Different graft thicknesses after Descemet stripping endothelial keratoplasty for bullous keratopathy in the two eyes of the same patient.

Objective: To describe a very unique case of two Descemet stripping automated endothelial keratoplasty (DSAEK) surgeries performed in both eyes of the same patient with an extremely different graft thickness and overall corneal thickness but with the same corrected distance visual acuity (CDVA) 2 years after surgery.

Case Presentation: A 75-year-old woman with bilateral bullous keratopathy (BK) was submitted to DSAEK surgeries in both eyes, first in right and after 6 months in left eye. CDVA was 20/160 in the right eye and 20/63 in the left eye.

Processing closely spaced lesions during Nucleotide Excision Repair triggers mutagenesis in E. coli.

It is generally assumed that most point mutations are fixed when damage containing template DNA undergoes replication, either right at the fork or behind the fork during gap filling. Here we provide genetic evidence for a pathway, dependent on Nucleotide Excision Repair, that induces mutations when processing closely spaced lesions. This pathway, referred to as Nucleotide Excision Repair-induced Mutagenesis (NERiM), exhibits several characteristics distinct from mutations that occur within the course of replication: i) following UV irradiation, NER-induced mutations are fixed much more rapidly (t ½ ≈ 30 min) than replication dependent mutations (t ½ ≈ 80-100 min) ii) NERiM specifically requires DNA Pol IV in addition to Pol V iii) NERiM exhibits a two-hit dose-response curve that suggests processing of closely spaced lesions.

Increase in dNTP pool size during the DNA damage response plays a key role in spontaneous and induced-mutagenesis in Escherichia coli.

Exposure of Escherichia coli to UV light increases expression of NrdAB, the major ribonucleotide reductase leading to a moderate increase in dNTP levels. The role of elevated dNTP levels during translesion synthesis (TLS) across specific replication-blocking lesions was investigated. Here we show that although the specialized DNA polymerase PolV is necessary for replication across UV-lesions, such as cyclobutane pyrimidine dimers or pyrimidine(6-4)pyrimidone photoproduct, Pol V per se is not sufficient.