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求大神幫個(gè)忙，四級(jí)沒過(guò)孩子，老板要翻譯文獻(xiàn)（還不是我方向的）�？啾啤�。。
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siRNAs: GENOMIC DEFENDERS RNA silencing via siRNAs is thought to have originated as a system by which cells protect themselves against the actions of molecular pathogens, including viruses and transposable elements. Silencing phenomena were recognized in plants in the 1980s during investigations of viral resistance and early studies of transgenic plants. In parallel, similar phenomena were identified in the nematode Caenorhabditis elegans. (The gradual enlightenment of the scientific community to the meaning of these studies is vividly described by Matzke and Matzke [2004].) siRNAs are produced from long dsRNA molecules, which can be produced via the replication of two overlapping genes, a viral genome, or an intermediate in viral replication , or they can be the product of an RdRP. Whatever their origin, dsRNAs are perceived by the cell as unwanted and so are rapidly cleaved by DCL RNases into siRNAs (usually 21 or 24 nucleotides in length). The siRNAs bind to AGO and can cleave or interfere with translation of complementary sequences (posttranscriptional gene silencing) or interfere with transcription of a cognate DNA sequence (tran-scriptional gene silencing). When the long RNA has a viral origin, this process is often called viral-induced gene silencing. VIRAL-INDUCED GENE SILENCING Plants, like animals, are susceptible to infections by viruses. Unlike some animals, plants do not produce antibodies to defend against viral infections. Nevertheles s, like those of us with antibody-based immunity, plants can recover from an infection and acquire a specific resistance to subsequent infection by the same or a closely related virus. Viral resistance can be systemic, meaning that uninfected tissues acquire immunity to the virus, and suggesting that some sort of signal is produced that moves throughout the plant. Plant viral immunity can be conferred by the introduction of viral genes into the plant and requires either transcription of a viral gene or viral replication via an RNA intermediate. In 1999, Hamilton and Baulcombe proposed that viral RNAs are copied into antisense RNAs, which form the basis of viral resistance, and they identified short antisense RNAs correlated with gene silencing. We now know that dsRNAs are processed by DCL into siRNAs, which then target AGO proteins to the virus or related sequence. In some cases, a dsRNA viral replication intermediate is the template for DCL cleavage, but DCL also apparently recognizes and processes hairpin-like structures formed by some viral single-stranded RNA. Mutant plants that are unable to produce siRNAs are more susceptible to viral disease. Systemic viral resistance is also mediated by siRNA-based silencing, which spreads outwards to the uninfected parts of the plant from the site of infection. The signal sprea ds locally through the plasmodesmata (cytoplasmic connections between plant cells) and more widely through the phloem. Systemic resistance requires that the primary signal is amplified by host cell RdRPs. The systemic signal has long been suspected to be siRNA, and in 2010, two groups showed that small RNAs can move systemically through the plant and are necessary and sufficient for systemic silencing. The most recent data suggest that the siRNA moves systemically as a short RNA duplex. In a typical host-pathogen arms race, most viruses encode suppressors of the host cell’s RNA silencing pathways; virus strains in which the suppressors have been experimentally eliminated are significantly less pathogeni c. Targets of viral suppressors include DCLs, RdRPs, and AGOs. Recently, siRNAs were recognized as suppressors of bacterial pathogens as well, indicating that siRNA silencing is an integral and essential component of the plant’s defensive arsenal. It is interesting to note that most components of the small RNA silencing pathway are amplified through gene duplication in plants compared with other eukaryotes and that this amplifica-tion has conferred greater reliability (through redundancy) and greater diversity in pathogen silencing. |
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【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★
愛與雨下: 金幣+1 2013-06-21 18:45:24
peaceqing(phu_grassman代發(fā)): 金幣+5, 翻譯EPI+1, thanks 2013-11-07 10:31:17
愛與雨下: 金幣+1 2013-06-21 18:45:24
peaceqing(phu_grassman代發(fā)): 金幣+5, 翻譯EPI+1, thanks 2013-11-07 10:31:17
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siRNA:遺傳防御 通過(guò)siRNA介導(dǎo)的RNA沉默，被認(rèn)為是通過(guò)細(xì)胞自我防御外界的病原分子，包括病毒和轉(zhuǎn)座子。沉默現(xiàn)象是在1980s對(duì)轉(zhuǎn)基因植物的病毒防御機(jī)制研究中發(fā)現(xiàn)的。 類似的沉默現(xiàn)在后來(lái)也在秀麗隱桿線蟲中發(fā)現(xiàn)。（這些發(fā)現(xiàn)被 Matzke 和 Matzke在2004年生動(dòng)地描述過(guò)。 ） siRNA由長(zhǎng)的dsRNA(就是雙鏈RNA，RNA一般情況下是單鏈的，即ssRNA)產(chǎn)生，在兩個(gè)重疊基因的復(fù)制過(guò)程中會(huì)生成，或者是通過(guò)病毒基因組、病毒增殖的中間分子介導(dǎo)而生成，或者是通過(guò)RdRP（RNA-dependent RNA polymerase,就是RNA聚合酶）產(chǎn)生。無(wú)論是通過(guò)什么途徑生成的，dsRNA都是被細(xì)胞不情愿地識(shí)別，然后迅速地被DCL RNases（Dicer-like 酶）降解成siRNA（通常長(zhǎng)度為21-24bp）。 小師弟，你自己翻譯一遍，我來(lái)潤(rùn)色，鍛煉了你，也節(jié)省了我的時(shí)間，你覺得可好？ |
2樓2013-06-21 18:09:15
3樓2013-06-21 18:10:38
【答案】應(yīng)助回帖
★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★ ★
peaceqing(phu_grassman代發(fā)): 金幣+15, good job 2013-11-07 10:31:31
peaceqing(phu_grassman代發(fā)): 金幣+15, good job 2013-11-07 10:31:31
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siRNA：基因組衛(wèi)士 RNA沉默的siRNA被認(rèn)為是作為系統(tǒng)的細(xì)胞保護(hù)自己免受病原體的分子的行動(dòng)，包括病毒和轉(zhuǎn)座子。沉默現(xiàn)象是植物中公認(rèn)的世紀(jì)80年代早期的病毒抗性的轉(zhuǎn)基因植物的研究調(diào)查。同時(shí)，類似的現(xiàn)象在秀麗隱桿線蟲鑒定。（科學(xué)界的漸進(jìn)啟示的意義這些研究是由馬茨和馬茨[ 2004 ]進(jìn)行了生動(dòng)的描述。）從長(zhǎng)dsRNA siRNA分子產(chǎn)生，它可以通過(guò)兩個(gè)重疊的基因復(fù)制產(chǎn)生，病毒基因組，或中間在病毒復(fù)制，或者他們可以RdRp的產(chǎn)品。不論其來(lái)源，雙鏈RNA被認(rèn)為以細(xì)胞為不必要的和正在迅速被DCL切割成siRNAs核糖核酸酶（通常21或24個(gè)核苷酸的長(zhǎng)度）。siRNA綁定到前，可以切割或干擾的互補(bǔ)序列的翻譯（轉(zhuǎn)錄后基因沉默）或干擾的同源DNA序列的轉(zhuǎn)錄因子（轉(zhuǎn)錄基因沉默）。當(dāng)長(zhǎng)的RNA病毒的起源，這個(gè)過(guò)程通常被稱為病毒誘導(dǎo)的基因沉默。 病毒誘導(dǎo)的基因沉默植物，像動(dòng)物一樣，是由病毒感染易感。不像一些動(dòng)物，植物不產(chǎn)生抗體來(lái)抵御病毒感染。盡管如此，像我們這些抗體為基礎(chǔ)的免疫，植物可以從感染中恢復(fù)過(guò)來(lái)，以相同或密切相關(guān)的病毒獲得后續(xù)感染的特異性抵抗。病毒抗性是全身性的，這意味著未受感染的組織中獲得對(duì)病毒的免疫力，并暗示某種信號(hào)的產(chǎn)生，將整個(gè)工廠。植物病毒的免疫力，可由病毒基因?qū)胫参镔x予和需要的病毒基因或病毒的復(fù)制或轉(zhuǎn)錄通過(guò)RNA中間體。1999，漢密爾頓和鮑爾庫(kù)姆提出病毒RNA復(fù)制到反義RNA，形成病毒耐藥的基礎(chǔ)，他們確定的短反義RNA基因沉默相關(guān)。我們現(xiàn)在知道，雙鏈RNA由DCL為siRNA處理，然后目標(biāo)前蛋白對(duì)病毒或相關(guān)序列。在某些情況下，一個(gè)dsRNA病毒復(fù)制中間體DCL切割模板，但是DCL顯然也識(shí)別和處理的發(fā)夾樣結(jié)構(gòu)的一些病毒單鏈RNA形成。突變體是無(wú)法產(chǎn)生的siRNA更易感染病毒病。 全身性病毒性也介導(dǎo)的siRNA的沉默，而向外傳播到植物的未受感染的部位感染的部位。信號(hào)將DS局部通過(guò)胞間連絲（細(xì)胞質(zhì)之間的連接植物細(xì)胞）和通過(guò)韌皮部更廣泛。全身性需要的主要信號(hào)是由宿主細(xì)胞的RNA依賴的RNA擴(kuò)增。系統(tǒng)的信號(hào)被懷疑是siRNA，和2010，兩組結(jié)果表明小RNAs可以系統(tǒng)地通過(guò)植物是必要的和足夠的系統(tǒng)性沉默。最近的數(shù)據(jù)表明，siRNA的移動(dòng)系統(tǒng)的短RNA雙鏈。在一個(gè)典型的病原體宿主的軍備競(jìng)賽，大多數(shù)病毒編碼的RNA沉默途徑抑制宿主細(xì)胞的病毒株的抑制；在實(shí)驗(yàn)已消除了顯著減少致病的病毒抑制C.目標(biāo)包括DCLS，程式，和前。最近，siRNA公認(rèn)的細(xì)菌病原體以及抑制，表明siRNA沉默是不可或缺的植物的防御武器庫(kù)組件。它是注意，小RNA沉默途徑的大多數(shù)組件是通過(guò)基因復(fù)制在植物與其他真核生物，這擴(kuò)大倍數(shù)賦予了更高的可靠性比較有趣的（冗余）和擴(kuò)增更大的多樣性病原體的沉默。 |
4樓2013-06-25 13:01:58
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