scholarly journals Characterization of valproic acid-initiated homologous recombination

2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Kevin Sha ◽  
Louise M. Winn
Keyword(s):  
Valproic Acid ◽  
Homologous Recombination

scholarly journals Characterization of homologous recombination induced by replication inhibition in mammalian cells

2001 ◽  
Vol 20 (14) ◽  
pp. 3861-3870 ◽  
Author(s):  
Y. Saintigny
Keyword(s):  
Homologous Recombination ◽  
Mammalian Cells

scholarly journals RAD54 is essential for RAD51-mediated repair of meiotic DSB in Arabidopsis

PLoS Genetics ◽  
2021 ◽  
Vol 17 (5) ◽  
pp. e1008919
Author(s):  
Miguel Hernandez Sanchez-Rebato ◽  
Alida M. Bouatta ◽  
Maria E. Gallego ◽  
Charles I. White ◽  
Olivier Da Ines
Keyword(s):  
Homologous Recombination ◽  
Meiotic Recombination ◽  
Dna Supercoiling ◽  
Homology Search ◽  
Detectable Effect ◽  
Damage Repair ◽  
Meiotic Dsbs ◽  
Dna Translocase

An essential component of the homologous recombination machinery in eukaryotes, the RAD54 protein is a member of the SWI2/SNF2 family of helicases with dsDNA-dependent ATPase, DNA translocase, DNA supercoiling and chromatin remodelling activities. It is a motor protein that translocates along dsDNA and performs multiple functions in homologous recombination. In particular, RAD54 is an essential cofactor for regulating RAD51 activity. It stabilizes the RAD51 nucleofilament, remodels nucleosomes, and stimulates homology search and strand invasion activity of RAD51. Accordingly, deletion of RAD54 has dramatic consequences on DNA damage repair in mitotic cells. In contrast, its role in meiotic recombination is less clear. RAD54 is essential for meiotic recombination in Drosophila and C. elegans, but plays minor roles in yeast and mammals. We present here characterization of the roles of RAD54 in meiotic recombination in the model plant Arabidopsis thaliana. Absence of RAD54 has no detectable effect on meiotic recombination in otherwise wild-type plants but RAD54 becomes essential for meiotic DSB repair in absence of DMC1. In Arabidopsis, dmc1 mutants have an achiasmate meiosis, in which RAD51 repairs meiotic DSBs. Lack of RAD54 leads to meiotic chromosomal fragmentation in absence of DMC1. The action of RAD54 in meiotic RAD51 activity is thus mainly downstream of the role of RAD51 in supporting the activity of DMC1. Equivalent analyses show no effect on meiosis of combining dmc1 with the mutants of the RAD51-mediators RAD51B, RAD51D and XRCC2. RAD54 is thus required for repair of meiotic DSBs by RAD51 and the absence of meiotic phenotype in rad54 plants is a consequence of RAD51 playing a RAD54-independent supporting role to DMC1 in meiotic recombination.

Molecular cloning and characterization of mutant and wild-type human beta-actin genes

1984 ◽  
Vol 4 (10) ◽  
pp. 1961-1969
Author(s):  
J Leavitt ◽  
P Gunning ◽  
P Porreca ◽  
S Y Ng ◽  
C S Lin ◽  
...  
Keyword(s):  
Homologous Recombination ◽  
Human Fibroblasts ◽  
Actin Gene ◽  
Actin Genes ◽  
Beta Actin ◽  
Gene Libraries ◽  
Actin Mrna ◽  
Dna Fragment ◽  
Specific Sequences

There are more than 20 beta-actin-specific sequences in the human genome, many of which are pseudogenes. To facilitate the isolation of potentially functional beta-actin genes, we used the new method of B. Seed (Nucleic Acids Res. 11:2427-2446, 1983) for selecting genomic clones by homologous recombination. A derivative of the pi VX miniplasmid, pi AN7 beta 1, was constructed by insertion of the 600-base-pair 3' untranslated region of the beta-actin mRNA expressed in human fibroblasts. Five clones containing beta-actin sequences were selected from an amplified human fetal gene library by homologous recombination between library phage and the miniplasmid. One of these clones contained a complete beta-actin gene with a coding sequence identical to that determined for the mRNA of human fibroblasts. A DNA fragment consisting of mostly intervening sequences from this gene was then used to identify 13 independent recombinant copies of the analogous gene from two specially constructed gene libraries, each containing one of the two types of mutant beta-actin genes found in a line of neoplastic human fibroblasts. The amino acid and nucleotide sequences encoded by the unmutated gene predict that a guanine-to-adenine transition is responsible for the glycine-to-aspartic acid mutation at codon 244 and would also result in the loss of a HaeIII site. Detection of this HaeIII polymorphism among the fibroblast-derived clones verified the identity of the beta-actin gene expressed in human fibroblasts.

Synthesis and characterization of valproic acid ester pro-drug micelles via an amphiphilic polycaprolactone block copolymer design

2015 ◽  
Vol 6 (13) ◽  
pp. 2386-2389 ◽  
Author(s):  
Suchithra A. Senevirathne ◽  
Suthida Boonsith ◽  
David Oupicky ◽  
Michael C. Biewer ◽  
Mihaela C. Stefan
Keyword(s):  
Valproic Acid ◽  
Block Copolymer ◽  
Block Copolymers ◽  
Histone Deacetylase ◽  
Hdac Inhibitors ◽  
Research Direction ◽  
Synthesis And Characterization ◽  
Covalent Bonds ◽  
New Research

The attachment of Histone deacetylase (HDAC) inhibitors via covalent bonds to biocompatible and biodegradable block copolymers provides a new research direction for cancer treatment.

Construction by homologous recombination and phenotypic characterization of a DNA polymerase domain polA mutant of Mycobacterium smegmatis

Gene ◽  
1996 ◽  
Vol 178 (1-2) ◽  
pp. 125-130 ◽  
Author(s):  
B.G. Gordhan ◽  
S.J. Andersen ◽  
A.R. De Meyer ◽  
V. Mizrahi
Keyword(s):  
Homologous Recombination ◽  
Dna Polymerase ◽  
Mycobacterium Smegmatis ◽  
Phenotypic Characterization ◽  
Polymerase Domain

Characterization of Inhibitory Effect of Carbapenem Antibiotics on the Deconjugation of Valproic Acid Glucuronide

2010 ◽  
Vol 38 (10) ◽  
pp. 1828-1835 ◽  
Author(s):  
Yusuke Masuo ◽  
Kousei Ito ◽  
Takehito Yamamoto ◽  
Akihiro Hisaka ◽  
Masashi Honma ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Inhibitory Effect

scholarly journals Deficient SUMO Attachment to Flp Recombinase Leads to Homologous Recombination-dependent Hyperamplification of the Yeast 2 μm Circle Plasmid

2009 ◽  
Vol 20 (4) ◽  
pp. 1241-1251 ◽  
Author(s):  
Ling Xiong ◽  
Xiaole L. Chen ◽  
Hannah R. Silver ◽  
Noreen T. Ahmed ◽  
Erica S. Johnson
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Homologous Recombination ◽  
Homologous Recombination Repair ◽  
Secondary Effects ◽  
Rolling Circle ◽  
Flp Recombinase ◽  
Recombination Repair ◽  
Sumo Pathway ◽  
Break Induced Replication

Many Saccharomyces cerevisiae mutants defective in the SUMO pathway accumulate elevated levels of the native 2 μm circle plasmid (2 μm). Here we show that accumulation of 2 μm in the SUMO pathway mutants siz1Δ siz2Δ, slx5Δ, and slx8Δ is associated with formation of an aberrant high-molecular-weight (HMW) form of 2 μm. Characterization of this species from siz1Δ siz2Δ showed that it contains tandem copies of the 2 μm sequence as well as single-stranded DNA. Accumulation of this species requires both the 2 μm–encoded Flp recombinase and the cellular homologous recombination repair (HRR) pathway. Importantly, reduced SUMO attachment to Flp is sufficient to induce formation of this species. Our data suggest a model in which Flp that cannot be sumoylated causes DNA damage, whose repair via HRR produces an intermediate that generates tandem copies of the 2 μm sequence. This intermediate may be a rolling circle formed via break-induced replication (BIR), because mutants defective in BIR contain reduced levels of the HMW form. This work also illustrates the importance of using cir° strains when studying mutants that affect the yeast SUMO pathway, to avoid confusing direct functions of the SUMO pathway with secondary effects of 2 μm amplification.

Sign in / Sign up

Export Citation Format

Share Document