کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5511015 | 1539378 | 2017 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cell cycle-dependent positive and negative functions of Fun30 chromatin remodeler in DNA damage response
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کلمات کلیدی
CPTDSBTLSG6PDDNA topoisomerase IMMSssDNAddC - DDCsingle stranded DNA - DNA تک رشته ایCell cycle checkpoint - ایست بازرسی چرخه سلولیDNA damage tolerance - تحمل آسیب DNATemplate switching - تعویض الگوTopo I - توپو IDDT - دیکرو دیفنیل تری کلرواتانtranslesion synthesis - سنتز ترجمهmethyl methanesulfonate - متیل متان سولفوناتDNA damage checkpoint - نقطه بازرسی آسیب DNAHomologous recombination - نوترکیبی همولوگDNA replication - همانندسازی DNA، تکثیر DNAHydroxyurea - هیدروکسی اورهDNA damage response - واکنش به آسیب DNA Genotoxin - ژنوتوکسینcamptothecin - کامپتوتسین glucose-6-phosphate dehydrogenase - گلوکز 6-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
The evolutionally conserved Fun30 chromatin remodeler in Saccharomyces cerevisiae has been shown to contribute to cellular resistance to genotoxic stress inflicted by camptothecin (CPT), methyl methanesulfonate (MMS) and hydroxyurea (HU). Fun30 aids in extensive DNA resection of DNA double stranded break (DSB) ends, which is thought to underlie its role in CPT-resistance. How Fun30 promotes MMS- or HU-resistance has not been resolved. Interestingly, we have recently found Fun30 to also play a negative role in cellular tolerance to MMS and HU in the absence of the Rad5-dependent DNA damage tolerance pathway. In this report, we show that Fun30 acts to down regulate Rad9-dependent DNA damage checkpoint triggered by CPT or MMS, but does not affect Rad9-independent intra-S phase replication checkpoint induced by MMS or HU. These results support the notion that Fun30 contributes to cellular response to DSBs by preventing excessive DNA damage checkpoint activation in addition to its role in facilitating DNA end resection. On the other hand, we present evidence suggesting that Fun30's negative function in MMS- and HU-tolerance in the absence of Rad5 is not related to its regulation of checkpoint activity. Moreover, we find Fun30 to be cell cycle regulated with its abundance peaking in G2/M phase of the cell cycle. Importantly, we demonstrate that artificially restricting Fun30 expression to G2/M does not affect its positive or negative function in genotoxin-resistance, but confining Fun30 to S phase abolishes its functions. These results indicate that both positive and negative functions of Fun30 in DNA damage response occur mainly in G2/M phase.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: DNA Repair - Volume 50, February 2017, Pages 61-70
Journal: DNA Repair - Volume 50, February 2017, Pages 61-70
نویسندگان
Jasmine Siler, Bowen Xia, Carina Wong, Morgan Kath, Xin Bi,