7,127 research outputs found
ruvA Mutants that resolve Holliday junctions but do not reverse replication forks
No full textRuvAB and RuvABC complexes catalyze branch migration and resolution of Holliday junctions (HJs) respectively. In addition to their action in the last steps of homologous recombination, they process HJs made by replication fork reversal, a reaction which occurs at inactivated replication forks by the annealing of blocked leading and lagging strand ends. RuvAB was recently proposed to bind replication forks and directly catalyze their conversion into HJs. We report here the isolation and characterization of two separation-of-function ruvA mutants that resolve HJs, based on their capacity to promote conjugational recombination and recombinational repair of UV and mitomycin C lesions, but have lost the capacity to reverse forks. In vivo and in vitro evidence indicate that the ruvA mutations affect DNA binding and the stimulation of RuvB helicase activity. This work shows that RuvA's actions at forks and at HJs can be genetically separated, and that RuvA mutants compromised for fork reversal remain fully capable of homologous recombination
Cover Image Credit
No full textCover Image Credit by NASA Johnson
Caption: July 1, 2018: Winnipeg, Manitoba and the Assiniboine and Red Rivers are pictured as the International Space Station was orbiting at the northern-most point of its 51.7-degree orbital inclination
Localization of an accessory helicase at the replisome is critical in sustaining efficient genome duplication
No full text© The Author(s) 2010. Published by Oxford University PressGenome duplication requires accessory helicases to displace proteins ahead of advancing replication forks. Escherichia coli contains three helicases, Rep, UvrD and DinG, that might promote replication of protein-bound DNA. One of these helicases, Rep, also interacts with the replicative helicase DnaB. We demonstrate that Rep is the only putative accessory helicase whose absence results in an increased chromosome duplication time. We show also that the interaction between Rep and DnaB is required for Rep to maintain rapid genome duplication. Furthermore, this Rep–DnaB interaction is critical in minimizing the need for both recombinational processing of blocked replication forks and replisome reassembly, indicating that colocalization of Rep and DnaB minimizes stalling and subsequent inactivation of replication forks. These data indicate that E. coli contains only one helicase that acts as an accessory motor at the fork in wild-type cells, that such an activity is critical for the maintenance of rapid genome duplication and that colocalization with the replisome is crucial for this function. Given that the only other characterized accessory motor, Saccharomyces cerevisiae Rrm3p, associates physically with the replisome, our demonstration of the functional importance of such an association indicates that colocalization may be a conserved feature of accessory replicative motors.Biotechnology and Biological Sciences Research Council (BB/G005915/1 and BB/E0020690 to P.M.); MRC (G0800970 to R.G.L.); Leverhulme Trust (to C.J.R.). Funding for open access charge: BBSRC
President Nixon Supporters at the Grand Forks Airport, 1970
No full textPresident Richard Nixon flew into the Grand Forks Airport on October 19, 1970, to support Congressman Thomas Kleppe\u27s campaign for the U.S. Senate. Supporters of the President greeted him with homemade signs.https://commons.und.edu/nd-politics-photos/1540/thumbnail.jp
FANCM regulates repair pathway choice at stalled replication forks.
No full textRepair pathway choice at stalled mammalian replication forks is an important determinant of genome stability; however, the underlying mechanisms are poorly understood. FANCM encodes a multi-domain scaffolding and motor protein that interacts with several distinct repair protein complexes at stalled forks. Here, we use defined mutations engineered within endogenous Fancm in mouse embryonic stem cells to study how Fancm regulates stalled fork repair. We find that distinct FANCM repair functions are enacted by molecularly separable scaffolding domains. These findings define FANCM as a key mediator of repair pathway choice at stalled replication forks and reveal its molecular mechanism. Notably, mutations that inactivate FANCM ATPase function disable all its repair functions and trap FANCM at stalled forks. We find that Brca1 hypomorphic mutants are synthetic lethal with Fancm null or Fancm ATPase-defective mutants. The ATPase function of FANCM may therefore represent a promising druggable target for therapy of BRCA1-linked cancer
Introduction: Here At the (Digital) Forks
No full textAt the Forks is a new platform developed by the Centre for Human Rights Research and Mamawipawin, both located at the University of Manitoba. Our goal is to disseminate timely, accessible research and thinking about Indigenous people and colonialism, in the past and the present, seen through the lenses of Indigenous rights and human rights
President Nixon at Grand Forks Airport, October 1970
No full textPhotograph of President Nixon after deboarding the plane at the Grand Forks Airport. Nixon is shown shaking hands with Representative Mark Andrews, while Andrews\u27 wife, Mary, stands between besides him next to an unknown person. The president\u27s private plane sits in the background with one Secret Service man standing besides the stairs of plane.https://commons.und.edu/gf-city-photos/1257/thumbnail.jp
The DNA helicase Pfh1 promotes fork merging at replication termination sites to ensure genome stability
No full textBidirectionally moving DNA replication forks merge at termination sites composed of accidental or programmed DNA-protein barriers. If merging fails, then regions of unreplicated DNA can result in the breakage of DNA during mitosis, which in turn can give rise to genome instability. Despite its importance, little is known about the mechanisms that promote the final stages of fork merging in eukaryotes. Here we show that the Pif1 family DNA helicase Pfh1 plays a dual role in promoting replication fork termination. First, it facilitates replication past DNA-protein barriers, and second, it promotes the merging of replication forks. A failure of these processes in Pfh1-deficient cells results in aberrant chromosome segregation and heightened genome instability. © 2012 by Cold Spring Harbor Laboratory Press
Protesting Nixon\u27s Visit to Grand Forks, 1970
No full textProtestors greet President Richard Nixon at the Grand Forks Airport on October 19, 1970. The President flew into town to support Congressman Thomas Kleppe\u27s campaign for the U.S. Senate.https://commons.und.edu/nd-politics-photos/1541/thumbnail.jp
Demo 10-03 Tuning Forks
No full textThree tuning forks of frequencies 256, 512, and 1024 Hz (at octave frequency intervals) are sounded and their waves displayed on an oscilloscope. The wave produced by a tuning fork is sinusoidal, as can be heard on the video and illustrated in Figure 1
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