a model to study the regulation of satDNA transcription and chromatin. Here we show that complex satDNAs (>100-bp repeat units) are transcribed into long noncoding RNAs and processed into piRNAs (PIWI interacting RNAs). This satDNA piRNA production depends on the Rhino-Deadlock-Cutoff complex and the transcription factor Moonshiner—a previously-described non-canonical pathway that licenses heterochromatin-dependent transcription of dual-strand piRNA clusters. We show that this pathway is important for establishing heterochromatin at satDNAs. Therefore, satDNAs are regulated by piRNAs originating from their own genomic loci. This novel mechanism of satDNA regulation provides insight into the role of piRNA pathways in heterochromatin formation and genome stability.

scholarly journals Cytogenetic Analysis of the Third Chromosome Heterochromatin of Drosophila melanogaster

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 509-517
Author(s):  
Dmitry E Koryakov ◽  
Igor F Zhimulev ◽  
Patrizio Dimitri
Keyword(s):  
Drosophila Melanogaster ◽  
Mitotic Chromosome ◽  
Essential Genes ◽  
Chromosome 3 ◽  
Cytogenetic Map ◽  
Satellite Dnas ◽  
Genetic Organization ◽  
The Third ◽  
Heterochromatic Genes ◽  
Insight Into

Abstract Previous cytological analysis of heterochromatic rearrangements has yielded significant insight into the location and genetic organization of genes mapping to the heterochromatin of chromosomes X, Y, and 2 of Drosophila melanogaster. These studies have greatly facilitated our understanding of the genetic organization of heterochromatic genes. In contrast, the 12 essential genes known to exist within the mitotic heterochromatin of chromosome 3 have remained only imprecisely mapped. As a further step toward establishing a complete map of the heterochomatic genetic functions in Drosophila, we have characterized several rearrangements of chromosome 3 by using banding techniques at the level of mitotic chromosome. Most of the rearrangement breakpoints were located in the dull fluorescent regions h49, h51, and h58, suggesting that these regions correspond to heterochromatic hotspots for rearrangements. We were able to construct a detailed cytogenetic map of chromosome 3 heterochromatin that includes all of the known vital genes. At least 7 genes of the left arm (from l(3)80Fd to l(3)80Fj) map to segment h49–h51, while the most distal genes (from l(3)80Fa to l(3)80Fc) lie within the h47–h49 portion. The two right arm essential genes, l(3)81Fa and l(3)81Fb, are both located within the distal h58 segment. Intriguingly, a major part of chromosome 3 heterochromatin was found to be “empty,” in that it did not contain either known genes or known satellite DNAs.

scholarly journals The Paramount Role of Drosophila melanogaster in the Study of Epigenetics: From Simple Phenotypes to Molecular Dissection and Higher-Order Genome Organization

Insects ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 884
Author(s):  
Jean-Michel Gibert ◽  
Frédérique Peronnet
Keyword(s):  
Drosophila Melanogaster ◽  
Regulation Of Gene Expression ◽  
Higher Order ◽  
Post Translational Modifications ◽  
Histone Marks ◽  
Heterochromatin Formation ◽  
Regulatory Processes ◽  
Chromatin Regulators ◽  
Chromatin Remodeling Complexes

Drosophila melanogaster has played a paramount role in epigenetics, the study of changes in gene function inherited through mitosis or meiosis that are not due to changes in the DNA sequence. By analyzing simple phenotypes, such as the bristle position or cuticle pigmentation, as read-outs of regulatory processes, the identification of mutated genes led to the discovery of major chromatin regulators. These are often conserved in distantly related organisms such as vertebrates or even plants. Many of them deposit, recognize, or erase post-translational modifications on histones (histone marks). Others are members of chromatin remodeling complexes that move, eject, or exchange nucleosomes. We review the role of D. melanogaster research in three epigenetic fields: Heterochromatin formation and maintenance, the repression of transposable elements by piRNAs, and the regulation of gene expression by the antagonistic Polycomb and Trithorax complexes. We then describe how genetic tools available in D. melanogaster allowed to examine the role of histone marks and show that some histone marks are dispensable for gene regulation, whereas others play essential roles. Next, we describe how D. melanogaster has been particularly important in defining chromatin types, higher-order chromatin structures, and their dynamic changes during development. Lastly, we discuss the role of epigenetics in a changing environment.

scholarly journals Fixation of transposable elements in the Drosophila melanogaster genome

2005 ◽  
Vol 85 (3) ◽  
pp. 195-203 ◽  
Author(s):  
XULIO MASIDE ◽  
STAVROULA ASSIMACOPOULOS ◽  
BRIAN CHARLESWORTH
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Elements ◽  
Genomic Dna ◽  
Molecular Level ◽  
Hybridization Technique ◽  
Small Interfering Rnas ◽  
Heterochromatin Formation ◽  
Large Clusters

We have investigated at the molecular level four cases in which D. melanogaster middle repetitive DNA probes consistently hybridized to a particular band on chromosomes sampled from a D. melanogaster natural population. Two corresponded to true fixations of a roo and a Stalker element, and the others were artefacts of the in situ hybridization technique caused by the presence of genomic DNA flanking the transposable elements (TEs) in the probes. The two fixed elements are located in the β-heterochromatin (20A and 80B, respectively) and are embedded in large clusters of other elements, many of which may also be fixed. We also found evidence that this accumulation is an ongoing process. These results support the hypothesis that TEs accumulate in the non-recombining part of the genome. Their implications for the effects of TEs on determining the chromatin structure of the host genomes are discussed in the light of recent evidence for the role of TE-derived small interfering-RNAs as cis-acting determinants of heterochromatin formation.

Sister chromatid cohesion and genome stability in vertebrate cells

2003 ◽  
Vol 31 (1) ◽  
pp. 263-265 ◽  
Author(s):  
C. Morrison ◽  
P. Vagnarelli ◽  
E. Sonoda ◽  
S. Takeda ◽  
W.C. Earnshaw
Keyword(s):  
Dna Repair ◽  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Genome Stability ◽  
Sister Chromatid Cohesion ◽  
Spindle Poles ◽  
Chromatid Cohesion ◽  
Chromosomal Passenger ◽  
Passenger Protein

For successful eukaryotic mitosis, sister chromatid pairs remain linked after replication until their kinetochores have been attached to opposite spindle poles by microtubules. This linkage is broken at the metaphase–anaphase transition and the sisters separate. In budding yeast, this sister chromatid cohesion requires a multi-protein complex called cohesin. A key component of cohesin is Scc1/Mcd1 (Rad21 in fission yeast). Disruption of the chicken orthologue of Scc1 by gene targeting in DT40 cells causes premature sister chromatid separation. Cohesion between sister chromatids is likely to provide a substrate for post-replicative DNA repair by homologous recombination. In keeping with this role of cohesion, Scc1 mutants also show defects in the repair of spontaneous and induced DNA damage. Scc1-deficient cells frequently fail to complete metaphase chromosome alignment and show chromosome segregation defects, suggesting aberrant kinetochore function. Consistent with this, the chromosomal passenger protein, INCENP (inner centromere protein) fails to localize to centromeres. Survivin, another passenger protein and one which interacts with INCENP, also fails to localize to centromeres in Scc1-deficient cells. These results show that cohesin maintains genomic stability by ensuring appropriate DNA repair and equal chromosome segregation at mitosis.

scholarly journals Sumo-mediated recruitment allows timely function of the Yen1 nuclease in mitotic cells

2021 ◽  
Author(s):  
Hugo Dorison ◽  
Ibtissam Talhaoui ◽  
Gerard Mazón
Keyword(s):  
Chromosome Segregation ◽  
Genome Stability ◽  
Genome Instability ◽  
Covalent Binding ◽  
Critical Role ◽  
Strand Break ◽  
Damage Response ◽  
Covalently Linked ◽  
Break Formation

The modification of DNA damage response proteins with Sumo is an important mechanism to orchestrate a timely and orderly recruitment of repair factors to damaged sites. After replication stress and double-strand break formation a number of repair factors are Sumoylated and interact with other Sumoylated factors, including the nuclease Yen1. Yen1 plays a critical role to ensure genome stability and unperturbed chromosome segregation by removing covalently linked DNA intermediates that are formed by homologous recombination. Here we show how this important role of Yen1 is dependent on interactions mediated by non-covalent binding to Sumoylated partners. Mutations in the motifs that allow Sumo-mediated recruitment of Yen1 impair its ability to resolve DNA intermediates and result in increased genome instability and chromosome missegregation.

scholarly journals The role of ATXR6 expression in modulating genome stability and transposable element repression in Arabidopsis

2022 ◽  
Vol 119 (3) ◽  
pp. e2115570119
Author(s):  
Magdalena E. Potok ◽  
Zhenhui Zhong ◽  
Colette L. Picard ◽  
Qikun Liu ◽  
Truman Do ◽  
...  
Keyword(s):  
Dna Damage ◽  
Genome Stability ◽  
Null Allele ◽  
Epigenetic Changes ◽  
Germline Development ◽  
Tissue Specific ◽  
Damage Response ◽  
Female Germline

ARABIDOPSIS TRITHORAX-RELATED PROTEIN 5 (ATXR5) AND ATXR6 are required for the deposition of H3K27me1 and for maintaining genomic stability in Arabidopsis. Reduction of ATXR5/6 activity results in activation of DNA damage response genes, along with tissue-specific derepression of transposable elements (TEs), chromocenter decompaction, and genomic instability characterized by accumulation of excess DNA from heterochromatin. How loss of ATXR5/6 and H3K27me1 leads to these phenotypes remains unclear. Here we provide extensive characterization of the atxr5/6 hypomorphic mutant by comprehensively examining gene expression and epigenetic changes in the mutant. We found that the tissue-specific phenotypes of TE derepression and excessive DNA in this atxr5/6 mutant correlated with residual ATXR6 expression from the hypomorphic ATXR6 allele. However, up-regulation of DNA damage genes occurred regardless of ATXR6 levels and thus appears to be a separable process. We also isolated an atxr6-null allele which showed that ATXR5 and ATXR6 are required for female germline development. Finally, we characterize three previously reported suppressors of the hypomorphic atxr5/6 mutant and show that these rescue atxr5/6 via distinct mechanisms, two of which involve increasing H3K27me1 levels.

scholarly journals Parasites Acquired Beta Satellite DNAs from Hominid Hosts via Horizontal Gene Transfer

2019 ◽  
Author(s):  
Jiawen Yang ◽  
Yiting Zhou ◽  
Guangwei Ma ◽  
Xueyan Zhang ◽  
Yabin Guo
Keyword(s):  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Chromosome Segregation ◽  
Genome Stability ◽  
Great Apes ◽  
Primate Species ◽  
List Type ◽  
Repeated Dna ◽  
Satellite Dnas ◽  
Dna Elements

AbstractBeta satellite DNA (satDNA) sequences are repeated DNA elements located in primate centromeres and telomeres, and might play roles in genome stability and chromosome segregation. Beta satDNAs mainly exist in great apes. Previous studies suggested that beta satDNAs may originate in old world monkeys. In this study, we searched both GenBank and SRA database, and identified beta satDNA sequences from the genomic sequences of 22 species. The beta satDNA sequences found in Prosimian, Dermoptera and Scandentia indicated that the origin of beta satDNAs might be as early as 80 MYA. Strikingly, beta satDNA sequences were also found in a number of some species evolutionarily far from primates, including several endoparasites of human and other great apes, which could be the results of multiple horizontal gene transfer (HGT) events. The similar phylogenic profiles between beta satDNAs in the parasite genomes and the human genome indicates that the parasite beta satDNAs have undergone similar concerted evolution and play similar roles as the beta satDNAs in primates.HighlightsThe ever largest scale analysis on beta satDNAs.The origin of beta satDNAs was traced back to ∼80 MYA.Mass existence of beta satDNAs in non-primate species was contributed by multiple HGT events.

scholarly journals Histone H3G34R mutation causes replication stress, homologous recombination defects and genomic instability in S. pombe

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Rajesh K Yadav ◽  
Carolyn M Jablonowski ◽  
Alfonso G Fernandez ◽  
Brandon R Lowe ◽  
Ryan A Henry ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Fission Yeast ◽  
Genomic Instability ◽  
Chromosome Segregation ◽  
Replication Fork ◽  
Replication Stress ◽  
Damage Repair ◽  
Replication Intermediates ◽  
Insight Into

Recurrent somatic mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R/V mutant histone H3.3. H3.3-G34R/V mutants are common in tumors with mutations in p53 and ATRX, an H3.3-specific chromatin remodeler. To gain insight into the role of H3-G34R, we generated fission yeast that express only the mutant histone H3. H3-G34R specifically reduces H3K36 tri-methylation and H3K36 acetylation, and mutants show partial transcriptional overlap with set2 deletions. H3-G34R mutants exhibit genomic instability and increased replication stress, including slowed replication fork restart, although DNA replication checkpoints are functional. H3-G34R mutants are defective for DNA damage repair by homologous recombination (HR), and have altered HR protein dynamics in both damaged and untreated cells. These data suggest H3-G34R slows resolution of HR-mediated repair and that unresolved replication intermediates impair chromosome segregation. This analysis of H3-G34R mutant fission yeast provides mechanistic insight into how G34R mutation may promote genomic instability in glioma.

scholarly journals Novel mechanistic insights into the role of Mer2 as the keystone of meiotic DNA break formation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Dorota Rousova ◽  
Vaishnavi Nivsarkar ◽  
Veronika Altmannova ◽  
Vivek B Raina ◽  
Saskia K Funk ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Protein Complexes ◽  
Strand Break ◽  
Yeast Genetics ◽  
Biochemical Basis ◽  
Dna Double Strand Break ◽  
Break Formation ◽  
Insight Into

In meiosis, DNA double strand break (DSB) formation by Spo11 initiates recombination and enables chromosome segregation. Numerous factors are required for Spo11 activity, and couple the DSB machinery to the development of a meiosis-specific “axis-tethered loop” chromosome organization. Through in vitro reconstitution and budding yeast genetics we here provide architectural insight into the DSB machinery by focussing on a foundational DSB factor, Mer2. We characterise the interaction of Mer2 with the histone reader Spp1, and show that Mer2 directly associates to nucleosomes, likely highlighting a contribution of Mer2 to tethering DSB factors to chromatin. We reveal the biochemical basis of Mer2 association with Hop1, a HORMA domain-containing chromosomal axis factor. Finally, we identify a conserved region within Mer2 crucial for DSB activity, and show that this region of Mer2 interacts with the DSB factor Mre11. In combination with previous work, we establish Mer2 as a keystone of the DSB machinery by bridging key protein complexes involved in the initiation of meiotic recombination.

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