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植物细胞器DNA聚合酶是复制性和跨损伤DNA合成聚合酶。

Plant organellar DNA polymerases are replicative and translesion DNA synthesis polymerases.

作者信息

Baruch-Torres Noe, Brieba Luis G

机构信息

Langebio-Cinvestav Sede Irapuato, Km. 9.6 Libramiento Norte Carretera. Irapuato-León, 36821 Irapuato Guanajuato, México.

出版信息

Nucleic Acids Res. 2017 Oct 13;45(18):10751-10763. doi: 10.1093/nar/gkx744.

DOI:10.1093/nar/gkx744
PMID:28977655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5737093/
Abstract

Genomes acquire lesions that can block the replication fork and some lesions must be bypassed to allow survival. The nuclear genome of flowering plants encodes two family-A DNA polymerases (DNAPs), the result of a duplication event, that are the sole DNAPs in plant organelles. These DNAPs, dubbed Plant Organellar Polymerases (POPs), resemble the Klenow fragment of bacterial DNAP I and are not related to metazoan and fungal mitochondrial DNAPs. Herein we report that replicative POPs from the plant model Arabidopsis thaliana (AtPolI) efficiently bypass one the most insidious DNA lesions, an apurinic/apyrimidinic (AP) site. AtPolIs accomplish lesion bypass with high catalytic efficiency during nucleotide insertion and extension. Lesion bypass depends on two unique polymerization domain insertions evolutionarily unrelated to the insertions responsible for lesion bypass by DNAP θ, an analogous lesion bypass polymerase. AtPolIs exhibit an insertion fidelity that ranks between the fidelity of replicative and lesion bypass DNAPs, moderate 3'-5' exonuclease activity and strong strand-displacement. AtPolIs are the first known example of a family-A DNAP evolved to function in both DNA replication and lesion bypass. The lesion bypass capabilities of POPs may be required to prevent replication fork collapse in plant organelles.

摘要

基因组会出现能够阻碍复制叉的损伤,一些损伤必须被绕过才能保证细胞存活。开花植物的核基因组编码了两种A类DNA聚合酶(DNAPs),这是一次基因复制事件的结果,它们是植物细胞器中仅有的DNAPs。这些DNAPs被称为植物细胞器聚合酶(POPs),类似于细菌DNAP I的Klenow片段,与后生动物和真菌的线粒体DNAPs没有关系。在此我们报道,来自植物模式生物拟南芥的复制性POPs(AtPolI)能够有效地绕过一种最隐匿的DNA损伤,即无嘌呤/无嘧啶(AP)位点。AtPolI在核苷酸插入和延伸过程中以高催化效率完成损伤绕过。损伤绕过依赖于两个独特的聚合结构域插入,这两个插入在进化上与由DNAP θ(一种类似的损伤绕过聚合酶)负责损伤绕过的插入无关。AtPolI表现出的插入保真度介于复制性和损伤绕过DNAPs的保真度之间,具有适度的3'-5'核酸外切酶活性和较强的链置换能力。AtPolI是已知的首个进化为在DNA复制和损伤绕过中都起作用的A类DNAP的例子。POPs的损伤绕过能力可能是防止植物细胞器中复制叉坍塌所必需的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7fc7ce7d27d2/gkx744fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7312f4ca5945/gkx744fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/38a913bfc486/gkx744fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/82a476834bd4/gkx744fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/5322551e3473/gkx744fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/47c790ea9251/gkx744fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/cd504df7adf2/gkx744fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7f49836a253a/gkx744fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7fc7ce7d27d2/gkx744fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7312f4ca5945/gkx744fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/38a913bfc486/gkx744fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/82a476834bd4/gkx744fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/5322551e3473/gkx744fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/47c790ea9251/gkx744fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/cd504df7adf2/gkx744fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7f49836a253a/gkx744fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4765/5737093/7fc7ce7d27d2/gkx744fig8.jpg

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