dna polymerase [gamma] and disease: what we have learned from yeast

Clicks: 122
ID: 249803
2015
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #257 of 264 articles by views in chemical record (new york, ny)

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 264 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Mip1 is the Saccharomyces cerevisiae DNA polymerase [gamma] (Pol [gamma]), which is responsible for the replication of mitochondrial DNA (mtDNA). It belongs to the family A of the DNA polymerases and it is orthologous to human POLGA. In humans, mutations in POLG(1) cause many mitochondrial pathologies, such as PEO, Alpers’ syndrome and ataxia-neuropathy syndrome, all of which present instability of mtDNA, which results in impaired mitochondrial function in several tissues with variable degrees of severity. In this review, we summarize the genetic and biochemical knowledge published on yeast mitochondrial DNA polymerase from 1989, when the MIP1 gene was first cloned, up until now. The role of yeast is particularly emphasized in i) validating the pathological mutations found in human POLG and modeled in MIP1, ii) determining the molecular defects caused by these mutations and iii) finding the correlation between mutations/polymorphisms in POLGA and mtDNA toxicity induced by specific drugs. We also describe recent findings regarding the discovery of molecules able to rescue the phenotypic defects caused by pathological mutations in Mip1, and the construction of a model system in which the human Pol [gamma] holoenzyme is expressed in yeast and complements the loss of Mip1.
Reference Key
elodi2015frontiersdna Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Tiziana eLodi;Cristina eDallabona;Cecilia eNolli;Paola eGoffrini;Claudia eDonnini;Enrico eBaruffini
Journal chemical record (new york, ny)
Year 2015
DOI
10.3389/fgene.2015.00106
URL
http://journal.frontiersin.org/Journal/10.3389/fgene.2015.00106/full
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.