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Biology subjects

Dannenberg, R. L.

Publications and source records attributed to Dannenberg, R. L..

2 recordsLinked to original sources

Interplay of macromolecular interactions during assembly of human DNA polymerase δ holoenzymes and initiation of DNA synthesis

In humans, DNA polymerase {delta} (Pol {delta}) holoenzymes, comprised of Pol {delta} and the processivity sliding clamp, proliferating cell nuclear antigen (PCNA), carry out DNA synthesis during lagging strand DNA replication, initiation of leading strand DNA replication, and the major DNA damage repair and tolerance pathways. Pol {delta} holoenzymes are assembled at primer/template (P/T) junctions and initiate DNA synthesis in a coordinated process involving the major single strand DNA-binding protein complex, replication protein A (RPA), the processivity sliding clamp loader, replication factor C (RFC), PCNA, and Pol {delta}. Each of these factors interact uniquely with a P/T junction and most directly engage one another. Currently, the interplay between these macromolecular interactions is largely unknown. In the present study, novel Forster Resonance Energy Transfer (FRET) assays reveal that dynamic interactions of RPA with a P/T junction during assembly of a Pol {delta} holoenzyme and initiation of DNA synthesis maintain RPA at a P/T junction and accommodate RFC, PCNA, and Pol {delta}, maximizing the efficiency of each process. Collectively, these studies significantly advance our understanding of human DNA replication and DNA repair.

biochemistry↗

High resolution studies of DNA lesion bypass by human DNA polymerase δ holoenzymes

During DNA replication, DNA lesions present in lagging strand templates are initially encountered by DNA polymerase {delta} (pol {delta}). The historical view for what transpires from these encounters is that replication of the afflicted lagging strand template abruptly stops, activating DNA damage tolerance (DDT) pathways that replicate the offending lesion and adjacent DNA sequence, allowing pol {delta} to resume downstream. However, qualitative studies observed that human pol {delta} is capable of replicating various DNA lesions, albeit to unknown extents, which raises issues regarding the roles of pol {delta} and DDT in the replication of DNA lesions. To address these issues, we re-constituted human lagging strand replication to quantitatively characterize initial encounters of pol {delta} holoenzymes with DNA lesions. The results indicate that pol {delta} holoenzymes support stable dNTP incorporation opposite and beyond multiple lesions and the extent of these activities depends on the lesion and pol {delta} proofreading. Furthermore, after encountering a given DNA lesion, subsequent dissociation of pol {delta} is distributed around the lesion and a portion of pol {delta} does not dissociate at all. The distributions of these events are dependent on the lesion and pol {delta} proofreading. These results challenge our understanding of DNA lesion replication and DDT.

biochemistry↗