scholarly journals A DNA Replication Mechanism for Generating Nonrecurrent Rearrangements Associated with Genomic Disorders

Cell ◽  
2007 ◽  
Vol 131 (7) ◽  
pp. 1235-1247 ◽  
Author(s):  
Jennifer A. Lee ◽  
Claudia M.B. Carvalho ◽  
James R. Lupski
2012 ◽  
Vol 131 (12) ◽  
pp. 1895-1910 ◽  
Author(s):  
Svetlana A. Yatsenko ◽  
Patricia Hixson ◽  
Erin K. Roney ◽  
Daryl A. Scott ◽  
Christian P. Schaaf ◽  
...  

Author(s):  
Peter C. van der Vliet ◽  
Marijke M. Kwant ◽  
Bram G. M. van Bergen ◽  
Wim van Driel

Plants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 533 ◽  
Author(s):  
Brieba

Plants are sessile organisms, and their DNA is particularly exposed to damaging agents. The integrity of plant mitochondrial and plastid genomes is necessary for cell survival. During evolution, plants have evolved mechanisms to replicate their mitochondrial genomes while minimizing the effects of DNA damaging agents. The recombinogenic character of plant mitochondrial DNA, absence of defined origins of replication, and its linear structure suggest that mitochondrial DNA replication is achieved by a recombination-dependent replication mechanism. Here, I review the mitochondrial proteins possibly involved in mitochondrial DNA replication from a structural point of view. A revision of these proteins supports the idea that mitochondrial DNA replication could be replicated by several processes. The analysis indicates that DNA replication in plant mitochondria could be achieved by a recombination-dependent replication mechanism, but also by a replisome in which primers are synthesized by three different enzymes: Mitochondrial RNA polymerase, Primase-Helicase, and Primase-Polymerase. The recombination-dependent replication model and primers synthesized by the Primase-Polymerase may be responsible for the presence of genomic rearrangements in plant mitochondria.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Shauna L Houlihan ◽  
Yuanyi Feng

Successfully completing the S phase of each cell cycle ensures genome integrity. Impediment of DNA replication can lead to DNA damage and genomic disorders. In this study, we show a novel function for NDE1, whose mutations cause brain developmental disorders, in safeguarding the genome through S phase during early steps of neural progenitor fate restrictive differentiation. Nde1 mutant neural progenitors showed catastrophic DNA double strand breaks concurrent with the DNA replication. This evoked DNA damage responses, led to the activation of p53-dependent apoptosis, and resulted in the reduction of neurons in cortical layer II/III. We discovered a nuclear pool of Nde1, identified the interaction of Nde1 with cohesin and its associated chromatin remodeler, and showed that stalled DNA replication in Nde1 mutants specifically occurred in mid-late S phase at heterochromatin domains. These findings suggest that NDE1-mediated heterochromatin replication is indispensible for neuronal differentiation, and that the loss of NDE1 function may lead to genomic neurological disorders.


1991 ◽  
Vol 56 (0) ◽  
pp. 303-313 ◽  
Author(s):  
L.F. Erdile ◽  
K.L. Collins ◽  
A. Russo ◽  
P. Simancek ◽  
D. Small ◽  
...  

1998 ◽  
Vol 111 (6) ◽  
pp. 675-679
Author(s):  
D.L. Guilbride ◽  
P.T. Englund

Kinetoplast DNA, a giant network of interlocked DNA circles, replicates by an unusual mechanism. Minicircles are released individually from the network by a topoisomerase II, and then, after replication, their progeny are reattached at antipodal positions on the network periphery. Studies to date have revealed two distinct variations on this model. In Crithidia fasciculata the newly replicated minicircles quickly become uniformly distributed around the network periphery, whereas in Trypanosoma brucei the minicircles accumulate near their two points of attachment. The kinetoplast DNA replication mechanism used by other related trypanosomatid species was until now unknown. Here we used a novel method, involving fluorescence microscopy of isolated networks, to investigate kinetoplast DNA replication in Leishmania tarentolae, Leishmania donovani, Trypanosoma cruzi and Phytomonas serpens. We found that all of these species have a replication mechanism resembling that of C. fasciculata and that the polar replication mechanism observed in T. brucei is so far unique to this species.


2021 ◽  
Author(s):  
Samuel Clamons ◽  
Richard M Murray

Biocircuit modeling sometimes requires explicit tracking of a self-replicating DNA species. The most obvious, straightforward way to model a replicating DNA is structurally unstable and leads to pathological model behavior. We describe a simple, stable replication mechanism with good model behavior and show how to derive it from a mechanistic model of ColE1 replication.


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