246 research outputs found
Effects of Oxygen and Respiratory Inhibitors on Induction and Release of Dormancy in Aerial Tubers of Begonia evansiana
A Competitive Enzyme-Linked Immunosorbent Assay to Quantify Acetaldehyde-Protein Adducts That Accumulate in Dry Seeds during Aging
Debris-free in-air laser dicing for multi-layer MEMS by perforated internal transformation and thermally-induced crack propagation
MEMS 2008, Tucson, AZ, USA, January 13-17, 200
RASSF1AâLATS1 signalling stabilizes replication forks by restricting CDK2-mediated phosphorylation of BRCA2
Genomic instability is a key hallmark of cancer leading to tumour heterogeneity and therapeutic resistance. âBRCA2 has a fundamental role in error-free DNA repair but also sustains genome integrity by promoting âRAD51 nucleofilament formation at stalled replication forks. âCDK2 phosphorylates âBRCA2 (pS3291-âBRCA2) to limit stabilizing contacts with polymerized âRAD51; however, how replication stress modulates âCDK2 activity and whether loss of pS3291-âBRCA2 regulation results in genomic instability of tumours are not known. Here we demonstrate that the Hippo pathway kinase âLATS1 interacts with âCDK2 in response to genotoxic stress to constrain pS3291-âBRCA2 and support âRAD51 nucleofilaments, thereby maintaining genomic fidelity during replication stalling. We also show that âLATS1 forms part of an âATR-mediated response to replication stress that requires the tumour suppressor âRASSF1A. Importantly, perturbation of the âATRââRASSF1AââLATS1 signalling axis leads to genomic defects associated with loss of âBRCA2 function and contributes to genomic instability and âBRCA-nessâ in lung cancers
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Ptychographic amplitude and phase reconstruction of bichromatic vortex beams
We experimentally demonstrate that ptychographic coherent diffractive imaging can be used to simultaneously characterize the amplitude and phase of bichromatic orbital angular momenta-shaped vortex beams, which consist of a fundamental field, together with its copropagating second-harmonic field. In contrast to most other orbital angular momentum characterization methods, this approach solves for the complex field of a hyperspectral beam. This technique can also be used to characterize other phase-structured illumination beams, and, in the future, will be able to be extended to other complex fields in the extreme ultraviolet or X-ray spectral regions, as well as to matter waves.The NSF STROBE STC (DMR-1548924); DOE BES AMOS grant (DE-FG02-99ER14982); the NSF GRFP (DGE 1650115); 2017 Leonardo Grant for Researchers and Cultural Creators, BBVA Foundation; Junta de Castilla y LeĂłn (SA046U16); Ministerio de EconomĂa y Competitividad (FIS2016-75652-P)
Fatores que afetam a germinação e a emergĂȘncia de Xanthium strumarim L.: dormĂȘncia, qualidade da luz e profundidade de semeadura
CDK targets Sae2 to control DNA-end resection and homologous recombination
DNA double-strand breaks (DSBs) are repaired by two principal mechanisms: non-homologous end-joining (NHEJ) and homologous recombination (HR)1. HR is the most accurate DSB repair mechanism but is generally restricted to the S and G2 phases of the cell cycle, when DNA has been replicated and a sister chromatid is available as a repair template2-5. By contrast, NHEJ operates throughout the cell cycle but assumes most importance in G1 (refs 4â, â6). The choice between repair pathways is governed by cyclin-dependent protein kinases (CDKs)2,3,5,7, with a major site of control being at the level of DSB resection, an event that is necessary for HR but not NHEJ, and which takes place most effectively in S and G2 (refs 2â, â5). Here we establish that cell-cycle control of DSB resection in Saccharomyces cerevisiae results from the phosphorylation by CDK of an evolutionarily conserved motif in the Sae2 protein. We show that mutating Ser 267 of Sae2 to a non-phosphorylatable residue causes phenotypes comparable to those of a sae2Î null mutant, including hypersensitivity to camptothecin, defective sporulation, reduced hairpin-induced recombination, severely impaired DNA-end processing and faulty assembly and disassembly of HR factors. Furthermore, a Sae2 mutation that mimics constitutive Ser 267 phosphorylation complements these phenotypes and overcomes the necessity of CDK activity for DSB resection. The Sae2 mutations also cause cell-cycle-stage specific hypersensitivity to DNA damage and affect the balance between HR and NHEJ. These findings therefore provide a mechanistic basis for cell-cycle control of DSB repair and highlight the importance of regulating DSB resection
Cooperation of breast cancer proteins PALB2 and piccolo BRCA2 in stimulating homologous recombination.
Inherited mutations in human PALB2 are associated with a predisposition to breast and pancreatic cancers. PALB2's tumor-suppressing effect is thought to be based on its ability to facilitate BRCA2's function in homologous recombination. However, the biochemical properties of PALB2 are unknown. Here we show that human PALB2 binds DNA, preferentially D-loop structures, and directly interacts with the RAD51 recombinase to stimulate strand invasion, a vital step of homologous recombination. This stimulation occurs through reinforcing biochemical mechanisms, as PALB2 alleviates inhibition by RPA and stabilizes the RAD51 filament. Moreover, PALB2 can function synergistically with a BRCA2 chimera (termed piccolo, or piBRCA2) to further promote strand invasion. Finally, we show that PALB2-deficient cells are sensitive to PARP inhibitors. Our studies provide the first biochemical insights into PALB2's function with piBRCA2 as a mediator of homologous recombination in DNA double-strand break repair
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