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PMID: 8831782 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

A tyrosyl-tRNA synthetase suppresses structural defects in the two major helical domains of the group I intron catalytic core.

Journal of molecular biology ·Vol. 262 ·No. 2 ·1996-09-20 ·Pages 87-104

Myers CA, Wallweber GJ, Rennard R, Kemel Y, Caprara MG, Mohr G, Lambowitz AM

Abstract

The Neurospora crassa mitochondrial tyrosyl-tRNA synthetase, the CYT-18 protein, functions in splicing group I introns by promoting the formation of the catalytically active structure of the intron RNA. The group I intron catalytic core is thought to consist of two extended helical domains, one formed by coaxial stacking of P5, P4, P6, and P6a (P4-P6 domain) and the other consisting of P8, P3, P7, and P9 (P3-P9 domain). To investigate how CYT-18 stabilizes the active RNA structure, we used an Escherichia coli genetic assay based on the phage T4 td intron to systematically test the ability of CYT-18 to compensate for structural defects in three key regions of the catalytic core: J3/4 and J6/7, connecting regions that form parts of the triple-helical-scaffold structure with the P4-P6 domain, and P7, a long-range base-pairing interaction that forms the guanosine-binding site and is part of the P3-P9 domain. Our results show that CYT-18 can suppress numerous mutations that disrupt the J3/4 and J6/7 nucleotide-triple interactions, as well as mutations that disrupt base-pairing in P7. CYT-18 suppressed mutations of phylogenetically conserved nucleotide residues at all positions tested, except for the universally conserved G-residue at the guanosine-binding site. Structure mapping experiments with selected mutant introns showed that the CYT-18-suppressible J3/4 mutations primarily impaired folding of the P4-P6 domain, while the J6/7 mutations impaired folding of both the P4-P6 and P3-P9 domains to various degrees. The P7 mutations impaired the formation of both P7 and P3, thereby grossly disrupting the P3-P9 domain. The finding that the P7 mutations also impaired formation of P3 provides evidence that the formation of these two long-range pairings is interdependent in the td intron. Considered together with previous work, the nature of mutations suppressed by CYT-18 supports a model in which CYT-18 helps assemble the P4-P6 domain and then stabilizes the two major helical domains of the catalytic core in the correct relative orientation to form the intron's active site.

MeSH Terms
Bacteriophage T4/chemistry Base Sequence Chromosome Mapping Escherichia coli Introns Kinetics Mitochondria/enzymology Molecular Sequence Data Mutagenesis, Site-Directed Neurospora crassa/enzymology,genetics Nucleic Acid Conformation Phenotype RNA Splicing RNA, Viral/chemistry Tyrosine-tRNA Ligase/chemistry
Chemicals
RNA, Viral Tyrosine-tRNA Ligase
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Myers C A
Department of Molecular Genetics, Ohio State University 43210-1292, USA.
Wallweber G J
Rennard R
Kemel Y
Caprara M G
Mohr G
Lambowitz A M
Article Info
Journal
Journal of molecular biology
Abbr.
J Mol Biol
ISSN
0022-2836
Published
1996-09-20
Pages
87-104
Language
English
Region
England
NLM ID
2985088R
Subset
IM
Grants
NIGMS NIH HHS · F32 GM16468 · United States
NIGMS NIH HHS · GM37951 · United States
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