Research output: Contribution to journal › Article › peer-review
Replication timing analysis in polyploid cells reveals rif1 uses multiple mechanisms to promote underreplication in drosophila. / Das, Souradip; Caballero, Madison; Kolesnikova, Tatyana et al.
In: Genetics, Vol. 219, No. 3, iyab147, 11.2021.Research output: Contribution to journal › Article › peer-review
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TY - JOUR
T1 - Replication timing analysis in polyploid cells reveals rif1 uses multiple mechanisms to promote underreplication in drosophila
AU - Das, Souradip
AU - Caballero, Madison
AU - Kolesnikova, Tatyana
AU - Zhimulev, Igor
AU - Koren, Amnon
AU - Nordman, Jared
N1 - This work was supported by a National Science Foundation grant (MCB-818019 to J.T.N.); National Institutes of Health (DP2-GM123495 to A.K.) and the National Science Foundation (MCB1921341 to A.K.); and a Joint Russian-German grant from the Russian Foundation for Basic Research (No. 20-54-12016) and Deutsche Forschungsgemeinschaft Schu762/12-1. Illumina sequencing was performed at the VANTAGE core at Vanderbilt University Medical Center, which is supported by the CTSA Grant (5UL1 RR024975-03), the Vanderbilt-Ingram Cancer Center (P30 CA68485), the Vanderbilt Vision Center (P30 EY08126), and NIH/NCRR (G20 RR030956). Publisher Copyright: © 2021 Genetics Society of America. All rights reserved.
PY - 2021/11
Y1 - 2021/11
N2 - Regulation of DNA replication and copy number is necessary to promote genome stability and maintain cell and tissue function. DNA replication is regulated temporally in a process known as replication timing (RT). Rap1-interacting factor 1 (Rif1) is a key regulator of RT and has a critical function in copy number control in polyploid cells. Previously, we demonstrated that Rif1 functions with SUUR to inhibit replication fork progression and promote underreplication (UR) of specific genomic regions. How Rif1-dependent control of RT factors into its ability to promote UR is unknown. By applying a computational approach to measure RT in Drosophila polyploid cells, we show that SUUR and Rif1 have differential roles in controlling UR and RT. Our findings reveal that Rif1 acts to promote late replication, which is necessary for SUUR-dependent underreplication. Our work provides new insight into the process of UR and its links to RT.
AB - Regulation of DNA replication and copy number is necessary to promote genome stability and maintain cell and tissue function. DNA replication is regulated temporally in a process known as replication timing (RT). Rap1-interacting factor 1 (Rif1) is a key regulator of RT and has a critical function in copy number control in polyploid cells. Previously, we demonstrated that Rif1 functions with SUUR to inhibit replication fork progression and promote underreplication (UR) of specific genomic regions. How Rif1-dependent control of RT factors into its ability to promote UR is unknown. By applying a computational approach to measure RT in Drosophila polyploid cells, we show that SUUR and Rif1 have differential roles in controlling UR and RT. Our findings reveal that Rif1 acts to promote late replication, which is necessary for SUUR-dependent underreplication. Our work provides new insight into the process of UR and its links to RT.
KW - Common fragile sites
KW - DNA replication
KW - Drosophila
KW - Genome stability
KW - Replication timing
UR - http://www.scopus.com/inward/record.url?scp=85120670851&partnerID=8YFLogxK
U2 - 10.1093/genetics/iyab147
DO - 10.1093/genetics/iyab147
M3 - Article
C2 - 34740250
AN - SCOPUS:85120670851
VL - 219
JO - Genetics
JF - Genetics
SN - 0016-6731
IS - 3
M1 - iyab147
ER -
ID: 34967944