Histone H3 lysine 56 acetylation by Rtt109 is crucial for chromosome positioning

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SAF-A promotes origin licensing and replication fork progression to ensure robust DNA replication

Funding CC was supported by a BBSRC EASTBIO Doctoral Training programme PhD studentship. SH was supported by Daiwa Anglo-Japanese Foundation 812 (12928/13746). Work in the Hiraga-Donaldson lab supported by Cancer Research UK awards C1445/A19059 and DRCPGM\100013. NG is supported by Medical Research Council (MC_UU_00007/13) Acknowledgements Information for SAF-A expression was obtained at The Cancer Genome Atlas TCGA) Research Network (https://www.cancer.gov/tcga). We thank Dr Ryu-suke Nozawa for help in the early stage of the project, and Professor Julian Blow for advice on the 3D licensing assay. Thanks to the staff of the Iain Fraser Cytometry Centre, and Microscopy and Histology facility at the University of Aberdeen.Peer reviewedPostprin

Protein phosphatase 1 acts as a RIF1 effector to suppress DSB resection prior to Shieldin action

Funding Information: We thank K. Murakami, H. Kimura, H. Kurumizaka, and J.M. Stark for materials. This work was supported by JSPS KAKENHI grant nos. JP19H03156 , JP18H04713 , JP18H05532 , and JP25116004 (to C.O.), JP17H06426 (to K.N.), JP18H04900 and JP19H04267 (to H.S.), the Mitsubishi Foundation (to H.S.), and by Cancer Research UK awards C1445/A19059 and DRCPGM/100013 (to S.H. and A.D.D. lab). Publisher Copyright: © 2021 The Author(s)Peer reviewedPublisher PD

Human RIF1-Protein Phosphatase 1 Prevents Degradation and Breakage of Nascent DNA on Replication Stalling

We thank the Microscopy Core and Proteomics Core Facilities at Aberdeen University for assistance and analysis. pCMV-Flag-WRN plasmid was kindly gifted by Pietro Pichierri. NSC-105808 from Grzegorz Ira lab was gifted by Alessandro Vindigni. We thank all the members of our lab and Takashi Kubota for helpful discussions. This research was supported by Cancer Research UK Programme Award A19059 to ADD and SH.Peer reviewedPublisher PD

Budding yeast Rif1 binds to replication origins and protects DNA at blocked replication forks

We thank Javier Garzon and Vamsi Krishna Gali for discussion and advice on methods, and Takashi Kubota for helpful comments on the manuscript. This work was supported by Cancer Research UK Programme Award A19059 to ADD and SH. KS was supported by Grant‐in‐Aid for Scientific Research on Priority Areas (15H05970 and 15K21761) from Ministry of Education, Culture, Sports, Science and Technology, Japan. Funding Cancer Research UK (CRUK) A19059 Ministry of Education, Culture, Sports, Science and Technology (MEXT) 15H0597015K21761 Data availability ChIP‐Seq data and corresponding input data were submitted to ArrayExpress under accession number E‐MTAB‐6736.Peer reviewedPublisher PD

OriDB: a DNA replication origin database

Replication of eukaryotic chromosomes initiates at multiple sites called replication origins. Replication origins are best understood in the budding yeast Saccharomyces cerevisiae, where several complementary studies have mapped their locations genome-wide. We have collated these datasets, taking account of the resolution of each study, to generate a single list of distinct origin sites. OriDB provides a web-based catalogue of these confirmed and predicted S.cerevisiae DNA replication origin sites. Each proposed or confirmed origin site appears as a record in OriDB, with each record comprising seven pages. These pages provide, in text and graphical formats, the following information: genomic location and chromosome context of the origin site; time of origin replication; DNA sequence of proposed or experimentally confirmed origin elements; free energy required to open the DNA duplex (stress-induced DNA duplex destabilization or SIDD); and phylogenetic conservation of sequence elements. In addition, OriDB encourages community submission of additional information for each origin site through a User Notes facility. Origin sites are linked to several external resources, including the Saccharomyces Genome Database (SGD) and relevant publications at PubMed. Finally, a Chromosome Viewer utility allows users to interactively generate graphical representations of DNA replication data genome-wide. OriDB is available at www.oridb.org

The RIF1-Long splice variant promotes G1 phase 53BP1 nuclear bodies to protect against replication stress

Acknowledgements Thanks to members of the Aberdeen Chromosome Biology Group for helpful comments, and Ronan Broderick and Wojciech Niedzwiedz for advice on mitotic bridge analysis. We thank Raif Yuecel and his team at the Iain Fraser Cytometry Centre for assistance, and Kevin Mackenzie and his team at the Microscopy and Histology Core Facility. Work was supported by Cancer Research UK Studentship Award C1445/A20596 and CRUK Programme Award C1445/A19059; by JSPS KAKENHI Grants Numbers 17K15068, 18H02170 and 18H04719; by research grants from the Daiichi Sankyo’s Foundation of Life Science and the Takeda Science Foundation; and by the UK Medical Research Council (MC_UU_00007/13). Collaboration was supported by a 2017 JSPS Summer Programme Fellowship. Funding Cancer Research UK (C1445/A20596) Anne D Donaldson Cancer Research UK (C1445/A19059) Anne D Donaldson Japan Society for the Promotion of Science (17K15068) Masato T Kanemaki Japan Society for the Promotion of Science (18H02170) Masato T Kanemaki Japan Society for the Promotion of Science (18H04719) Masato T Kanemaki Medical Research Council (MC_UU_00007/13) Nick GilbertPeer reviewedPublisher PD

Human RIF1 and protein phosphatase 1 stimulate DNA replication origin licensing but suppress origin activation

We thank David Stead at the Aberdeen Proteomics Service for help in mass spectrometry interpretation, and Raif Yücel and his team at the University of Aberdeen Iain Fraser Cytometry Centre for assistance with flow cytometry. We thank Robert Alver and Julian Blow at University of Dundee for advice on the use of tautomycetin. Peter Cherepanov of the Francis Crick Institute gifted XL413. Daniel Durocher of Lunenfeld-Tanenbaum Research Institute gifted DNA constructs. Work by ADD and SH was supported by Cancer Research UK Grant A13356, Cancer Research UK Programme Award A19059, and BBSRC grant (BB/K006304/1). AIL was supported by Wellcome Trust Awards (108058/Z/15/Z & 105024/Z/14/Z). This work was also supported by JSPS KAKENHI Grant # 16H04739, 25116004 to CO and 16J04327 to YO.Peer reviewedPublisher PD

Rif1 acts through Protein Phosphatase 1 but independent of replication timing to suppress telomere extension in budding yeast

ACKNOWLEDGEMENTS We thank Katsunori Sugimoto for strains, plasmids and technical advice. We thank Amanda Williams for Illumina NextSeq 500 technical support and advice. Takashi Kubota provided helpful comments on the manuscript. FUNDING Cancer Research UK Programme Award [A19059 to A.D., S.H.]; Wellcome Trust Investigator Award [110064/Z/15/Z to C.A.N., R.H.C.W.]; SULSA PhD Studentship (to S.K.). Funding for open access charge: Cancer Research UK via University of Aberdeen Open Access Fund. Conflict of interest statement. None declared.Peer reviewedPublisher PD

Protection of nascent DNA at stalled replication forks is mediated by phosphorylation of RIF1 intrinsically disordered region

Acknowledgements We thank all members of the Di Virgilio lab for their feedback and discussion; V Delgado-Benito (Di Virgilio lab, MDC, Berlin) for her contribution to the project development; L Keller (Di Virgilio lab, MDC, Berlin) for support with cloning, mutagenesis, and mice genotyping; C Brischetto (Scheidereit Lab, MDC, Berlin) for assistance with confocal microscopy; Aberdeen Proteomics facility (University of Aberdeen) for the mass spec analysis of Aph-induced hRIF1 phosphorylation; and the MDC FACS Core Facility and Dr. HP Rahn for support with cell sorting. Aliquots of ATRi and ATMi were gener- ously provided by AG Henssen (MDC and ECRC, Berlin). Figures 1B and D, 2A, and 4C contain items created with BioRender.com. This work was supported by ERC grant 638897 (to MDV), the Helmholtz- Gemeinschaft Zukunftsthema 'Immunology and Inflammation' ZT-0027 (to MDV), P41 GM109824 and P41 GM103314 (to BTC), and Cancer Research UK awards C1445/A19059 and DRCPGM\100,013 (to ADD and SH).Peer reviewedPublisher PD