Caprara M G, Mohr G, Lambowitz A M
Department of Molecular Genetics, The Ohio State University, Columbus, 43210-1292, USA.
J Mol Biol. 1996 Apr 5;257(3):512-31. doi: 10.1006/jmbi.1996.0182.
The Neurospora crassa mitochondrial tyrosyl-tRNA synthetase (CYT-18 protein) functions in splicing group I introns. We have used chemical-structure mapping and footprinting to investigate the interaction of the CYT-18 protein with the N. crassa mitochondrial large subunit ribosomal RNA (mt LSU) and ND1 introns, which are not detectably self-splicing in vitro. Our results show that both these non-self-splicing introns form most of the short range pairings of the conserved group I intron secondary structure in the absence of CYT-18, but otherwise remain largely unfolded, even at high Mg2+ concentrations. The binding of CYT-18 promotes the formation of the extended helical domains P6a-P6-P4-P5 (P4-P6 domain) and P8-P3-P7-P9 (P3-P9 domain) and their interaction to form the catalytic core. In iodine-footprinting experiments, CYT-18 binding results in the protection of regions of the phosphodiester backbone expected for tertiary folding of the catalytic core, as well as additional protections that may reflect proximity of the protein. In both introns, most of the putative CYT-18 protection sites are in the P4-P6 domain, the region of the SU intron previously shown to bind CYT-18 as a separate RNA molecule, but additional sites are found in the other major helical domain in P8 and P9 in both introns and in L9 and P7.1/P7.1a in the mt LSU intron. Protease digestion of the CYT-18/intron RNA complexes results in the loss of CYT-18-induced RNA tertiary structure and splicing activity. Considered together with previous studies, or results suggest that CYT-18 binds initially to the P4-P6 region of group I introns to form a scaffold for the assembly of the P3-P9 domain, which may contain additional binding sites for the protein. A three-dimensional model structure of the CYT-18 binding site in group I introns indicates that CYT-18 interacts with the surface of the catalytic core on the side opposite the active-site cleft and may primarily recognize a specific three-dimensional geometry of the phosphodiester backbone of group I introns.
粗糙脉孢菌线粒体酪氨酰 - tRNA合成酶(CYT - 18蛋白)在I组内含子剪接中发挥作用。我们利用化学结构图谱和足迹法研究了CYT - 18蛋白与粗糙脉孢菌线粒体大亚基核糖体RNA(mt LSU)和ND1内含子的相互作用,这些内含子在体外无法检测到自我剪接。我们的结果表明,在没有CYT - 18的情况下,这两个非自我剪接内含子都形成了保守I组内含子二级结构的大部分短程配对,但除此之外,即使在高镁离子浓度下也基本保持未折叠状态。CYT - 18的结合促进了延伸螺旋结构域P6a - P6 - P4 - P5(P4 - P6结构域)和P8 - P3 - P7 - P9(P3 - P9结构域)的形成以及它们相互作用形成催化核心。在碘足迹实验中,CYT - 18的结合导致催化核心三级折叠预期的磷酸二酯主链区域受到保护,以及可能反映蛋白质接近程度的额外保护区域。在这两个内含子中,大多数假定的CYT - 18保护位点都在P4 - P6结构域,即之前显示能作为单独RNA分子结合CYT - 18的SU内含子区域,但在两个内含子的P8和P9以及mt LSU内含子的L9和P7.1/P7.1a中的其他主要螺旋结构域中也发现了额外的位点。对CYT - 18/内含子RNA复合物进行蛋白酶消化会导致CYT - 18诱导的RNA三级结构和剪接活性丧失。结合之前的研究,我们的结果表明CYT - 18最初结合到I组内含子的P4 - P6区域,为P3 - P9结构域的组装形成一个支架,该结构域可能包含该蛋白质的额外结合位点。I组内含子中CYT - 18结合位点的三维模型结构表明,CYT - 18与催化核心在活性位点裂隙相对一侧的表面相互作用,并且可能主要识别I组内含子磷酸二酯主链的特定三维几何形状。