scholarly journals Origin and evolution of group I introns in cyanobacterial tRNA genes.

1997 ◽  
Vol 179 (21) ◽  
pp. 6798-6806 ◽  
Author(s):  
B Paquin ◽  
S D Kathe ◽  
S A Nierzwicki-Bauer ◽  
D A Shub
Protist ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 113-122 ◽  
Author(s):  
Debashish Bhattacharya

2002 ◽  
Vol 184 (14) ◽  
pp. 3917-3922 ◽  
Author(s):  
Minsu Ko ◽  
Hyang Choi ◽  
Chankyu Park

ABSTRACT Self-splicing introns are rarely found in bacteria and bacteriophages. They are classified into group I and II according to their structural features and splicing mechanisms. While the group I introns are occasionally found in protein-coding regions of phage genomes and in several tRNA genes of cyanobacteria and proteobacteria, they had not been found in protein-coding regions of bacterial genomes. Here we report a group I intron in the recA gene of Bacillus anthracis which was initially found by DNA sequencing as an intervening sequence (IVS). By using reverse transcriptase PCR, the IVS was shown to be removable from the recA precursor mRNA for RecA that was being translated in E. coli. The splicing was visualized in vitro with labeled free GTP, indicating that it is a group I intron, which is also implied by its predicted secondary structure. The RecA protein of B. anthracis expressed in E. coli was functional in its ability to complement a recA defect. When recA-negative E. coli cells were irradiated with UV, the Bacillus RecA reduced the UV susceptibility of the recA mutant, regardless of the presence of intron.


2002 ◽  
Vol 184 (3) ◽  
pp. 666-671 ◽  
Author(s):  
Knut Rudi ◽  
Tonje Fossheim ◽  
Kjetill S. Jakobsen

ABSTRACT The origin and evolution of bacterial introns are still controversial issues. Here we present data on the distribution and evolution of a recently discovered divergent tRNALeu(UAA) intron. The intron shows a higher sequence affiliation with introns in tRNAIle(CAU) and tRNAArg(CCU) genes in α- and β-proteobacteria, respectively, than with other cyanobacterial tRNALeu(UAA) group I introns. The divergent tRNALeu(UAA) intron is sporadically distributed both within the Nostoc and the Microcystis radiations. The complete tRNA gene, including flanking regions and intron from Microcystis aeruginosa strain NIVA-CYA 57, was sequenced in order to elucidate the evolutionary pattern of this intron. Phylogenetic reconstruction gave statistical evidence for different phylogenies for the intron and exon sequences, supporting an evolutionary model involving horizontal intron transfer. The distribution of the tRNA gene, its flanking regions, and the introns were addressed by Southern hybridization and PCR amplification. The tRNA gene, including the flanking regions, were absent in the intronless stains but present in the intron-containing strains. This suggests that the sporadic distribution of this intron within the Microcystis genus cannot be attributed to intron mobility but rather to an instability of the entire tRNALeu(UAA) intron-containing genome region. Taken together, the complete data set for the evolution of this intron can best be explained by a model involving a nested evolution of the intron, i.e., wherein the intron has been transferred horizontally (probably through a single or a few events) to a tRNALeu(UAA) gene which is located within a unstable genome region.


2000 ◽  
Vol 36 (s3) ◽  
pp. 6-7
Author(s):  
D. Bhattacharya ◽  
F. Lutzoni ◽  
V. Reeb ◽  
D. Simon ◽  
F. Fernandez ◽  
...  

2020 ◽  
Author(s):  
Kelly P. Williams

ABSTRACTBacterial tRNA have been found interrupted at various positions in the anticodon loop by group I introns, in four types. The primary bioinformatic tool for group I intron discovery is a covariance model that can identify conserved features in the catalytic core and can sometimes identify the typical uridine residue at the -1 position, preceding the 5-prime splice site, but cannot identify the typical guanidine residue at the omega position, preceding the 3-prime splice site, to achieve precise mapping. One approach to complete the automation of group I intron mapping is to focus instead on the exons, which is enabled by the regularity of tRNAs. We develop a software module, within a larger package (tFind) aimed at mapping bacterial tRNA and tmRNA genes precisely, that expands this list of four known classes of intron-interrupted tRNAs to 21 cases. A new covariance model for these introns is presented. The wobble base pair formed by the -1 uridine is considered a determinant of the 5-prime splice site, yet one reasonably large new type bears a cytidine nucleotide at that position.


1999 ◽  
Vol 181 (11) ◽  
pp. 3445-3451 ◽  
Author(s):  
Knut Rudi ◽  
Kjetill S. Jakobsen

ABSTRACT Based on the findings that plastids and cyanobacteria have similar group I introns inserted into tRNAUAA Leu genes, these introns have been suggested to be immobile and of ancient origin. In contrast, recent evidence suggests lateral transfer of cyanobacterial group I introns located in tRNAUAA Leu genes. In light of these new findings, we have readdressed the evolution and lateral transfer of tRNAUAA Leu group I introns in cyanobacteral radiation. We determined the presence of introns in 38 different strains, representing the major cyanobacterial lineages, and characterized the introns in 22 of the strains. Notably, two of these strains have two tRNAUAA Leu genes, with each of these genes interrupted by introns, while three of the strains have both interrupted and uninterrupted genes. Two evolutionary distinct clusters of tRNA genes, with the genes interrupted by introns belonging to two distinct intron clusters, were identified. We also compared 16S rDNA and intron evolution for both closely and distantly related strains. The distribution of the introns in the clustered groups, as defined from 16S rDNA analysis, indicates relatively recent gain and/or loss of the introns in some of these lineages. The comparative analysis also suggests differences in the phylogenetic trees for 16S rDNA and the tRNAUAA Leu group I introns. Taken together, our results show that the evolution of the intron is considerably more complex than previous studies found to be the case. We discuss, based on our results, evolutionary models involving lateral intron transfer and models involving differential loss of the intron.


2017 ◽  
Vol 54 (1) ◽  
pp. 66-78 ◽  
Author(s):  
Alicia del Hoyo ◽  
Raquel Álvarez ◽  
Francisco Gasulla ◽  
Leonardo Mario Casano ◽  
Eva María del Campo

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 2001
Author(s):  
Jigeesha Mukhopadhyay ◽  
Georg Hausner

Introns are ubiquitous in eukaryotic genomes and have long been considered as ‘junk RNA’ but the huge energy expenditure in their transcription, removal, and degradation indicate that they may have functional significance and can offer evolutionary advantages. In fungi, plants and algae introns make a significant contribution to the size of the organellar genomes. Organellar introns are classified as catalytic self-splicing introns that can be categorized as either Group I or Group II introns. There are some biases, with Group I introns being more frequently encountered in fungal mitochondrial genomes, whereas among plants Group II introns dominate within the mitochondrial and chloroplast genomes. Organellar introns can encode a variety of proteins, such as maturases, homing endonucleases, reverse transcriptases, and, in some cases, ribosomal proteins, along with other novel open reading frames. Although organellar introns are viewed to be ribozymes, they do interact with various intron- or nuclear genome-encoded protein factors that assist in the intron RNA to fold into competent splicing structures, or facilitate the turn-over of intron RNAs to prevent reverse splicing. Organellar introns are also known to be involved in non-canonical splicing, such as backsplicing and trans-splicing which can result in novel splicing products or, in some instances, compensate for the fragmentation of genes by recombination events. In organellar genomes, Group I and II introns may exist in nested intronic arrangements, such as introns within introns, referred to as twintrons, where splicing of the external intron may be dependent on splicing of the internal intron. These nested or complex introns, with two or three-component intron modules, are being explored as platforms for alternative splicing and their possible function as molecular switches for modulating gene expression which could be potentially applied towards heterologous gene expression. This review explores recent findings on organellar Group I and II introns, focusing on splicing and mobility mechanisms aided by associated intron/nuclear encoded proteins and their potential roles in organellar gene expression and cross talk between nuclear and organellar genomes. Potential application for these types of elements in biotechnology are also discussed.


Genetics ◽  
1989 ◽  
Vol 123 (1) ◽  
pp. 97-108 ◽  
Author(s):  
K F Dobinson ◽  
M Henderson ◽  
R L Kelley ◽  
R A Collins ◽  
A M Lambowitz

Abstract The nuclear cyt-4 mutants of Neurospora crassa have been shown previously to be defective in splicing the group I intron in the mitochondrial large rRNA gene and in 3' end synthesis of the mitochondrial large rRNA. Here, Northern hybridization experiments show that the cyt-4-1 mutant has alterations in a number of mitochondrial RNA processing pathways, including those for cob, coI, coII and ATPase 6 mRNAs, as well as mitochondrial tRNAs. Defects in these pathways include inhibition of 5' and 3' end processing, accumulation of aberrant RNA species, and inhibition of splicing of both group I introns in the cob gene. The various defects in mitochondrial RNA synthesis in the cyt-4-1 mutant cannot be accounted for by deficiency of mitochondrial protein synthesis or energy metabolism, and they suggest that the cyt-4-1 mutant is defective in a component or components required for processing and/or turnover of a number of different mitochondrial RNAs. Defective splicing of the mitochondrial large rRNA intron in the cyt-4-1 mutant may be a secondary effect of failure to synthesize pre-rRNAs having the correct 3' end. However, a similar explanation cannot be invoked to account for defective splicing of the cob pre-mRNA introns, and the cyt-4-1 mutation may directly affect splicing of these introns.


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