scholarly journals Relationship of DNA repair processes to mutagenesis and carcinogenesis in mammalian cells. Progress report, November 1, 1978-October 31, 1979. [EMS; cultured mouse embryo cells (C3H/10T 1/2)]

1979 ◽  
Author(s):  
H.H. Evans
Keyword(s):  
Dna Repair ◽  
Mouse Embryo ◽  
Mammalian Cells ◽  
Progress Report ◽  
Repair Processes ◽  
Embryo Cells ◽  
Relationship Of

scholarly journals Tools for Decoding Ubiquitin Signaling in DNA Repair

2021 ◽  
Vol 9 ◽  
Author(s):  
Benjamin Foster ◽  
Martin Attwood ◽  
Ian Gibbs-Seymour
Keyword(s):  
Dna Repair ◽  
Mammalian Cells ◽  
Genome Stability ◽  
Dna Lesions ◽  
Post Translational Modifications ◽  
Dna Repair Mechanisms ◽  
Repair Processes ◽  
Repair Mechanisms ◽  
Mechanistic Basis ◽  
Cellular Dna

The maintenance of genome stability requires dedicated DNA repair processes and pathways that are essential for the faithful duplication and propagation of chromosomes. These DNA repair mechanisms counteract the potentially deleterious impact of the frequent genotoxic challenges faced by cells from both exogenous and endogenous agents. Intrinsic to these mechanisms, cells have an arsenal of protein factors that can be utilised to promote repair processes in response to DNA lesions. Orchestration of the protein factors within the various cellular DNA repair pathways is performed, in part, by post-translational modifications, such as phosphorylation, ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs). In this review, we firstly explore recent advances in the tools for identifying factors involved in both DNA repair and ubiquitin signaling pathways. We then expand on this by evaluating the growing repertoire of proteomic, biochemical and structural techniques available to further understand the mechanistic basis by which these complex modifications regulate DNA repair. Together, we provide a snapshot of the range of methods now available to investigate and decode how ubiquitin signaling can promote DNA repair and maintain genome stability in mammalian cells.

Spontaneous Production of Type C Virus Particles in a Culture Derived from Rat Embryo Cells

1972 ◽  
Vol 30 ◽  
pp. 288-289
Author(s):  
Elizabeth S. Priori ◽  
T. Shigematsu ◽  
B. Myers ◽  
L. Dmochowski
Keyword(s):  
Virus Particle ◽  
Mouse Embryo ◽  
Calf Serum ◽  
Embryo Cell ◽  
Virus Particles ◽  
Extracellular Virus ◽  
Mouse Embryo Cell ◽  
Mature Virus Particle ◽  
Embryo Cells ◽  
Type C

Spontaneous release of type C virus particles in long-term cultures of mouse embryo cells as well as induction of similar particles in mouse embryo cell cultures with IUDR or BUDR have been reported. The presence of type C virus particles in cultures of normal rat embryos has not been reported.NB-1, a culture derived from embryos of a New Zealand Black (NB) rat (rats obtained from Mr. Samuel M. Poiley, N.C.I., Bethesda, Md.) and grown in McCoy's 5A medium supplemented with 20% fetal calf serum was passaged weekly. Extracellular virus particles similar to murine leukemia particles appeared in the 22nd subculture. General appearance of cells in passage 23 is shown in Fig. 1. Two budding figures and one immature type C virus particle may be seen in Fig. 2. The virus particles and budding were present in all further passages examined (currently passage 39). Various stages of budding are shown in Figs. 3a,b,c,d. Appearance of a mature virus particle is shown in Fig. 4.

scholarly journals Exploiting DNA Endonucleases to Advance Mechanisms of DNA Repair

Biology ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 530
Author(s):  
Marlo K. Thompson ◽  
Robert W. Sobol ◽  
Aishwarya Prakash
Keyword(s):  
Dna Repair ◽  
Mammalian Cells ◽  
Genome Stability ◽  
Gene Editing ◽  
Adaptive Immune System ◽  
Zinc Finger Nucleases ◽  
Specific Gene ◽  
Target Sequence ◽  
Transcription Activator ◽  
Low Cytotoxicity

The earliest methods of genome editing, such as zinc-finger nucleases (ZFN) and transcription activator-like effector nucleases (TALENs), utilize customizable DNA-binding motifs to target the genome at specific loci. While these approaches provided sequence-specific gene-editing capacity, the laborious process of designing and synthesizing recombinant nucleases to recognize a specific target sequence, combined with limited target choices and poor editing efficiency, ultimately minimized the broad utility of these systems. The discovery of clustered regularly interspaced short palindromic repeat sequences (CRISPR) in Escherichia coli dates to 1987, yet it was another 20 years before CRISPR and the CRISPR-associated (Cas) proteins were identified as part of the microbial adaptive immune system, by targeting phage DNA, to fight bacteriophage reinfection. By 2013, CRISPR/Cas9 systems had been engineered to allow gene editing in mammalian cells. The ease of design, low cytotoxicity, and increased efficiency have made CRISPR/Cas9 and its related systems the designer nucleases of choice for many. In this review, we discuss the various CRISPR systems and their broad utility in genome manipulation. We will explore how CRISPR-controlled modifications have advanced our understanding of the mechanisms of genome stability, using the modulation of DNA repair genes as examples.

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