bioRxiv Science⌕ Search

Biology subjects

Thiesen, C.

Publications and source records attributed to Thiesen, C..

2 recordsLinked to original sources

Extracellular G-quadruplex and Z-DNA protect biofilms from DNase I and forms a DNAzyme with peroxidase activity

Many bacteria form biofilms to protect themselves from predators or stressful environmental conditions. In the biofilm, bacteria are embedded in a protective extracellular matrix composed of polysaccharides, proteins and extracellular DNA (eDNA). eDNA most often arises from lysed cells, and it is the only matrix component most biofilms appear to have in common. However, little is known about the form DNA takes in the extracellular space, and how different non-canonical DNA structures such as Z-DNA or G-quadruplex formation might contribute to its function in the biofilm. The aim of this study was to determine if non-canonical DNA structures form in eDNA-rich staphylococcal biofilms, and if these structures protect the biofilm from degradation by nucleases. We grew Staphylococcus epidermidis biofilms in laboratory media amended with hemin and NaCl to stabilize secondary DNA structures and visualized their location by immunolabelling and fluorescence microscopy. We furthermore visualized the macroscopic biofilm structure by optical coherence tomography. We developed assays to quantify degradation of Z-DNA and G-quadruplex DNA oligos by different nucleases, and subsequently investigated how these enzymes affected eDNA in the biofilms. Z-DNA and G-quadruplex DNA were abundant in the biofilm matrix, and were often present in a web-like structure in biofilms grown in vitro and in vivo using a murine implant-associated osteomyelitis model. In vitro, the structures did not form in the absence of NaCl or mechanical shaking during biofilm growth, or in bacterial strains deficient in eDNA or exopolysaccharide production. We thus infer that eDNA and polysaccharides interact, leading to non-canonical DNA structures under mechanical stress when stabilized by salt, and we confirmed that G-quadruplex DNA and Z-DNA was also present in biofilms from infected implants. Mammalian DNase I lacked activity against Z-DNA and G-quadruplex DNA, while Micrococcal nuclease could degrade G-quadruplex DNA and S1 Aspergillus nuclease could degrade Z-DNA. Micrococcal nuclease, which originates from Staphylococcus aureus, may thus be key for dispersal of biofilm in staphylococci. In addition to its structural role, we show for the first time that the eDNA in biofilms forms a DNAzyme with peroxidase-like activity in the presence of hemin. While peroxidases are part of host defenses against pathogens, we now show that biofilms can possess intrinsic peroxidase activity in the extracellular matrix. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=152 SRC="FIGDIR/small/541711v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@c32012org.highwire.dtl.DTLVardef@6e8c7eorg.highwire.dtl.DTLVardef@1c9cc6corg.highwire.dtl.DTLVardef@18be51e_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

Nanoparticle mediated in vitro and in vivo CRISPR base correction of LCA16 causing nonsense mutation rescues Kir7.1 channel function

Clinical genome editing is emerging for rare disease treatment, but one of the major limitations is the targeted delivery of CRISPR editors. We delivered base editors to the retinal pigmented epithelium (RPE) in the mouse eye using silica nanocapsules (SNC) as a treatment for retinal degeneration. Leber Congenital Amaurosis (LCA16) is a rare pediatric blindness caused by point mutations in the KCNJ13 gene, a loss-of-function inwardly rectifying potassium channel (Kir7.1) in the RPE. SNC carrying adenine base editor (ABE8e) mRNA and single-guide RNA precisely and efficiently corrected KCNJ13W53X/W53X mutation. Editing in both patient fibroblasts (47%) and human-induced pluripotent stem cell-derived RPE (LCA16-iPSC-RPE) (17%) had a negligible off-target response. Functional Kir7.1 channels were recorded from the edited LCA16-iPSC-RPE. In the LCA16 mouse model (Kcnj13W53X/+{Delta}R), RPE cells targeted SNC delivery of ABE8e mRNA preserved normal visual function measured by full-field electroretinogram (ERG). Moreover, multifocal ERG confirmed the topographic measure of electrical activity primarily originating from the edited retinal area at the injection site. Preserved retina structure, post-treatment, was established by Optical Coherence Tomography (OCT). This preclinical validation of targeted ion channel functional rescue, a challenge for pharmacological and genomic interventions, reinforces the effectiveness of nonviral genome editing therapy for rare inherited disorders. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=174 SRC="FIGDIR/small/499808v3_ufig1.gif" ALT="Figure 1"> View larger version (56K): org.highwire.dtl.DTLVardef@1fb405eorg.highwire.dtl.DTLVardef@3f14c1org.highwire.dtl.DTLVardef@16bb82aorg.highwire.dtl.DTLVardef@107d862_HPS_FORMAT_FIGEXP M_FIG C_FIG

genetics↗