遺傳物質(zhì)脫氧核糖核酸（DNA）分子擁有雙鏈結(jié)構(gòu)，在一些生命活動中,，DNA分子鏈條就像“車道”一樣,，其上“行駛”著各種蛋白質(zhì)。英國的一項(xiàng)新研究顯示,，在DNA分子鏈條中也存在較高的“交通事故”風(fēng)險(xiǎn),，相關(guān)發(fā)現(xiàn)有助于解釋一些基因突變。
英國諾丁漢大學(xué)等機(jī)構(gòu)的研究人員在新一期《自然》雜志上報(bào)告了這項(xiàng)成果,。該校教授帕諾斯·蘇爾塔納斯說,，在細(xì)胞分裂需要復(fù)制DNA時，會有一種復(fù)制體沿DNA分子鏈條快速運(yùn)行,，它相當(dāng)于“快車”,。而在某一段DNA分子鏈條中的基因需要被轉(zhuǎn)錄而發(fā)揮作用時，會有一種聚合酶沿相應(yīng)的DNA片段運(yùn)行,，它的速度較慢,，相當(dāng)于“慢車”。
很多研究者曾一直認(rèn)為,，只有在復(fù)制體和聚合酶相向運(yùn)行時才會“撞車”,，如果它們同向運(yùn)行，復(fù)制體會減慢速度跟在聚合酶后面，等聚合酶完成工作離開后再正常運(yùn)行,。而本次研究發(fā)現(xiàn)了完全不同的情況：即使在復(fù)制體和聚合酶同向運(yùn)行時,，也會因?yàn)閮烧咝旭偹俣炔煌l(fā)生大量“交通事故”。
研究人員介紹說,，DNA分子中還有一種蛋白質(zhì)專門負(fù)責(zé)處理這類“交通事故”,，它們會把因“撞車”而“脫軌”的復(fù)制體推回正常軌道。然而,，“事故”畢竟已經(jīng)發(fā)生,，這個過程可能導(dǎo)致DNA復(fù)制出現(xiàn)錯誤，或造成一些后果惡劣的基因突變,，從而引發(fā)癌癥等疾病,。
研究人員表示，本次研究顯示DNA活動中的“交通事故”風(fēng)險(xiǎn)比過去認(rèn)為的要高得多,，尤其是在那些基因轉(zhuǎn)錄頻率很高的DNA片段中——也就是常有“慢車”運(yùn)行的地方,。因此，今后在研究基因突變時也應(yīng)該重點(diǎn)關(guān)注這些片段的恩所在區(qū)域,。（生物谷Bioon.com）
生物谷推薦相關(guān)文章：
Nature doi:10.1038/nature09758
Co-directional replication–transcription conflicts lead to replication restart
Houra Merrikh,1, 3 Cristina Machón,2, 3 William H. Grainger,2 Alan D. Grossman1 & Panos Soultanas2
Head-on encounters between the replication and transcription machineries on the lagging DNA strand can lead to replication fork arrest and genomic instability1, 2. To avoid head-on encounters, most genes, especially essential and highly transcribed genes, are encoded on the leading strand such that transcription and replication are co-directional. Virtually all bacteria have the highly expressed ribosomal RNA genes co-directional with replication3. In bacteria, co-directional encounters seem inevitable because the rate of replication is about 10–20-fold greater than the rate of transcription. However, these encounters are generally thought to be benign2, 4, 5, 6, 7, 8, 9. Biochemical analyses indicate that head-on encounters10 are more deleterious than co-directional encounters8 and that in both situations, replication resumes without the need for any auxiliary restart proteins, at least in vitro. Here we show that in vivo, co-directional transcription can disrupt replication, leading to the involvement of replication restart proteins. We found that highly transcribed rRNA genes are hotspots for co-directional conflicts between replication and transcription in rapidly growing Bacillus subtilis cells. We observed a transcription-dependent increase in association of the replicative helicase and replication restart proteins where head-on and co-directional conflicts occur. Our results indicate that there are co-directional conflicts between replication and transcription in vivo. Furthermore, in contrast to the findings in vitro, the replication restart machinery is involved in vivo in resolving potentially deleterious encounters due to head-on and co-directional conflicts. These conflicts probably occur in many organisms and at many chromosomal locations and help to explain the presence of important auxiliary proteins involved in replication restart and in helping to clear a path along the DNA for the replisome.
