Protein regulation by ubiquitin technology
Research in my lab centres on the contributions of two posttranslational protein modifiers, ubiquitin and SUMO, to DNA replication, repair and genome stability. We focus in particular on DNA damage bypass, a system that allows genome replication in the presence of DNA-damaging agents. This pathway helps cells resist genotoxic agents, but also has the potential to cause genome instability and must be tightly regulated.
Regulation of DNA damage bypass in eukaryotic cells is achieved by posttranslational modification of the replication factor PCNA with monoubiquitin, polyubiquitin or SUMO. We are investigating how ubiquitin and SUMO modulate PCNA to initiate damage bypass, what cellular signals determine the balance between the different modifications, and how DNA damage bypass pathway is coordinated with genome replication and the overall cellular DNA damage response.
Positions held
2018-2019: Executive Director, IMB, Mainz
Since 2013: Scientific Director, Institute of Molecular Biology (IMB), Mainz; Professor, Faculty of Biology, University of Mainz
2004-2012: Group Leader, Cancer Research UK London Research Institute, Clare Hall Laboratories
2000-2004: Group Leader, Max Planck Institute for Terrestrial Microbiology, Marburg
1998-2000: Postdoc, Max Planck Institute for Biochemistry, Martinsried
1997-1998: Postdoc, University of Heidelberg
Education
2004: Habilitation, Faculty of Biology (Genetics), Philipps University Marburg
1996: PhD in Chemistry, University of California, Berkeley
1992: Diploma in Biology, Georg-August-University Göttingen
Selected publications by Helle Ulrich
Sriramachandran AM, Petrosino G, Méndez-Lago M, Schäfer AJ, Batista-Nascimento LS, Zilio N# and Ulrich HD# (2020) Genome-wide Nucleotide-Resolution Mapping of DNA Replication Patterns, Single-Strand Breaks, and Lesions by GLOE-Seq. Mol Cell, 78:975-985.e7 (#indicates joint correspondence) Link
Wong RP, García-Rodríguez N, Zilio N, Hanulová M and Ulrich HD (2020) Processing of DNA Polymerase-Blocking Lesions during Genome Replication Is Spatially and Temporally Segregated from Replication Forks. Mol Cell, 77:3–16.e4 Link
Sriramachandran AM, Meyer-Teschendorf K, Pabst S, Ulrich HD, Gehring NH, Hofmann K, Praefcke GJK and Dohmen RJ (2019) Arkadia/RNF111 is a SUMO-targeted ubiquitin ligase with preference for substrates marked with SUMO1-capped SUMO2/3 chain. Nat Commun, 10:3678 Link
García‐Rodríguez N, Morawska M, Wong RP, Daigaku Y and Ulrich HD (2018) Spatial separation between replisome‐ and template‐induced replication stress signaling. EMBO J, 37:e98369 Link
Hung SH, Wong RP, Ulrich HD# and Kao CF# (2017) Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication. Proc Natl Acad Sci USA, 114:E2205–E2214 (#indicates joint correspondence) Link