Age-Related Differences in DNA Polymerase Alpha Specific Activity: Potential for Interaction in DNA Repair

2020 ◽  
pp. 65-87
Author(s):  
David L. Busbee ◽  
Victor L. Sylvia ◽  
Geoffrey M. Curtin
1981 ◽  
Vol 199 (2) ◽  
pp. 453-455 ◽  
Author(s):  
N Hardt ◽  
G Pedrali-Noy ◽  
F Focher ◽  
S Spadari

A radioautographic examination of nuclear DNA synthesis in unirradiated and u.v.-irradiated HeLa cells, in the presence and in the absence of aphidicolin, showed that aphidicolin inhibits nuclear DNA replication and has no detectable effect on DNA repair synthesis. Although the results establish that in u.v.-irradiated HeLa cells most of the DNA repair synthesis is not due to DNA polymerase alpha, they do not preclude a significant role for this enzyme in DNA repair processes.


2011 ◽  
Vol 9 (1) ◽  
pp. 53-61
Author(s):  
Nora Babudri ◽  
Alessandro Achilli ◽  
Chiara Martinelli ◽  
Elizabeth Moore ◽  
Hovirag Lancioni ◽  
...  

In nature, microorganisms experience numerous environmental stresses and generally grow poorly most of the time. In the last two decades it has become evident that mutations arise not only in actively dividing cells but also in nonreplicating or slowly replicating cells starved for nutrients. In yeast, precise base selection and proofreading by replicative DNA polymerases δ and ε keep starvation-associated mutagenesis (SAM) at basal levels. Less is known about the role of replicative DNA polymerase α (Pol α). Here we provide evidence that Pol α is involved in the control of SAM in yeast cells starved for adenine by participation in sporadic replication and/or DNA repair under these conditions. 


Biology ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 163
Author(s):  
Swapnil Gupta ◽  
Panpan You ◽  
Tanima SenGupta ◽  
Hilde Nilsen ◽  
Kulbhushan Sharma

Genomic integrity is maintained by DNA repair and the DNA damage response (DDR). Defects in certain DNA repair genes give rise to many rare progressive neurodegenerative diseases (NDDs), such as ocular motor ataxia, Huntington disease (HD), and spinocerebellar ataxias (SCA). Dysregulation or dysfunction of DDR is also proposed to contribute to more common NDDs, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), and Amyotrophic Lateral Sclerosis (ALS). Here, we present mechanisms that link DDR with neurodegeneration in rare NDDs caused by defects in the DDR and discuss the relevance for more common age-related neurodegenerative diseases. Moreover, we highlight recent insight into the crosstalk between the DDR and other cellular processes known to be disturbed during NDDs. We compare the strengths and limitations of established model systems to model human NDDs, ranging from C. elegans and mouse models towards advanced stem cell-based 3D models.


1983 ◽  
Vol 258 (11) ◽  
pp. 6698-6700 ◽  
Author(s):  
T Yagura ◽  
S Tanaka ◽  
T Kozu ◽  
T Seno ◽  
D Korn

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