single mutant exhibits growth delay and cell cycle abnormalities and shows a strong spontaneous mutator phenotype. All phenotypes of the dut1-1 mutant are suppressed by the simultaneous inactivation of the uracil DNA N-glycosylase, Ung1. However, the ung1 dut1-1 double mutant accumulates uracil in its

nuclear foci as a novel approach for monitoring the repair of DSBs, we show here that NHEJ-defective hamster cells (CHO mutant V3 cells) have strongly reduced repair in all cell cycle phases after 1 Gy of irradiation. In contrast, HR-defective CHO irs1SF cells have a minor repair defect in G 1, greater

-stranded oligonucleotide substrate less efficiently than double-stranded oligonucleotide. The CeUng-1 activity was inhibited by Bacillus subtilis Ung inhibitor, indicating that CeUng-1 is a member of the family-1 Ung group. The mutation in the ung-1 gene did not affect development, fertility and lifespan in C

Chromosomal double-strand breaks (DSBs) in mammalian cells are repaired by either homology-directed repair (HDR), using a homologous sequence as a repair template, or nonhomologous end-joining (NHEJ), which often involves sequence alterations at the DSB site. To characterize the interrelationship

-strand annealing between distant repeats while the remaining long-range resection activity depends on the exonuclease Exo1. In exo1D sgs1D double mutants, the MRX complex together with Sae2 nuclease generate, in a stepwise manner, only few hundred nucleotides of ssDNA at the break, resulting in inefficient gene

of endocytosis, respectively. Not only was vacuolar transport of a Golgi membrane protein blocked in the vpslA sec4-ts and vpslA end4-ts double mutant cells at the non-permissive temperature but

High level of antibiotic production in a double polyphosphate kinase and phosphate 1 binding protein mutant of Streptomyces lividans 2

the Pho4 recognition site. Eight of these genes, PHM1–PHM8, had no previously defined function in phosphate metabolism. The amino acid sequences of PHM1 (YFL004w), PHM2 (YPL019c), PHM3 (YJL012c), and PHM4 (YER072w) are 32–56 % identical. The phm3 and phm4 single mutants and the phm1 phm2 double mutant

nonstructural protein 1 (NS1) prevents the induction of the IFN- promoter by inhibiting the activation of transcription factors, including IRF-3, involved in IFN- transcriptional activation. The inhibitory properties of NS1 appear to be due at least in part to its binding to double-stranded RNA (ds

expresses the SA/NPR1–regulated PR genes (PR-1, BGL2, and PR-5) and displays enhanced resistance to Pseudomonas syringae pv maculicola ES4326 and Peronospora parasitica Noco2 in the absence of SAR induction. cpr6-1–induced PR gene expression is not suppressed in the cpr6-1 npr1-1 double mutant