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Weng, Z.

Publications and source records attributed to Weng, Z..

At least 55 records · Page 3Linked to original sources

CDCA-seq resolve the different chromatin structure on integral circular DNAs

Although extrachromosomal DNA (ecDNA) has been intensively studied for several decades, the mechanisms underlying its tumorigenic effects have been revealed only recently. In the majority of conventional sequencing studies, the high-throughput short-read sequencing largely ignores the epigenetic status of most ecDNA regions except for the junctional areas. Here, we developed the sequencing of enzyme-accessible chromatin in circular DNA (CCDA-seq) method, which uses methylase to label open chromatin without fragmentation and exonuclease to enrich the ecDNA sequencing depth, followed by long-read nanopore sequencing. Using CCDA-seq, we observed significantly different patterns in nucleosome/regulator binding in ecDNA at a single-molecule resolution. These results deepen the understanding of ecDNA regulatory mechanisms.

genomics↗

Somatic piRNAs and Transposons are Differentially Regulated During Skeletal Muscle Atrophy and Programmed Cell Death

PiWi-interacting RNAs (piRNAs) are small single-stranded RNAs that can repress transposon expression via epigenetic silencing and transcript degradation. They have been identified predominantly in the ovary and testis, where they serve essential roles in transposon silencing in order to protect the integrity of the genome in the germline. The potential expression of piRNAs in somatic cells has been controversial. In the present study we demonstrate the expression of piRNAs derived from both genic and transposon RNAs in the intersegmental muscles (ISMs) from the tobacco hawkmoth Manduca sexta. These piRNAs are abundantly expressed, are ~27 nt long, map antisense to transposons, are oxidation resistant, exhibit a uridine bias at their first nucleotide, and amplify via the canonical ping-pong pathway. An RNA-seq analysis demonstrated that 20 piRNA pathway genes are expressed in the ISMs and are developmentally regulated. The abundance of piRNAs does not change when the muscles initiate developmentally-regulated atrophy, but are repressed when cells become committed to undergo programmed cell death at the end of metamorphosis. This change in piRNA expression is associated with the targeted repression of several retrotransposons and the induction of specific DNA transposons. The developmental changes in the expression of piRNAs, piRNA pathway genes, and transposons are all regulated by 20-hydroxyecdysone, the steroid hormone that controls the timing of ISM death. Taken together, these data provide compelling evidence for the existence of piRNA in somatic tissues and suggest that they may play roles in developmental processes such as programmed cell death. Author SummarypiRNAs are a class of small non-coding RNAs that suppress the expression of transposable elements, parasitic DNA that if reintegrated, can harm the integrity of the host genome. The expression of piRNAs and their associated regulatory proteins has been studied predominantly in germ cells and some stem cells. We have found that they are also expressed in skeletal muscles in the moth Manduca sexta that undergo developmentally-regulated atrophy and programmed cell death at the end of metamorphosis. The expression of transposons becomes deregulated when the muscles become committed to die, which may play a functional role in the demise of the cell by inducing genome damage. piRNA-mediated control of transposons may represent a novel mechanism that contributes to the regulated death of highly differentiated somatic cells.

developmental biology↗

YAP and TAZ are transcriptional co-activators of AP-1 proteins and STAT3 during breast cellular transformation

The YAP and TAZ paralogues are transcriptional co-activators recruited to target sites, primarily by TEAD proteins. Here, we show that YAP and TAZ are also recruited by JUNB and STAT3, key factors that mediate an epigenetic switch linking inflammation to cellular transformation. YAP and TAZ directly interact with JUNB and STAT3 via a WW domain important for transformation, co-occupy many target sites in vivo via AP-1 and (to a lesser extent) STAT3 sequence motifs, and stimulate transcriptional activation by AP-1 proteins. A few target sites are YAP- or TAZ-specific, and they are associated with different sequence motifs and gene classes. YAP/TAZ, JUNB, and STAT3 directly regulate a common set of target genes that overlap, but are distinct from, those regulated by YAP/TAZ and TEADs. The set of genes regulated by YAP/TAZ, STAT3, and JUNB is associated with poor survival in breast cancer patients with the triple-negative form of the disease.

molecular biology↗

Genetic and Epigenetic Features of Promoters with Ubiquitous Chromatin Accessibility Support Ubiquitous Transcription of Cell-essential Genes

Gene expression is controlled by regulatory elements with accessible chromatin. Although the majority of regulatory elements are cell type-specific, being in the open chromatin state in only one or a few cell types, approximately 16,000 regions in the human genome and 13,000 regions in the mouse genome are in the open chromatin state in nearly all of the 517 human and 94 mouse cell and tissue types assayed by the ENCODE consortium, respectively. We performed a systematic analysis on the subset of 9,000 human and 8,000 mouse ubiquitously (ubi) open chromatin regions that were also classified as candidate cis-regulatory elements (cCREs) with promoter-like signatures (PLSs) by the ENCODE consortium, which we refer to as ubi-PLSs. We found that these ubi-PLSs had higher levels of CG dinucleotides and corresponded to the genes with ubiquitously high levels of transcriptional activities. Furthermore, the transcription start sites of a vast majority of cell-essential genes are located in ubi-PLSs. ubi-PLSs are enriched in the motifs of ubiquitously expressed transcription factors and preferentially bound by transcriptional cofactors that regulate ubiquitously expressed genes. Finally, ubi-PLSs are highly conserved between human and mouse at the synteny level, but not as conserved at the sequence level, with a high turnover of transcription factor motif sites. Thus, there is a distinct set of roughly 9,000 promoters in the mammalian genome that are actively maintained in the open chromatin state in nearly all cell types to ensure the transcriptional program of cell-essential genes.

genomics↗

Genome-Wide Mapping of Human DNA Replication by Optical Replication Mapping Supports a Stochastic Model of Eukaryotic Replication Timing

DNA replication is regulated by the location and timing of replication initiation. Therefore, much effort has been invested in identifying and analyzing the sites of human replication initiation. However, the heterogeneous nature of eukaryotic replication kinetics and the low efficiency of individual initiation site utilization in metazoans has made mapping the location and timing of replication initiation in human cells difficult. A potential solution to the problem of human replication mapping is single-molecule analysis. However, current approaches do not provide the throughput required for genome-wide experiments. To address this challenge, we have developed Optical Replication Mapping (ORM), a high-throughput single-molecule approach to map newly replicated DNA, and used it to map early initiation events in human cells. The single-molecule nature of our data, and a total of more than 2000-fold coverage of the human genome on 27 million fibers averaging ~300 kb in length, allow us to identify initiation sites and their firing probability with high confidence. In particular, for the first time, we are able to measure genome-wide the absolute efficiency of human replication initiation. We find that the distribution of human replication initiation is consistent with inefficient, stochastic initiation of heterogeneously distributed potential initiation complexes enriched in accessible chromatin. In particular, we find sites of human replication initiation are not confined to well-defined replication origins but are instead distributed across broad initiation zones consisting of many initiation sites. Furthermore, we find no correlation of initiation events between neighboring initiation zones. Although most early initiation events occur in early-replicating regions of the genome, a significant number occur in late-replicating regions. The fact that initiation sites in typically late-replicating regions have some probability of firing in early S phase suggests that the major difference between initiation events in early and late replicating regions is their intrinsic probability of firing, as opposed to a qualitative difference in their firing-time distributions. Moreover, modeling of replication kinetics demonstrates that measuring the efficiency of initiation-zone firing in early S phase suffices to predict the average firing time of such initiation zones throughout S phase, further suggesting that the differences between the firing times of early and late initiation zones are quantitative, rather than qualitative. These observations are consistent with stochastic models of initiation-timing regulation and suggest that stochastic regulation of replication kinetics is a fundamental feature of eukaryotic replication, conserved from yeast to humans.

genomics↗

Annotation of Chromatin States in 66 Complete Mouse Epigenomes During Development

The morphologically and functionally distinct cell types of a multicellular organism are maintained by epigenomes and gene expression programs. Phase III of the ENCODE Project profiled 66 mouse epigenomes across twelve tissues at daily intervals from embryonic day 10.5 to birth. Applying the ChromHMM algorithm to these epigenomes, we annotated eighteen chromatin states with characteristics of promoters, enhancers, transcribed regions, repressed regions, and quiescent regions throughout the developmental time course. Our integrative analyses delineate the tissue specificity and developmental trajectory of the loci in these chromatin states. Approximately 0.3% of each epigenome is assigned to a bivalent chromatin state, which harbors both active marks and the repressive mark H3K27me3. Highly evolutionarily conserved, these loci are enriched in silencers bound by Polycomb Repressive Complex proteins and the transcription start sites of their silenced target genes. This collection of chromatin state assignments provides a useful resource for studying mammalian development.

bioinformatics↗

A curated benchmark of enhancer-gene interactions for evaluating enhancer-target gene prediction methods

Many genome-wide collections of candidate cis-regulatory elements (cCREs) have been defined using genomic and epigenomic data, but it remains a major challenge to connect these elements to their target genes. To facilitate the development of computational methods for predicting target genes, we developed a Benchmark of candidate Enhancer-Gene Interactions (BENGI) by integrating the Registry of cCREs we developed recently with experimentally-derived genomic interactions. We used BENGI to test several published computational methods for linking enhancers with genes, including signal correlation and the supervised learning methods TargetFinder and PEP. We found that while TargetFinder was the best performing method, it was modestly better than a baseline distance method for most benchmark datasets while trained and tested within the same cell type and that TargetFinder often did not outperform the distance method when applied across cell types. Our results suggest that current computational methods need to be improved and that BENGI presents a useful framework for method development and testing.

bioinformatics↗

Assessment of human diploid genome assembly with 10x Linked-Reads data

BackgroundProducing cost-effective haplotype-resolved personal genomes remains challenging. 10x Linked-Read sequencing, with its high base quality and long-range information, has been demonstrated to facilitate de novo assembly of human genomes and variant detection. In this study, we investigate in depth how the parameter space of 10x library preparation and sequencing affects assembly quality, on the basis of both simulated and real libraries.\n\nFindingsWe prepared and sequenced eight 10x libraries with a diverse set of parameters from standard cell lines NA12878 and NA24385 and performed whole genome assembly on the data. We also developed the simulator LRTK-SIM to follow the workflow of 10x data generation and produce realistic simulated Linked-Read data sets. We found that assembly quality could be improved by increasing the total sequencing coverage (C) and keeping physical coverage of DNA fragments (CF) or read coverage per fragment (CR) within broad ranges. The optimal physical coverage was between 332X and 823X and assembly quality worsened if it increased to greater than 1,000X for a given C. Long DNA fragments could significantly extend phase blocks, but decreased contig contiguity. The optimal length-weighted fragment length (WFL) was around 50 - 150kb. When broadly optimal parameters were used for library preparation and sequencing, ca. 80% of the genome was assembled in a diploid state.\n\nConclusionThe Linked-Read libraries we generated and the parameter space we identified provide theoretical considerations and practical guidelines for personal genome assemblies based on 10x Linked-Read sequencing.

bioinformatics↗

Compartment-dependent chromatin interaction dynamics revealed by liquid chromatin Hi-C

Chromosomes are folded so that active and inactive chromatin domains are spatially segregated. Compartmentalization is thought to occur through polymer phase/microphase separation mediated by interactions between loci of similar type. The nature and dynamics of these interactions are not known. We developed liquid chromatin Hi-C to map the stability of associations between loci. Before fixation and Hi-C, chromosomes are fragmented removing the strong polymeric constraint to enable detection of intrinsic locus-locus interaction stabilities. Compartmentalization is stable when fragments are over 10-25 kb. Fragmenting chromatin into pieces smaller than 6 kb leads to gradual loss of genome organization. Dissolution kinetics of chromatin interactions vary for different chromatin domains. Lamin-associated domains are most stable, while interactions among speckle and polycomb-associated loci are more dynamic. Cohesin-mediated loops dissolve after fragmentation, possibly because cohesin rings slide off nearby DNA ends. Liquid chromatin Hi-C provides a genome-wide view of chromosome interaction dynamics.\n\nHighlightsO_LILiquid chromatin Hi-C detects chromatin interaction dissociation rates genome-wide\nC_LIO_LIChromatin conformations in distinct nuclear compartments differ in stability\nC_LIO_LIStable heterochromatic associations are major drivers of chromatin phase separation\nC_LIO_LICTCF-CTCF loops are stabilized by encirclement of loop bases by cohesin rings\nC_LI

genomics↗

Adaptive evolution targets a piRNA precursor transcription network

In Drosophila, transposon-silencing piRNAs are derived from heterochromatic clusters and a subset of euchromatic transposon insertions, which are transcribed from internal non-canonical initiation sites and flanking canonical promoters. Rhino binds to Deadlock, which recruits TRF2 to promote non-canonical transcription of these loci. Cuff co-localizes with Rhino and Del. The role of Cuff is less well understood, but the cuff gene shows hallmarks of adaptive evolution, which frequently targets functional interactions within host defense systems. We show that Drosophila simulans cuff is a dominant negative allele when expressed in Drosophila melanogaster, where it traps Deadlock, TRF2 and the transcriptional co-repressor CtBP in stable nuclear complexes. Cuff promotes Rhino and Deadlock localization, driving non-canonical transcription. CtBP, by contrast, suppresses canonical cluster and transposon transcription, which interferes with downstream non-canonical transcription and piRNA production. Cuff, TRF2 and CtBP thus form a network that balances canonical and non-canonical piRNA precursor transcription.

genetics↗

Aquila: diploid personal genome assembly and comprehensive variant detection based on linked reads

Variant discovery in personal, whole genome sequence data is critical for uncovering the genetic contributions to health and disease. We introduce a new approach, Aquila, that uses linked-read data for generating a high quality diploid genome assembly, from which it then comprehensively detects and phases personal genetic variation. Assemblies cover >95% of the human reference genome, with over 98% in a diploid state. Thus, the assemblies support detection and accurate genotyping of the most prevalent types of human genetic variation, including single nucleotide polymorphisms (SNPs), small insertions and deletions (small indels), and structural variants (SVs), in all but the most difficult regions. All heterozygous variants are phased in blocks that can approach arm-level length. The final output of Aquila is a diploid and phased personal genome sequence, and a phased VCF file that also contains homozygous and a few unphased heterozygous variants. Aquila represents a cost-effective evolution of whole-genome reconstruction that can be applied to cohorts for variation discovery or association studies, or to single individuals with rare phenotypes that could be caused by SVs or compound heterozygosity.

genomics↗

The piRNA Response to Retroviral Invasion of the Koala Genome

Transposons are ubiquitous mobile elements with the potential to trigger genome instability and mutations linked to diseases1,2. Antisense piRNAs guide an adaptive genome immune system that silences established transposons during germline development3, but how the germline responds to new genome invaders is not understood. The KoRV retrovirus infects somatic and germline cells and is sweeping through wild koala populations by a combination of horizontal and vertical transfers, providing a unique opportunity to directly analyze the germline response to retroviral invasions of a mammalian genome4,5. We analyzed genome organization and long RNA and short RNA transcriptomes in testis, liver, and brain from two wild koalas infected with KoRV, while integrating our results with earlier genomic data. Consistent with data from other mammals6,7, koala piRNAs were detected in testis and mapped to both isolated transposon insertions and genic and intergenic piRNA clusters. Established transposon subfamilies produced roughly equal levels of antisense piRNAs, which are the effectors of trans-silencing, and sense piRNAs, which drive ping-pong amplification of these effectors8,9. KoRV piRNAs, in striking contrast, were strongly sense biased in both animals analyzed. These two koalas each carried 60 germline KoRV-A insertions, but only 14 of the insertions were shared, and none of the insertions mapped to piRNA clusters. The sense piRNAs thus appear to be produced by direct processing of the transcripts from isolated proviral insertions. A typical gammaretrovirus, KoRV produces spliced Env mRNAs and unspliced transcripts encoding Gag, Pol, and the viral genome. KoRV Env mRNAs were 5-fold more abundant than the unspliced pre-mRNAs, but 92% of piRNAs were derived from the unspliced pre-mRNAs. We show that this biased piRNA production from unspliced retrotransposon transcripts is conserved from flies to mice. Retroviruses must bypass splicing to replicate; thus, we propose that failed splicing produces a \"molecular pattern\" on transcripts from retroviral invaders that is recognized by an innate genome immune system, which silences transposons in cis by processing their transcripts into piRNAs. This innate immune response defends the germline until antisense piRNA production--from clusters or isolated insertions--is established to provide sequence-specific adaptive immunity and memory of the genome invader.

genetics↗

The RNA-binding ATPase, Armitage, Couples piRNA Amplification in Nuage to Phased piRNA Production on Mitochondria

PlWI-interacting RNAs (piRNAs) silence transposons in Drosophila ovaries, ensuring female fertility. Two coupled pathways generate germline piRNAs: the ping-pong cycle, in which the PIWI proteins Aubergine and Ago3 increase the abundance of pre-existing piRNAs, and the phased piRNA pathway, which generates strings of tail-to-head piRNAs, one after another. Proteins acting in the ping-pong cycle localize to nuage, whereas phased piRNA production requires Zucchini, an endonuclease on the mitochondrial surface. Here, we report that Armitage (Armi), an RNA-binding ATPase localized to both nuage and mitochondria, links the ping-pong cycle to the phased piRNA pathway. Mutations that block phased piRNA production deplete Armi from nuage. Armi ATPase mutants cannot support phased piRNA production and inappropriately bind mRNA instead of piRNA precursors. We propose that Armi shuttles between nuage and mitochondria, feeding precursor piRNAs generated by Ago3 cleavage into the Zucchini-dependent production of Aubergine- and Piwi-bound piRNAs on the mitochondrial surface.

genetics↗

Comprehensive Genomic Characterization of Breast Tumors with BRCA1 and BRCA2 Mutations

BackgroundGermline mutations in the BRCA1 and BRCA2 genes predispose carriers to breast and ovarian cancer, and there remains a need to identify the specific genomic mechanisms by which cancer evolves in these patients. Here we present a systematic genomic analysis of breast tumors with BRCA1 and BRCA2 mutations.\n\nMethodsWe analyzed genomic data from breast tumors, with a focus on comparing tumors with BRCA1/BRCA2 gene mutations with common classes of sporadic breast tumors.\n\nResultsWe identify differences between BRCA-mutated and sporadic breast tumors in patterns of point mutation, DNA methylation and structural variation. We show that structural variation disproportionately affects tumor suppressor genes and identify specific driver gene candidates that are enriched for structural variation.\n\nConclusionsCompared to sporadic tumors, BRCA-mutated breast tumors show signals of reduced DNA methylation, more ancestral cell divisions, and elevated rates of structural variation that tend to disrupt highly expressed protein-coding genes and known tumor suppressors. Our analysis suggests that BRCA-mutated tumors are more aggressive than sporadic breast cancers because loss of the BRCA pathway causes multiple processes of mutagenesis and gene dysregulation.

cancer biology↗

An Evolutionarily Conserved piRNA-producing Locus Required for Male Mouse Fertility

Pachytene piRNAs, which comprise >80% of small RNAs in the adult mouse testis, have been proposed to bind and regulate target RNAs like miRNAs, cleave targets like siRNAs, or lack biological function altogether. Although piRNA pathway protein mutants are male sterile, no biological function has been identified for any mammalian piRNA-producing locus. Here, we report that males lacking piRNAs from a conserved mouse pachytene piRNA locus on chromosome 6 (pi6) produce sperm with defects in capacitation and egg fertilization. Moreover, heterozygous embryos sired by pi6-/- fathers show reduced viability in utero. Molecular analyses suggest that pi6 piRNAs repress gene expression by cleaving mRNAs encoding proteins required for sperm function. pi6 also participates in a network of piRNA-piRNA precursor interactions that initiate piRNA production from a second piRNA locus on chromosome 10 as well as pi6 itself. Our data establish a direct role for pachytene piRNAs in spermiogenesis and embryo viability.\n\nHighlightsO_LINormal male mouse fertility and spermiogenesis require piRNAs from the pi6 locus\nC_LIO_LISperm capacitation and binding to the zona pellucida of the egg require pi6 piRNAs\nC_LIO_LIHeterozygous embryos sired by pi6-/- fathers show reduced viability in utero\nC_LIO_LIDefects in pi6 mutant sperm reflect changes in the abundance of specific mRNAs.\nC_LI

genetics↗

Maelstrom Represses Canonical Polymerase II Transcription within Bi-Directional piRNA Clusters in Drosophila melanogaster

In Drosophila, 23-30 nt long PIWI-interacting RNAs (piRNAs) direct the protein Piwi to silence germline transposon transcription. Most germline piRNAs derive from dual-strand piRNA clusters, heterochromatic transposon graveyards that are transcribed from both genomic strands. These piRNA sources are marked by the Heterochromatin Protein 1 homolog, Rhino (Rhi), which facilitates their promoter-independent transcription, suppresses splicing, and inhibits transcriptional termination. Here, we report that the protein Maelstrom (Mael) represses canonical, promoter-dependent transcription in dual-strand clusters, allowing Rhi to initiate piRNA precursor transcription. In addition to Mael, the piRNA biogenesis factors Armitage and Piwi, but not Rhi, are required to repress canonical transcription in dual-strand clusters. We propose that Armitage, Piwi, and Mael collaborate to repress potentially dangerous transcription of individual transposon mRNAs within clusters, while Rhi allows non-canonical transcription of the clusters into piRNA precursors without generating transposase-encoding mRNAs.

genetics↗

Integrating cross-linking experiments with ab initio protein-protein docking

Ab initio protein-protein docking algorithms often rely on experimental data to identify the most likely complex structure. We integrated protein-protein docking with the experimental data of chemical cross-linking followed by mass spectrometry. We tested our approach using 12 cases that resulted from an exhaustive search of the Protein Data Bank for protein complexes with cross-links identified in our experiments. We implemented cross-links as constraints based on Euclidean distance or void-volume distance. For most test cases the rank of the top-scoring near-native prediction was improved by at least two fold compared with docking without the cross-link information, and the success rates for the top 5 and top 10 predictions doubled. Our results demonstrate the delicate balance between retaining correct predictions and eliminating false positives. Several test cases had multiple components with distinct interfaces, and we present an approach for assigning cross-links to the interfaces. Employing the symmetry information for these cases further improved the performance of complex structure prediction.\n\nHighlightsO_LIIncorporating low-resolution cross-linking experimental data in protein-protein docking algorithms improves performance more than two fold.\nC_LIO_LIIntegration of protein-protein docking with chemical cross-linking reveals information on the configuration of higher order complexes.\nC_LIO_LISymmetry analysis of protein-protein docking results improves the predictions of multimeric complex structures\nC_LI

bioinformatics↗

Culture-free generation of microbial genomes from human and marine microbiomes

Our understanding of natural microbial communities is shaped by the careful investigation of a relatively small number of isolated and cultured organisms, and by analysis of genomic sequences obtained by culture-free metagenomic sequencing approaches. Metagenomic shotgun sequencing has facilitated partial reconstruction of strain-level community structure and functional repertoire. Unfortunately, it remains difficult to cost-effectively produce high quality genome drafts for individual microbes without isolation and culture. Recent molecular techniques that partition long DNA fragments and then barcode short fragments derived from them produce \"read clouds\", which are short-read sequences containing long-range information. Here, we present a novel application of a read cloud technique to microbiome samples, as well as Athena, a de novo assembler that uses these barcodes to produce improved metagenomic assemblies. We apply our approach to sequence human stool samples from two healthy individuals, and compare it to existing short read and synthetic long read metagenomic sequencing approaches. We find that read cloud metagenomic sequencing and Athena assembly produce the most complete individual genome drafts. These genome drafts are also highly contiguous (>200kb N50, <10 contigs), even for bacteria that have relatively low (20x) raw short read sequence coverage. We also apply this approach to a significantly more complex marine sediment sample and obtain 23 genome drafts with valuable 16S ribosomal RNA taxonomic marker sequences, nine of which are complete genome drafts. Read cloud metagenomic sequencing allows culture-free generation of high quality microbial genome drafts using only a single shotgun experiment.

genomics↗