Evolutionary relationship of plant catalase genes inferred from exon-intron structures: isozyme divergence after the separation of monocots and dicots

Iwamoto, Masao; Maekawa, Masato; Saito, Akira; Higo, Hiromi; Higo, Kenichi

doi:10.1007/s001220050861

Cited by 84 publications

(50 citation statements)

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“…These low rates in Plasmodium could reflect the lack of known retrotransposons and associated reverse transcriptase activity, since intron loss likely occurs via reverse transcription of spliced mRNAs (see below), and intron gain likely occurs either via reverse transcription of spliced mRNAs or via transposon insertion (Crick 1979;Cavalier-Smith 1985;Palmer and Logsdon Jr. 1991;Giroux et al 1994;Iwamoto et al 1998Iwamoto et al , 1999Coghlan and Wolfe 2004;Logsdon Jr. 2004;Roy 2004;Sverdlov et al 2004). Alternative models of intron loss by simple genomic deletion and of intron gain by genomic duplication do not predict low rates in Plasmodium (Rogers 1989;Robertson 1998;Venkatesh et al 1998;Kent and Zahler 2000;Llopart et al 2002;Banyai and Patthy 2004;Cho et al 2004).…”

Section: Discussionmentioning

confidence: 99%

“…New introns might arise either by (1) insertion of type II self-splicing introns laterally transferred from endosymbionts (Sharp 1985;Cavalier-Smith 1991;Stoltzfus 1999), (2) insertion of transposable elements into coding sequences (Crick 1979;Iwamoto et al 1998Iwamoto et al , 1999Roy 2004), or (3) reinsertion of a spliced RNA copy of an intron into a previously intron-less site of a transcript, followed by reverse transcription of this transcript and gene conversion (Cavalier-Smith 1985;Palmer and Logsdon Jr. 1991;Coghlan and Wolfe 2004;Logsdon Jr. 2004;Sverdlov et al 2004). Intron loss might occur by recombination with a reversetranscribed copy of a spliced mRNA transcript (Perler et al 1980;Bernstein et al 1983;Lewin 1983;Weiner et al 1986;Fink 1987;Long and Langley 1993;Derr 1998;Sakurai et al 2002;Wada et al 2002;Lin et al 2003;Mourier and Jeffares 2003;Sverdlov et al 2004;Niu et al 2005;Roy and Gilbert 2005a) or by simple genomic deletion of the intron sequence (Robertson 1998;Kent and Zahler 2000;Banyai and Patthy 2004;Cho et al 2004).…”

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confidence: 99%

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Very little intron loss/gain in Plasmodium: Intron loss/gain mutation rates and intron number

Roy¹,

Hartl²

2006

Genome Res.

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We compared intron positions in conserved regions of 3479 orthologous gene pairs from Plasmodium falciparum and Plasmodium yoelii, which likely diverged Ն100 million years ago (Mya). Only 27 out of 2212 positions were specific to one of the two species. Intron presence in related species shows that at least 19 and possibly 26 of the changes are due to intron loss, depending on phylogeny. The implied intron loss and gain rates are much lower than previously estimated for nematodes, arthropods, fungi, and plants, and are comparable only with the rates in vertebrates. That all observed changes were exact, occurring without loss or gain of flanking coding sequence, suggests intron loss via an mRNA intermediate, as does a nonsignificant trend toward loss of introns at adjacent positions. Many of the intron changes occurred in genes encoding proteins involved in nucleic acid-related processes, as previously found for intron gains in nematodes. Two changes occurred in the chloroquine resistance transporter, suggesting a role for positive selection in intron loss in Plasmodium. The dearth of intron loss and gain could be explained by the lack of known transposable elements in Plasmodium, since transposable elements and/or reverse transcriptase are thought to be necessary for both processes. The observed pattern suggests that the availability of stochastic intron loss and gain mutations can be a major determinant of changes in intron number.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Very little intron loss/gain in Plasmodium: Intron loss/gain mutation rates and intron number

Roy¹,

Hartl²

2006

Genome Res.

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“…There are a few ways a retrocopy can gain an intron (Roy and Gilbert, 2006). After a retroposition event, nucleotide sequences, such as transposable elements, can be inserted into the intronless copy and can become an intron (Iwamoto et al, 1998;Lin et al, 2006). In most cases, if a transposable element inserts itself into an exon, the coding sequence will become interrupted, and therefore the gene will not be functional.…”

Section: Hypothesis For Ir-type Duplicated Genesmentioning

confidence: 99%

Evolution of Gene Structural Complexity: An Alternative-Splicing-Based Model Accounts for Intron-Containing Retrogenes

Chen

Gschwend

Ouyang³

et al. 2014

Plant Physiology

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The structure of eukaryotic genes evolves extensively by intron loss or gain. Previous studies have revealed two models for gene structure evolution through the loss of introns: RNA-based gene conversion, dubbed the Fink model and retroposition model. However, retrogenes that experienced both intron loss and intron-retaining events have been ignored; evolutionary processes responsible for the variation in complex exon-intron structure were unknown. We detected hundreds of retroduplicationderived genes in human (Homo sapiens), fly (Drosophila melanogaster), rice (Oryza sativa), and Arabidopsis (Arabidopsis thaliana) and categorized them either as duplicated genes that have all introns lost or as duplicated genes that have at least lost one and retained one intron compared with the parental copy (intron-retaining [IR] type). Our new model attributes intron retention alternative splicing to the generation of these IR-type gene pairs. We presented 25 parental genes that have an intron retention isoform and have retained introns in the same locations in the IR-type duplicate genes, which directly support our hypothesis. Our alternative-splicing-based model in conjunction with the retroposition and Fink models can explain the IR-type gene observed. We discovered a greater percentage of IR-type genes in plants than in animals, which may be due to the abundance of intron retention cases in plants. Given the prevalence of intron retention in plants, this new model gives a support that plant genomes have very complex gene structures.

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“…Many spliceosomal introns in higher eukaryotes are considered to be relatively recent (4-6), but there is very little direct evidence for the mechanisms by which they arose. Intron insertion by transposition of a p-SINE1 element has occurred in the rice catalase A gene (7). Likewise, transposon insertion supports the creation of a new intron in the Sh2 gene of maize (8).…”

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confidence: 99%

Modern origin of numerous alternatively spliced human introns from tandem arrays

Zhuo

Madden

Elela

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Despite the widespread occurrence of spliceosomal introns in the genomes of higher eukaryotes, their origin remains controversial. One model proposes that the duplication of small genomic portions could have provided the boundaries for new introns. If this mechanism has occurred recently, the 5 and 3 boundaries of each resulting intron should display distinctive sequence similarity. Here, we report that the human genome contains an excess of introns with perfect matching sequences at boundaries. One-third of these introns interrupt the protein-coding sequences of known genes. Introns with the best-matching boundaries are invariably found in tandem arrays of direct repeats. Sequence analysis of the arrays indicates that many intron-breeding repeats have disseminated in several genes at different times during human evolution. A comparison with orthologous regions in mouse and chimpanzee suggests a young age for the human introns with the most-similar boundaries. Finally, we show that these human introns are alternatively spliced with exceptionally high frequency. Our study indicates that genomic duplication has been an important mode of intron gain in mammals. The alternative splicing of transcripts containing these intron-breeding repeats may provide the plasticity required for the rapid evolution of new human proteins.evolution ͉ polymorphism ͉ repeats ͉ splicing T he origin of spliceosomal introns and their dissemination in higher eukaryotes are controversial issues. Different mechanisms have been proposed to explain how introns have arisen at different times during eukaryotic evolution (1). Ancestral spliceosomal introns may have evolved from organellar type II introns (2). In a manner similar to type II introns, the transposition of a spliceosomal intron through its reverse splicing into an intronless gene has been proposed as an ancient dissemination mechanism (3). Many spliceosomal introns in higher eukaryotes are considered to be relatively recent (4-6), but there is very little direct evidence for the mechanisms by which they arose. Intron insertion by transposition of a p-SINE1 element has occurred in the rice catalase A gene (7). Likewise, transposon insertion supports the creation of a new intron in the Sh2 gene of maize (8). Reverse splicing and the genomic insertion of transposons have been proposed to explain recent intron gains in nematodes (5, 9). Intron transfer among paralogues is consistent with the distribution of introns in the globin genes of Chironomus (10). The tandem genomic duplication of a portion of coding sequences with an AGGT cryptic splice site was initially proposed by Rogers (11) as a mechanism to produce the boundaries of a new intron. Although this model was rejected almost immediately based on the lack of similarity at the boundaries of introns that were examined, this mechanism was revived 10 years later to explain the origin of introns in several fish genes (12).A new intron can also arise when a known boundary is spliced to a novel junction created by point mutations, as is...

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Evolutionary relationship of plant catalase genes inferred from exon-intron structures: isozyme divergence after the separation of monocots and dicots

Cited by 84 publications

References 30 publications

Very little intron loss/gain in Plasmodium: Intron loss/gain mutation rates and intron number

Very little intron loss/gain in Plasmodium: Intron loss/gain mutation rates and intron number

Evolution of Gene Structural Complexity: An Alternative-Splicing-Based Model Accounts for Intron-Containing Retrogenes

Modern origin of numerous alternatively spliced human introns from tandem arrays

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