Geometrical Aberration Suppression for Large Aperture Sub-THz Lenses

Advanced THz setups require high performance optical elements with large numerical apertures and small focal lengths. This is due to the high absorption of humid air and relatively low efficiency of commercially available detectors. Here, we propose a new type of double-sided sub-THz diffractive optical element with suppressed geometrical aberration for narrowband applications (0.3 THz). One side of the element is designed as thin structure in non-paraxial approach which is the exact method, but only for ideally flat elements. The second side will compensate phase distribution differences between ideal thin structure and real volume one. The computer-aided optimization algorithm is performed to design an additional phase distribution of correcting layer assuming volume designing of the first side of the element. The experimental evaluation of the proposed diffractive component created by 3D printing technique shows almost two times larger performance in comparison with uncorrected basic diffractive lens

Replication and Recombination Factors Contributing to Recombination-Dependent Bypass of DNA Lesions by Template Switch

Damage tolerance mechanisms mediating damage-bypass and gap-filling are crucial for genome integrity. A major damage tolerance pathway involves recombination and is referred to as template switch. Template switch intermediates were visualized by 2D gel electrophoresis in the proximity of replication forks as X-shaped structures involving sister chromatid junctions. The homologous recombination factor Rad51 is required for the formation/stabilization of these intermediates, but its mode of action remains to be investigated. By using a combination of genetic and physical approaches, we show that the homologous recombination factors Rad55 and Rad57, but not Rad59, are required for the formation of template switch intermediates. The replication-proficient but recombination-defective rfa1-t11 mutant is normal in triggering a checkpoint response following DNA damage but is impaired in X-structure formation. The Exo1 nuclease also has stimulatory roles in this process. The checkpoint kinase, Rad53, is required for X-molecule formation and phosphorylates Rad55 robustly in response to DNA damage. Although Rad55 phosphorylation is thought to activate recombinational repair under conditions of genotoxic stress, we find that Rad55 phosphomutants do not affect the efficiency of X-molecule formation. We also examined the DNA polymerase implicated in the DNA synthesis step of template switch. Deficiencies in translesion synthesis polymerases do not affect X-molecule formation, whereas DNA polymerase δ, required also for bulk DNA synthesis, plays an important role. Our data indicate that a subset of homologous recombination factors, together with DNA polymerase δ, promote the formation of template switch intermediates that are then preferentially dissolved by the action of the Sgs1 helicase in association with the Top3 topoisomerase rather than resolved by Holliday Junction nucleases. Our results allow us to propose the choreography through which different players contribute to template switch in response to DNA damage and to distinguish this process from other recombination-mediated processes promoting DNA repair