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  1. Article ; Online: The interplay of 3D genome organization with UV-induced DNA damage and repair.

    Akköse, Ümit / Adebali, Ogün

    The Journal of biological chemistry

    2023  Volume 299, Issue 5, Page(s) 104679

    Abstract: The 3D organization of the eukaryotic genome is crucial for various cellular processes such as gene expression and epigenetic regulation, as well as for maintaining genome integrity. However, the interplay between UV-induced DNA damage and repair with ... ...

    Abstract The 3D organization of the eukaryotic genome is crucial for various cellular processes such as gene expression and epigenetic regulation, as well as for maintaining genome integrity. However, the interplay between UV-induced DNA damage and repair with the 3D structure of the genome is not well understood. Here, we used state-of-the-art Hi-C, Damage-seq, and XR-seq datasets and in silico simulations to investigate the synergistic effects of UV damage and 3D genome organization. Our findings demonstrate that the peripheral 3D organization of the genome shields the central regions of genomic DNA from UV-induced damage. Additionally, we observed that potential damage sites of pyrimidine-pyrimidone (6-4) photoproducts are more prevalent in the nucleus center, possibly indicating an evolutionary pressure against those sites at the periphery. Interestingly, we found no correlation between repair efficiency and 3D structure after 12 min of irradiation, suggesting that UV radiation alters the genome's 3D organization in a short period of time. Interestingly, however, 2 h after UV induction, we observed more efficient repair levels in the center of the nucleus relative to the periphery. These results have implications for understanding the etiology of cancer and other diseases, as the interplay between UV radiation and the 3D genome may play a role in the development of genetic mutations and genomic instability.
    MeSH term(s) DNA Damage ; DNA Repair ; Epigenesis, Genetic ; Pyrimidine Dimers/metabolism ; Ultraviolet Rays/adverse effects
    Chemical Substances Pyrimidine Dimers
    Language English
    Publishing date 2023-04-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.104679
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Boquila: NGS read simulator to eliminate read nucleotide bias in sequence analysis.

    Akköse, Ümit / Adebali, Ogün

    Turkish journal of biology = Turk biyoloji dergisi

    2023  Volume 47, Issue 2, Page(s) 158–163

    Abstract: Sequence content is heterogeneous throughout genomes. Therefore, genome-wide next-generation sequencing (NGS) reads biased towards specific nucleotide profiles are affected by the genome-wide heterogeneous nucleotide distribution. Boquila generates ... ...

    Abstract Sequence content is heterogeneous throughout genomes. Therefore, genome-wide next-generation sequencing (NGS) reads biased towards specific nucleotide profiles are affected by the genome-wide heterogeneous nucleotide distribution. Boquila generates sequences that mimic the nucleotide profile of true reads, which can be used to correct the nucleotide-based bias of genome-wide distribution of NGS reads. Boquila can be configured to generate reads from only specified regions of the reference genome. It also allows the use of input DNA sequencing to correct the bias due to the copy number variations in the genome. Boquila uses standard file formats for input and output data, and it can be easily integrated into any workflow for high-throughput sequencing applications.
    Language English
    Publishing date 2023-02-21
    Publishing country Turkey
    Document type Journal Article
    ZDB-ID 2046470-8
    ISSN 1303-6092 ; 1303-6092
    ISSN (online) 1303-6092
    ISSN 1303-6092
    DOI 10.55730/1300-0152.2650
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Sibling rivalry among the ZBTB transcription factor family: homodimers versus heterodimers.

    Piepoli, Sofia / Barakat, Sarah / Nogay, Liyne / Şimşek, Büşra / Akkose, Umit / Taskiran, Hakan / Tolay, Nazife / Gezen, Melike / Yeşilada, Canberk Yarkın / Tuncay, Mustafa / Adebali, Ogün / Atilgan, Canan / Erman, Batu

    Life science alliance

    2022  Volume 5, Issue 11

    Abstract: The BTB domain is an oligomerization domain found in over 300 proteins encoded in the human genome. In the family of BTB domain and zinc finger-containing (ZBTB) transcription factors, 49 members share the same protein architecture. The N-terminal BTB ... ...

    Abstract The BTB domain is an oligomerization domain found in over 300 proteins encoded in the human genome. In the family of BTB domain and zinc finger-containing (ZBTB) transcription factors, 49 members share the same protein architecture. The N-terminal BTB domain is structurally conserved among the family members and serves as the dimerization site, whereas the C-terminal zinc finger motifs mediate DNA binding. The available BTB domain structures from this family reveal a natural inclination for homodimerization. In this study, we investigated the potential for heterodimer formation in the cellular environment. We selected five BTB homodimers and four heterodimer structures. We performed cell-based binding assays with fluorescent protein-BTB domain fusions to assess dimer formation. We tested the binding of several BTB pairs, and we were able to confirm the heterodimeric physical interaction between the BTB domains of PATZ1 and PATZ2, previously reported only in an interactome mapping experiment. We also found this pair to be co-expressed in several immune system cell types. Finally, we used the available structures of BTB domain dimers and newly constructed models in extended molecular dynamics simulations (500 ns) to understand the energetic determinants of homo- and heterodimer formation. We conclude that heterodimer formation, although frequently described as less preferred than homodimers, is a possible mechanism to increase the combinatorial specificity of this transcription factor family.
    MeSH term(s) Amino Acid Sequence ; Gene Expression Regulation ; Humans ; Transcription Factors/genetics ; Zinc Fingers/genetics
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2022-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202201474
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events.

    Akkose, Umit / Kaya, Veysel Ogulcan / Lindsey-Boltz, Laura / Karagoz, Zeynep / Brown, Adam D / Larsen, Peter A / Yoder, Anne D / Sancar, Aziz / Adebali, Ogun

    BMC genomics

    2021  Volume 22, Issue 1, Page(s) 600

    Abstract: Background: Nucleotide excision repair is the primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), ... ...

    Abstract Background: Nucleotide excision repair is the primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair in gray mouse lemur, Microcebus murinus, in comparison to human.
    Results: We derived fibroblast cell lines from mouse lemur, exposed them to UV irradiation, and analyzed the repair events genome-wide using the XR-seq protocol. Mouse lemur repair profiles were analyzed in comparison to the equivalent human fibroblast datasets. We found that overall UV sensitivity, repair efficiency, and transcription-coupled repair levels differ between the two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions are highly correlated, and this correlation is stronger for highly expressed genes. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts of the two primates repair UV-induced DNA lesions in a more similar pattern than two distinct human cell lines do.
    Conclusion: Our results suggest that mouse lemurs and humans, and possibly primates in general, share a homologous repair mechanism as well as genomic variance distribution, albeit with their variable repair efficiency. This result also emphasizes the deep homologies of individual tissue types across the eukaryotic phylogeny.
    MeSH term(s) Animals ; DNA Damage/genetics ; DNA Repair/genetics ; Genome, Human ; Humans ; Primates/genetics ; Pyrimidine Dimers ; Ultraviolet Rays
    Chemical Substances Pyrimidine Dimers
    Language English
    Publishing date 2021-08-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041499-7
    ISSN 1471-2164 ; 1471-2164
    ISSN (online) 1471-2164
    ISSN 1471-2164
    DOI 10.1186/s12864-021-07898-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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