生物谷援引華文生技網(wǎng)報(bào)道:Uppsala大學(xué)研究人員最近發(fā)現(xiàn)了一種全新RNA抑制途徑,,即反義RNA與核糖體競爭mRNA的起始位點(diǎn),,從而達(dá)到抑制或影響RNA轉(zhuǎn)錄的作用。文章發(fā)表于近日出版的Molecular Cell上,。
以往人們一直認(rèn)為反義RNA通過與mRNA結(jié)合,,從而抑制核糖體閱讀目標(biāo)基因,抑制了mRNA轉(zhuǎn)錄,。研究人員已經(jīng)在細(xì)菌中證實(shí),,反義RNA與核糖體閱讀起始位點(diǎn)的特定mRNA而形成堿基對(duì),抑制了mRNA轉(zhuǎn)錄,。
然而,,Uppsala大學(xué)原核生物微生物學(xué)教授Gerhart Wagner發(fā)現(xiàn)一種調(diào)節(jié)蛋白合成的全新機(jī)制,不能用反義RNA阻礙核糖體在 mRNA上的起始位點(diǎn)解釋,,相反的,,反義RNA與遠(yuǎn)離閱讀起始位點(diǎn)的mRNA外成堿基對(duì),但仍然能夠阻斷閱讀,。 意外的是,,核糖體到達(dá)一個(gè)封閉的起始位點(diǎn)時(shí),它會(huì)選擇遠(yuǎn)離此位點(diǎn)的開放性位點(diǎn),,而等待正確位點(diǎn)恢復(fù),。研究人員認(rèn)為反義RNA與核糖體競爭結(jié)合這個(gè)后備位點(diǎn)。如果反義RNA先到,,便中止蛋白合成,。
(資料來源 : Bio.com)
英文原文鏈接:
原始出處:
Molecular Cell,Volume 26, Issue 3, 11 May 2007, Pages 381-392
Article
An Antisense RNA Inhibits Translation by Competing with Standby Ribosomes
Fabien Darfeuille1, 3, 4, Cecilia Unoson1, 3, Jörg Vogel2 and E. Gerhart H. Wagner1, ,
1Department of Cell and Molecular Biology, Biomedical Center, Uppsala University, Box 596, S-75124 Uppsala, Sweden
2RNA Biology Group, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117 Berlin, Germany
Received 21 February 2007; revised 25 March 2007; accepted 5 April 2007. Published: May 10, 2007. Available online 10 May 2007.
Summary
Most antisense RNAs in bacteria inhibit translation by competing with ribosomes for translation initiation regions (TIRs) on nascent mRNA. We propose a mechanism by which an antisense RNA inhibits translation without binding directly to a TIR. The tisAB locus encodes an SOS-induced toxin, and IstR-1 is the antisense RNA that counteracts toxicity. We show that full-length tisAB mRNA (+1) is translationally inactive and endonucleolytic processing produces an active mRNA (+42). IstR-1 binding inhibits translation of this mRNA, and subsequent RNase III cleavage generates a truncated, inactive mRNA (+106). In vitro translation, toeprinting, and structure mapping suggest that active, but not inactive, tisAB mRNAs contain an upstream ribosome loading or “standby” site. Standby binding is required for initiation at the highly structured tisB TIR. This may involve ribosome sliding to a transiently open tisB TIR. IstR-1 competes with ribosomes by base pairing to the standby site located 100 nucleotides upstream.
Author Keywords: RNA