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Results for “Genome protection”

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At least 19 recordsLinked to original sources

PubMed2023

The multi-functional Smc5/6 complex in genome protection and disease.

Structural maintenance of chromosomes (SMC) complexes are ubiquitous genome regulators with a wide range of functions. Among the three types of SMC complexes in eukaryotes, cohesin and condensin fold the genome into different domains and structures, while Smc5/6 plays direct roles in promoting chromosomal replication and repair and in restraining pathogenic viral extra-chromosomal DNA. The importance of Smc5/6 for growth, genotoxin resistance and host defense across species is highlighted by its involvement in disease prevention in plants and animals. Accelerated progress in recent years, including structural and single-molecule studies, has begun to provide greater insights into the mechanisms underlying Smc5/6 functions. Here we integrate a broad range of recent studies on Smc5/6 to identify emerging features of this unique SMC complex and to explain its diverse cellular functions and roles in disease pathogenesis. We also highlight many key areas requiring further investigation for achieving coherent views of Smc5/6-driven mechanisms.

Animals↗

PubMed2024

Private detection of relatives in forensic genomics using homomorphic encryption.

BACKGROUND: Forensic analysis heavily relies on DNA analysis techniques, notably autosomal Single Nucleotide Polymorphisms (SNPs), to expedite the identification of unknown suspects through genomic database searches. However, the uniqueness of an individual's genome sequence designates it as Personal Identifiable Information (PII), subjecting it to stringent privacy regulations that can impede data access and analysis, as well as restrict the parties allowed to handle the data. Homomorphic Encryption (HE) emerges as a promising solution, enabling the execution of complex functions on encrypted data without the need for decryption. HE not only permits the processing of PII as soon as it is collected and encrypted, such as at a crime scene, but also expands the potential for data processing by multiple entities and artificial intelligence services. METHODS: This study introduces HE-based privacy-preserving methods for SNP DNA analysis, offering a means to compute kinship scores for a set of genome queries while meticulously preserving data privacy. We present three distinct approaches, including one unsupervised and two supervised methods, all of which demonstrated exceptional performance in the iDASH 2023 Track 1 competition. RESULTS: Our HE-based methods can rapidly predict 400 kinship scores from an encrypted database containing 2000 entries within seconds, capitalizing on advanced technologies like Intel AVX vector extensions, Intel HEXL, and Microsoft SEAL HE libraries. Crucially, all three methods achieve remarkable accuracy levels (ranging from 96% to 100%), as evaluated by the auROC score metric, while maintaining robust 128-bit security. These findings underscore the transformative potential of HE in both safeguarding genomic data privacy and streamlining precise DNA analysis. CONCLUSIONS: Results demonstrate that HE-based solutions can be computationally practical to protect genomic privacy during screening of candidate matches for further genealogy analysis in Forensic Genetic Genealogy (FGG).

Humans↗

PubMed2026

Escape and survival: transposon adaptations in the face of insect host silencing.

Transposable elements (TEs) are mobile genetic sequences that have long resided within host genomes. Over this shared history, a continuous process of co-evolution has forged a diverse array of dynamic TE-host interactions. In an evolutionary arms race, hosts must silence TEs to protect genome integrity from deleterious mutations by TE insertions, while TEs must evade this silencing to survive. TE adaptations to host genomes have recently gained prominence, following many discoveries in eukaryotic genomes. Here, I discuss TE strategies to evade host silencing and ensure their long-term persistence within host genomes, focusing on insects as the primary model system. Furthermore, by describing host silencing, I postulate potential evasive mechanisms that may drive TE adaptation within host genomes.

Journal Article↗

PubMed2025

Beacon Reconstruction Attack: Reconstruction of genomes in genomic data-sharing beacons using summary statistics.

MOTIVATION: Genomic data-sharing beacon protocol, developed by the Global Alliance for Genomics and Health, offers a privacy-preserving mechanism for querying genomic datasets while restricting direct data access. Despite their design, beacons remain vulnerable to privacy attacks. This study introduces a novel privacy vulnerability of the protocol: one can reconstruct large portions of the genomes of all beacon participants by only using the summary statistics reported by the protocol. RESULTS: We introduce a novel optimization-based algorithm that leverages beacon responses and SNP correlations for reconstruction. By optimizing for the SNP correlations and allele frequencies, the proposed approach achieves genome reconstruction with a substantially higher F1-score (70%) compared to baseline methods (45%) on beacons generated using individuals from the HapMap and OpenSNP datasets. We show that reconstructed genomes can be used by downstream applications such as in membership inference attacks against other beacons. Our findings reveal that beacons releasing allele frequencies substantially increase the reconstruction risk, underscoring the need for enhanced privacy-preserving mechanisms to protect genomic data. AVAILABILITY AND IMPLEMENTATION: Our implementation is available at https://github.com/ASAP-Bilkent/Beacon-Reconstruction-Attack.

Genomics↗

PubMed2025

Functional integration of the bacteriophage T4 DNA replication complex: The multiple roles of the ssDNA binding protein (gp32).

Single-stranded DNA binding protein (gp32) serves as the central regulatory component of the multi-subunit T4 bacteriophage DNA replication system by coordinating the system's three functional sub-assemblies, resulting in phage DNA synthesis in T4-infected E. coli cells at the high speeds (~1,000 nts s-1) and the high fidelity (< 1 error per 107 nts) required for genomic function within this cellular eco-system. Gp32 proteins continuously bind to, slide as cooperatively-linked clusters on, and un-bind from transiently exposed single-stranded (ss) DNA templates to carry out their coordinating functions, as well as to protect genomic sequences from nuclease activity and block the formation of interfering secondary structures. The N-terminal domains (NTDs) of gp32 mediate cooperative interactions within ssb clusters, but the roles of the disordered C-terminal domains (CTD) in the nucleation of gp32-ssDNA filaments at ss-dsDNA junctions are less well understood. We here present microsecond-resolved single-molecule Förster resonance energy transfer studies of the initial steps of gp32 assembly on short oligo-deoxythymidine lattices of varying lattice length and polarity near model ss-dsDNA junctions. These data are analyzed to define the molecular steps and related free energy surfaces involved in initiating gp32 cluster formation, which show that the nucleation mechanisms and regulatory interactions driven by gp32 proteins at ss-dsDNA junctions are significantly directed by lattice polarity. We propose a model for the role of the CTDs in orienting gp32 monomers at lattice positions close to ss-dsDNA junctions that suggests how intrinsically disordered CTD domains might facilitate and control non-base-sequence-specific binding in both the nucleation and the dissociation of the gp32-ssDNA filaments involved in phage DNA replication and related processes.

Journal Article↗

PubMed2024

Transcriptional profiles of Microcystis reveal gene expression shifts that promote bloom persistence in in situ mesocosms.

Harmful algal blooms caused by cyanobacteria threaten aquatic ecosystems, the economy, and human health. Previous work has tried to identify the mechanisms that allow blooms to form, focusing on the role of nutrients. However, little is known about how introduced nutrients influence gene expression in situ. To address this knowledge gap, we used in situ mesocosms initiated with water experiencing a Microcystis bloom. We added pulses of nutrients that are commonly associated with anthropogenic sources to the mesocosms for 72 hours and collected samples for metatranscriptomics to examine how the physiological function of Microcystis and bloom status changed. The addition of nitrogen (N) as urea, but not the addition of PO4, resulted in conspicuous bloom persistence for at least 9 days after the final introduction of nutrients. The addition of urea initially resulted in the upregulation of photosynthesis machinery, as well as phosphate, carbon, and N transport and metabolism. Once Microcystis presumably became N-replete, upregulation of amino acid metabolism, microcystin biosynthesis, and other processes associated with biomass generation occurred. These capacities coincided with the upregulation of toxin-antitoxin systems, CRISPR-cas genes, and transposases suggesting that phage defense and genome rearrangement are critical in bloom persistence. Overall, our results show the stepwise transcriptional response of a Microcystis bloom to the introduction of nutrients, specifically urea, as it is sustained in a natural setting. The transcriptomic shifts observed herein may serve as markers of the longevity of blooms while providing insight into why Microcystis blooms over other cyanobacteria.IMPORTANCEHarmful algal blooms represent a threat to human health and ecosystems. Understanding why blooms persist may help us develop warning indicators of bloom persistence and create novel mitigation strategies. Using mesocosm experiments initiated with water with an active bloom, we measured the stepwise transcription changes of the toxin-producing cyanobacterium Microcystis in response to the addition of nutrients that are important in causing blooms. We found that nitrogen (N), but not phosphorus, promoted bloom longevity. The initial introduction of N resulted in the upregulation of genes involved in photosynthesis and N import. At later times in the bloom, upregulation of genes involved in biomass generation, phage protection, genomic rearrangement, and toxin production was observed. Our results suggest that Microcystis first fulfills nutritional requirements before investing energy in pathways associated with growth and protection against competitors, which allowed bloom persistence more than a week after the final addition of nutrients.

Microcystis↗

PubMed2026

Genetic Variants at the NAT2 and HLA-DOA are Associated With Anti-Tuberculosis Drug-Induced Liver Injury Susceptibility and Clinical Manifestations in Western Chinese Populations.

BACKGROUND: Anti-tuberculosis drug-induced liver injury (ATDILI) is one of the most prevalent and serious adverse reactions during anti-tuberculosis treatment and can potentially lead to liver failure or mortality. This study aims to investigate whether genetic variants in the N-acetyltransferase 2 gene (NAT2) and the HLA-DOA gene (HLA-DOA) are associated with ATDILI susceptibility and clinical manifestations in a Western Chinese population. METHODS: A total of 1358 participants with active tuberculosis were enrolled and genotyped for four NAT2 polymorphisms and five HLA-DOA loci. Associations between candidate genetic variants and ATDILI were evaluated using logistic regression analyses, with multiple comparisons adjusted by Bonferroni correction. RESULTS: The overall incidence of ATDILI was 28.4% (385/1358) in this cohort. Under a recessive model, NAT2 rs1799930 was found to increase the risk of ATDILI (odds ratio [OR] = 1.88, 95% confidence interval [CI]: 1.20-2.95, p = 0.006), which remained significant after Bonferroni correction (adjusted p = 0.048). Meanwhile, while HLA-DOA rs1367731 (OR = 0.41, 95% CI: 0.18-0.93, p = 0.033), rs6913008 (OR = 0.39, 95% CI: 0.17-0.89, p = 0.024), and rs9276975 (OR = 0.47, 95% CI: 0.23-0.98, p = 0.045) demonstrated a promising protective genomic characteristic that may mitigate the development of ATDILI. However, none of the reported HLA-DOA associations remained statistically significant after applying Bonferroni corrections. Regarding clinical manifestations, NAT2 rs1799930 and rs1799931 have been linked to poor ATDILI clinical presentations, whereas certain HLA-DOA variants (rs1367731, rs6913008, and rs9276975) were possibly linked to milder ATDILI severity. CONCLUSION: Our findings preliminarily suggest that the NAT2 and HLA-DOA genetic variants may play a role in ATDILI susceptibility and clinical outcomes. NAT2 rs1799930 represents a potential genetic risk marker, while HLA-DOA variants may serve as protective factors warranting further validation. These findings may contribute to the precision management of ATDILI and the prevention of anti-TB drug-associated liver injury.

Adult↗

PubMed2026

Control of foreign DNA: emerging roles of xenogeneic silencers.

Bacteria continuously acquire foreign DNA through horizontal gene transfer, yet its successful integration depends on regulatory mechanisms that balance genome protection with evolutionary innovation. Xenogeneic silencers are central to this process: they preferentially bind AT-rich DNA, a common feature of many horizontally acquired genetic elements, and repress its transcription. Recent studies, however, reveal a much broader regulatory repertoire. Beyond transcriptional repression, these proteins contribute to chromosome organization by forming higher-order nucleoprotein complexes and phase-separated condensates that shape bacterial nucleoid architecture. Furthermore, they play roles in regulating bacteriophage infection cycles, including mechanisms by which phages hijack host silencing activities for their own benefit. Their extensive regulatory reach, spanning virulence genes, biofilm formation, specialized metabolite production, and mobile genetic elements (MGEs), underscores their central role in connecting environmental signals, including fluctuations in the second messenger c-di-GMP, with gene expression, and genome organization. The diversification of xenogeneic silencers across bacterial chromosomes, plasmids, phages, and other MGEs highlights their evolutionary significance. Together, these recent findings position xenogeneic silencers as dynamic regulatory modules that shape the fate of foreign DNA across the horizontal gene transfer network.

Gene Transfer, Horizontal↗

PubMed2026

Small GTPase RAN-driven PNET2 oligomerization and phase separation at the nuclear lamina promote nuclear envelope integrity in plants.

The nuclear envelope is a fundamental organizer of eukaryotic cells, yet how plants regulate its architecture and integrity remains poorly understood. In this study, we identified the plant inner nuclear membrane protein PLANT NUCLEAR ENVELOPE TRANSMEMBRANE 2 (PNET2) as a scaffold that maintains nuclear envelope integrity and genome stability. Loss of PNET2 function compromises nuclear membrane structure and sensitizes cells to DNA damage, whereas overexpression drives aberrant nuclear membrane expansion. Biochemically, PNET2 cooperates with the nuclear lamin protein KAKU4 and CROWDED NUCLEI 1 within the nuclear lamina to promote nuclear membrane remodeling, a process driven by biomolecular condensate formation via their intrinsically disordered regions. We further uncovered a direct interaction between PNET2 and the small GTPase RAN. Structural modeling and biochemical analyses revealed that its active GTP-bound form stimulates PNET2 oligomerization, potentially promoting its phase separation to drive membrane expansion. Genetic analyses showed that PNET2 and RAN function in a shared pathway essential for nuclear membrane integrity. Together, our findings define a regulatory module that orchestrates GTPase signaling to sustain nuclear membrane homeostasis in plants, positioning PNET2 as a nexus linking membrane dynamics, nuclear lamina organization, and genome protection.

PNET2↗

PubMed2025

The small bacterial membrane protein YohP induces nucleoid condensation in E. coli and inhibits oligomerization of antimicrobial peptides.

Prokaryotic organisms execute multiple stress response mechanisms in order to cope with rapidly changing environments. Some mechanisms respond to specific cues, such as the OxyR-dependent response to hydrogen peroxide or the SOS-response that is induced upon DNA-damage. These specific responses complement general mechanisms that respond to multiple and diverse stressors. One example is nucleoid condensation, which is a rapid and effective mechanism for genome protection and observed in response to various stresses, including entry into stationary phase. Recently, the upregulation of small membrane proteins (SMPs) in response to stress was observed, but details on how this emerging class of proteins modulate the stress response is largely unknown. Here, we demonstrate that the production of two SMPs, YohP and YncL, cause nucleoid condensation in Escherichia coli. Nucleoid condensation is the result of YohP-/YncL-induced sublethal membrane depolarization, which induces the phage-shock response and leads to a reduction of global protein synthesis. YohP production also prevents the oligomerization of the antimicrobial peptide magainin-2 in the E. coli membrane and reduces the metabolic activity of E. coli cells. Thus, the synthesis of YohP and likely of other SMPs potentially protects bacterial cells against some unfavorable conditions by shifting them into a metabolically silent state.

YncL↗

PubMed2025

NuRD chromatin remodeling is required to repair exogenous DSBs in the Caenorhabditis elegans germline.

Organisms rely on coordinated networks of DNA repair pathways to protect genomes against toxic double-strand breaks (DSBs), particularly in germ cells. All repair mechanisms must successfully negotiate the local chromatin environment in order to access DNA. For example, nucleosomes can be repositioned by the highly conserved Nucleosome Remodeling and Deacetylase (NuRD) complex. In Caenorhabditis elegans, NuRD functions in the germline to repair DSBs - the loss of NuRD's ATPase subunit, LET-418/CHD4, prevents DSB resolution and therefore reduces fertility. In this study, we challenge germlines with exogenous DNA damage to better understand NuRD's role in repairing DSBs. We find that let-418 mutants are sensitive to cisplatin and hydroxyurea: exposure to either mutagen impedes DSB repair, generates aneuploid oocytes, and reduces fertility and embryonic survival. These defects resemble those seen when the Fanconi anemia (FA) DNA repair pathway is compromised, and we find that LET-418's activity is epistatic to that of the FA component FCD-2/FANCD2. We propose a model in which NuRD is recruited to the site of DNA lesions to remodel chromatin and allow access for FA pathway components. Together, these results implicate NuRD in the repair of both endogenous DSBs and exogenous DNA lesions to preserve genome integrity in developing germ cells.

DNA repair↗

PubMed2012

RETRACTED: Identification of sumoylation sites in CCDC6, the first identified RET partner gene in papillary thyroid carcinoma, uncovers a mode of regulating CCDC6 function on CREB1 transcriptional activity.

CCDC6 was originally identified in chimeric genes as caused by chromosomal translocation involving the RET protooncogene in some thyroid tumors. Recognised as a 65 kDa pro-apoptotic phosphoprotein, CCDC6 has been enrolled as an ATM substrate that contribute to protect genome integrity by modulating PP4c activity in response to genotoxic stress. Recently, CCDC6 has been identified as a repressor of CREB1-dependent transcription. Sumoylation has emerged as an important mechanism in transcriptional control. Here, we report the identification and characterization of three sites of sumoylation in CCDC6 (K74, K266 and K424) which are highly conserved in vertebrates. We demonstrate that the post-translational modifications by SUMO2 constrain most of the CCDC6 protein in the cytosol and affect its functional interaction with CREB1 with a decrease of CCDC6 repressive function on CREB1 transcriptional activity. Indeed, the impairment of functional outcome of sumoylated CCDC6 is obtained knocking down all three the sumoylation sites. Interestingly, in thyroid cells the SUMO2-mediated CCDC6 post-translational modifications are induced by Forskolin, a cAMP analog. Signal transduction via the cAMP pathway is known to be ubiquitous and represents a major line of communication between many organisms and their environment. We believe that CCDC6 could be an important player in the dynamics of cAMP signaling by fine regulating CREB1 transcriptional activity in normal and transformed thyroid cells.

Animals↗

PubMed2026

Biochemical, structural and mutational landscapes of base excision repair enzymes and cancer: from atomic resolution to tumor signatures.

PURPOSE: Base excision repair (BER) is the predominant pathway for repairing non‑bulky oxidized and alkylated DNA base lesions, and its fidelity depends on the coordinated action of lesion‑specific DNA glycosylases and downstream repair enzymes. This review aims to summarize recent structural, biochemical, and genomic insights into three base excision repair enzymes, MUTYH DNA glycosylase, NTHL1 DNA glycosylase, and DNA polymerase β. CONCLUSION: This review outlines how MUTYH, NTHL1 and DNA polymerase β protect the genome from mutagenesis, highlights major germline variants associated with disease, and synthesizes the current knowledge on the characteristic single base substitution (SBS) mutational signatures that occur when these repair enzymes are dysfunctional.

Base excision repair↗

PubMed2026

A novel DNA-protective function of Escherichia coli thioredoxin 2 mediated by its N-terminal zinc-binding domain.

Thioredoxins are ubiquitous thiol-disulfide oxidoreductases that maintain intracellular redox homeostasis. In addition to its conserved catalytic domain, Escherichia coli thioredoxin 2 (EcTrx2) possesses a unique N-terminal zinc-binding domain whose physiological function remains largely unknown. Here, we identify a previously unrecognized DNA-binding activity of EcTrx2 and demonstrate its role in protecting DNA during oxidative stress. Electrophoretic mobility shift assays showed that EcTrx2 bound plasmid DNA in a concentration-dependent and GST-tag-independent manner, whereas EcTrx1 exhibited no detectable DNA-binding activity. DNA binding was abolished by deletion of the N-terminal zinc-binding domain and was blocked by zinc occupancy, indicating that this unique domain is essential for DNA interaction. Consistent with these findings, EcTrx2 significantly protected plasmid DNA from DNase I digestion and hydroxyl radical-mediated oxidative damage in vitro. Furthermore, EcTrx2 enhanced bacterial tolerance to the DNA-damaging agents zeocin and diamide, supporting the physiological relevance of its DNA-binding activity. Our results reveal a DNA-binding role for EcTrx2 and identify its N-terminal zinc-binding domain as a key determinant of DNA binding and protection against oxidative DNA damage.

DNA binding↗

PubMed2025

Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.

Replication stress (RS) poses a threat to genome stability and drives genomic rearrangements. The homologous recombination (HR) pathway repairs stalled replication forks (RFs) and prevents such instability. Through an E3 ubiquitin ligase screen aimed at identifying regulators of RAD51, we identified macrophage erythroblast attacher (MAEA), a core component of C-terminal to Lish (CTLH) E3 ubiquitin ligase complex, as a regulator of the HR pathway. Loss of MAEA impairs RAD51 recruitment at stalled RFs, leading to increased sensitivity to RS-inducing agents and excessive degradation of nascent DNA strands. Mechanistically, MAEA associates with and mediates the ubiquitylation of Ku80, enabling its removal from RF ends and facilitating the loading of RAD51. Notably, MAEA deficiency is associated with a developmental disorder involving microcephaly, craniofacial abnormalities, ocular defects, and heart malformations. Functional assays show that disease-linked MAEA variants (R34C, E349G, Y394D, and M396R) are defective in RS response. These findings establish MAEA as an essential factor in RF protection and genome integrity.

Humans↗

PubMed2026

Oral melanoma in the immunotherapy era: Immune evasion, resistance, and therapeutic opportunities.

Oral melanoma (OM) is a rare and highly aggressive mucosal malignancy associated with poor survival and limited evidence to guide immunotherapy. This narrative review synthesizes current knowledge on OM immunobiology and its therapeutic implications. OM differs from cutaneous melanoma in its origin in sun-protected sites, genomic architecture, and heterogeneous immune microenvironments, features that can contribute to attenuated responses to immune checkpoint inhibitors. Anti-PD-1-based therapy has demonstrated clinical activity in mucosal melanoma, and selected OM cases have shown meaningful responses, including in multimodal and perioperative settings. However, OM-specific prospective data remain sparse, and the available evidence is largely derived from pooled mucosal melanoma cohorts or case reports. Emerging combination strategies, such as antiangiogenic agents, radiotherapy, and perioperative immunotherapy, remain insufficiently validated. This review critically reappraises the available evidence, identifies key knowledge gaps, and outlines future directions for biomarker-driven, OM-specific translational research.

Humans↗

PubMed2025

Noncompetitive Inhibition of DNA Polymerase β by a Nonnative Nucleotide.

Base excision repair (BER) is a DNA repair pathway responsible for protecting the genome against modified nucleotides. DNA polymerase β (Pol β) participates in this process by removing the remnants of a damaged nucleotide and filling in the resulting gap. Pol β is overexpressed in some cancers and is synthetic lethal in cells deficient in BRCA1/2, providing additional impetus for identifying inhibitors of this enzyme. We report noncovalent Pol β inhibitors that are nonnative nucleotides. The inhibitors were identified via a combination of structural and biochemical analysis, as well as serendipity, from an initial library of covalent inhibitor candidates in which diversity was introduced sequentially at the C3'- and C5-positions of pyrimidine nucleotides. The molecules are among the most potent Pol β inhibitors (Ki ≤ 70 nM) of the enzyme's polymerase and lyase activities. Kinetic analyses reveal that the molecules inhibit Pol β noncompetitively. Fluorescence anisotropy and kinetic experiments reveal that the more potent inhibitor binds in the lyase domain and does not prevent DNA binding. Neither the more potent noncompetitive inhibitor nor a neutral protide exhibits cytotoxic synergism with the DNA damaging agent methyl methanesulfonate in HeLa cells. Cell permeability experiments suggest that micromolar levels of the more potent noncompetitive inhibitor and corresponding protide are taken up by HeLa cells following 24 h incubation (25 μM). However, based upon a comparison with other molecules, it is possible that they are membrane bound. The molecules identified could be useful tools in biochemical studies and provide a starting point for creating new Pol β inhibitors that function in cells.

DNA Polymerase beta↗

PubMed1975

Isolation of RNA transcripts from the entire Sendai viral genome.

Three classes of viral transcripts (18S, 24S, and 33S) were isolated from viral ribonucleoproteins in Sendai virus-infected cells. Hybridization studies with virion minus strand genome RNA demonstrated that the 18S RNA contained transcripts from 60% of the viral genome while the 33S RNA contained transcripts from the entire viral genome. Brief heat of ME2SO treatment of the 33S RNA demonstrated that this RNA was composed of two classes: RNA which continued to sediment at 33S (33S RNA) and 18S RNA aggregates (18S RNA). The 33S RNA was determined to be a transcript from the 40% of the viral genome not protected by the 18S RNA. The aggregated 18S RNA does not appear to be an artifact of isolation.

Culture Techniques↗