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7 results for “Intron gain”
Fig. 5 in Loss and Gain of Group I Introns in the Mitochondrial Gene of the Scleractinia (Cnidaria; Anthozoa).
Fig. 5. Bayesian estimates of divergence times in scleractinians. The basal axis is a geologic time scale in units of million years ago (mya). Different time intervals are labeled with abbreviations (Cam, Cambrian; Ord, Ordovician; Sil, Silurian; Dev, Devonian; Car, Carboniferous; Per, Permian; Tri, Triassic; Jur, Jurassic; Cre, Cretaceous; Pal, Paleogene; Neo, Neogene). The chart below the phylogenetic tree gives the extinction rate (solid line) and origination rate (dashed line) in different geological periods, which were modified from Kiessling (2004) with major extinction events labeled with abbreviations (Rhae, Rhaetian; Plie, Pliensbachian; Kimm, Kimmeridgian; Ceno, Cenomanian; Maa, Maastrichtian, KT-extinction). Species with different types of intron are labeled with symbols: ●, Intron-729 (I729); ▲, Intron-893 (I893); ■, Intron-876 (I876).
Fig. 4 in Loss and Gain of Group I Introns in the Mitochondrial Gene of the Scleractinia (Cnidaria; Anthozoa).
Fig. 4. Comparison of phylogenetic trees between the cox1 exon (left side) and intron (right side) in complex corals and corallimorpharians (A) and in sponges and robust corals (B). Tree topologies presenting the phylogenetic relationships of exons and introns were consensus trees between the maximum-likelihood analysis and Bayesian algorism. Numbers on branches are Shimedaira- Hasegawa-like/posterior probabilities. Dashed lines are potential changes in phylogenetic positions between the exon and intron trees.
Fig. 3 in Loss and Gain of Group I Introns in the Mitochondrial Gene of the Scleractinia (Cnidaria; Anthozoa).
Fig. 3. Phylogeny and characteristics of cox1 intron traits in hexacorals. The tree topology was constructed with Mrbayes. Numbers labeled on branches are Shimodaira-Hasegawa-like support/posterior probabilities. Species with different types of introns are labeled with symbols: ●, Intron-729 (I729); ▲, Intron-893 (I893); ■, Intron-876 (I876).
Fig. 1 in Loss and Gain of Group I Introns in the Mitochondrial Gene of the Scleractinia (Cnidaria; Anthozoa).
Fig. 1. Secondary structures of representative cox1 introns in anthozoans. A: Corallimorpharian (Rhodactis howesii); B: basal and complex corals (Gardeneris hawaiinesis); C: robust corals (Diploastrea heliopora); D: actiniarian (Metridinium senile); E: poriferian (Plakortis angulospiculatus); F: zoantharian (Savalia savaglia). Features of the secondary structure indicate the characteristics of group I introns: 10 helical elements P1~P10; consensus primary structures P, Q, R, and S in hollow letters; internal guide sequence, IGS. Initial and terminal sites of the predicted open reading frame are labeled "ORF start" and "ORF stop", respectively.
Analysis of fungal genomes reveals commonalities of intron gain or loss and functions in intron-poor species
<p>Datasets for DOI: <a href="https://doi.org/10.1101/2020.08.11.247098">10.1101/2020.08.11.247098</a>. Jupyter notebooks to reproduce the analysis of this study is available at <a href="https://github.com/Brookesloci/fungi_intron_paper_2020">GitHub</a></p> <ul> <li>annotations.total.txt.gz - gene annotation file of 350 fungi species and outgroups <em>Homo sapiens</em> and <em>Fonticula alba</em></li> <li>site_histories_41490_51_2L_1G.txt.gz - intron site histories of 263 fungi species and outgroups <em>Homo sapiens</em> and <em>Fonticula alba.</em></li> </ul>
Data from: Nonsense-mediated decay enables intron gain in Drosophila
Intron number varies considerably among genomes, but despite their fundamental importance, the mutational mechanisms and evolutionary processes underlying the expansion of intron number remain unknown. Here we show that Drosophila, in contrast to most eukaryotic lineages, is still undergoing a dramatic rate of intron gain. These novel introns carry significantly weaker splice sites that may impede their identification by the spliceosome. Novel introns are more likely to encode a premature termination codon (PTC), indicating that nonsense-mediated decay (NMD) functions as a backup for weak splicing of new introns. Our data suggest that new introns originate when genomic insertions with weak splice sites are hidden from selection by NMD. This mechanism reduces the sequence requirement imposed on novel introns and implies that the capacity of the spliceosome to recognize weak splice sites was a prerequisite for intron gain during eukaryotic evolution.
Data from: Nonsense-mediated decay enables intron gain in Drosophila
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International Brain Laboratory public data
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