bioRxiv Science⌕ Search

bioRxiv · 10.1101/2020.04.10.036236

Visualizing Rev1 Catalyze Protein-template DNA Synthesis

Abstract

During DNA replication, replicative DNA polymerases may encounter DNA lesions, which can stall replication forks. One way to prevent replication fork stalling is through the recruitment of specialized translesion synthesis (TLS) polymerases that have evolved to incorporate nucleotides opposite DNA lesions. Rev1 is a specialized TLS polymerase that bypasses abasic sites as well as minor-groove and exocyclic guanine adducts. It does this by using a unique protein-template mechanism in which the template base is flipped out of the DNA helix and the incoming dCTP hydrogen bonds with an arginine side chain. To observe Rev1 catalysis at the atomic level, we employed time-lapse X-ray crystallography. We found that Rev1 flips out the template base prior to binding the incoming nucleotide. Binding the incoming nucleotide changes the conformation of the DNA substrate to orient it for nucleotidyl transfer, and this is not coupled to large structural changes in the protein like those observed with other DNA polymerases. Moreover, we found that following nucleotide incorporation, Rev1 converts the pyrophosphate product to two mono-phosphates, which drives the reaction in the forward direction. Following nucleotide incorporation, the hydrogen bonds between the incorporated nucleotide and the arginine side chain are broken, but the templating base remains extrahelical. These post-catalytic changes prevent potentially mutagenic processive synthesis by Rev1 and facilitate dissociation of the DNA product from the enzyme.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Weaver, T. M., Cortez, L. M., Khoang, T. H., Washington, M. T., Agarwal, P., Freudenthal, B. D.. 2020-04-12. Visualizing Rev1 Catalyze Protein-template DNA Synthesis. https://doi.org/10.1101/2020.04.10.036236

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The structures of two intermediates en route to DNA repair within a (6-4) photolyase

Pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) are mutagenic DNA lesions produced when UV light crosslinks two adjacent pyrimidine bases. These lesions must be repaired to maintain genome integrity, a function executed by the (6-4) photolyase enzymes. This repair chemistry is complex, involving the transfer of a hydroxyl group from one base to another, accompanied or followed by cleavage of an interbase bond. It remains unclear how the enzyme orchestrates this reaction. Typically, models invoke a stepwise process in which an oxetane intermediate is transiently populated, but despite over thirty years of investigation, such an intermediate has never been definitively observed. Conducting dose-controlled X-ray crystallography on the (6-4) photolyase from Vibrio cholerae, we observed the transformation of 6-4PP into an oxetane species. Furthermore, we identified a previously unanticipated hemi-cleaved intermediate. The progressive transformation of 6-4PP into oxetane, hemi-cleaved, and fully repaired species requires a reexamination of the existing models of DNA repair by (6-4) photolyases.

biochemistry↗

Endothelial protein C receptor is an entry receptor for Langya virus

Langya virus (LayV) was recently discovered in infected individuals with febrile illness and classified as a Parahenipavirus, a group of poorly understood pathogens. LayV is distantly related to Nipah henipavirus which causes recurring outbreaks with case fatality rates reaching up to 90%. No vaccines or therapeutics are approved for use in humans for any parahenipavirus or henipavirus despite their broad geographic distribution and pandemic potential. Here, we discovered that human endothelial protein C receptor (EPCR) is an entry receptor for LayV and that the tetrameric LayV attachment glycoprotein (G) binds EPCR avidly. We reveal the molecular basis of LayV G recognition of the EPCR receptor and provide a blueprint of the determinants of receptor ortholog usage. We found that human and shrew EPCR orthologs promote cell entry of LayV and of the closely related Mojiang pseudoviruses. These results along with the detection of several Parahenipaviruses in shrews set these pathogens apart from Henipaviruses, which use Pteropid fruit bats as reservoir hosts. Our data support future surveillance efforts, by enabling prediction of EPCR utilization among newly discovered Parahenipaviruses, and the development and evaluation of countermeasures targeting this emerging group of human pathogens.

biochemistry↗

RNA-targeted aminopyridine compounds provide a new antifungal strategy

While RNA is an emerging therapeutic target class, progress is limited by a shortage of well-defined targets in which ligand binding is coupled to measurable function. The group I intron, a self-splicing ribozyme essential in fungal mitochondria but absent from humans, offers both a tractable platform for exploring first principles of small molecule-RNA targeting and a selective antifungal target. We recalibrated an intron-splicing assay to approximate cellular conditions and performed an extensive, cryo-EM-guided structure-activity relationship campaign against the Candida albicans mtLSU intron. Ligands containing a flexible diamine outperformed conformationally constrained analogues, suggesting a general principle for engaging dynamic RNA surfaces and yielding lead aminopyridine 56 (IC 21.6 nM). Compound 56 synergizes with amphotericin B against C. albicans, suggesting a path for combination therapies. RT-qPCR confirmed direct target engagement in cells. This work establishes the fungal group I intron as a viable, mechanistically distinct antifungal target and a model platform for RNA-targeted discovery.

biochemistry↗