کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8320474 | 1539384 | 2016 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
High-resolution genomic assays provide insight into the division of labor between TLS and HDR in mammalian replication of damaged DNA
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کلمات کلیدی
MEFssDNAICLMMRPPRBERTSRNHEJTLSHDRXPAPCNACSTRdsDNAXeroderma pigmentosum variantXPVCRISPRDSBxeroderma pigmentosum complementation group Acpd - CPDSingle-stranded DNA - DNA تک رشته ایdouble-stranded DNA - DNA رشته ایNER - DOWNDNA damage - آسیبDNAProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیUltraviolet - اشعه فرابنفشDNA damage tolerance - تحمل آسیب DNAnucleotide excision repair - تعمیر مجدد نوکلئوتیدیmismatch repair - تعمیر ناسازگاریbase excision repair - تعمیر پایه پایهpostreplication repair - تعمیر پس از اعمالRecombination - دوباره سازیDDT - دیکرو دیفنیل تری کلرواتانcyclobutane pyrimidine dimer - دییریر پیریمیدین cyclobutanetranslesion DNA synthesis - سنتز DNA ترجمه شدهTemplate switch - سوئیچ الگوdouble strand break - شکست دو رشتهnon-homologous end joining - عدم پیوستن انتهای غیر همولوگmouse embryonic fibroblasts - موش فیبروبلاست جنینیpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازpol - پل
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The multitude of DNA lesions that continuously form in DNA cannot all be detected and removed prior to replication. Thus, encounters of the replication fork with DNA damage become inevitable. Such encounters inhibit fork progression, leading to replication fork arrest or to replication re-priming downstream of the damage site. Either of these events will result in the formation of gap-lesion structures, in which a damaged base is located in a single stranded stretch of DNA, that is vulnerable to subsequent nicking. The double strand break that would ensue if ssDNA becomes nicked constitutes escalation of the damage from nucleotide(s)-specific to chromosomal scale. Cells employ two universal DNA damage tolerance (DDT) strategies to resolve these situations, by converting the gap-lesion structures into dsDNA without repairing the damage. The first is translesion DNA synthesis (TLS), in which a specialized low-fidelity DNA polymerase inserts a nucleotide opposite the damaged one. TLS is inherently mutagenic, due to the miscoding nature of most damaged nucleotides. The second strategy is homology-dependent repair (HDR), which relies on the presence of an identical intact sister chromatid. The molecular mechanisms that regulate the division of labor between these pathways are poorly understood. This review focuses on the balance between TLS and HDR in mammalian cells, discussing recent findings that were made possible thanks to newly developed high resolution genomic assays, and highlighting the role of the DNA lesion's properties in DDT pathway choice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: DNA Repair - Volume 44, August 2016, Pages 59-67
Journal: DNA Repair - Volume 44, August 2016, Pages 59-67
نویسندگان
Zvi Livneh, Isadora S. Cohen, Tamar Paz-Elizur, Dana Davidovsky, Dalit Carmi, Umakanta Swain, Nataly Mirlas-Neisberg,