Species-specific homogeneity of the primate Alu family of repeated DNA sequences

Daniels, Gary R.; Fox, Gary M.; Loewensteiner, Daniel; Schmid, Carl W.; Deininger, Prescott L.

doi:10.1093/nar/11.21.7579

Cited by 51 publications

(27 citation statements)

References 31 publications

(56 reference statements)

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“…However, although the dimeric Alu structure appeared in the earliest primates, its amplification rate has been significantly lower in prosimians than in simians (anthropoids) (11, 12). Furthermore, while rodent and prosimian genomes amplified 7SL-related SINEs in addition to tRNA-related SINEs, simian genomes expanded only one dominant SINE, i.e., Alu (3,11,13).Classification of Alu repeats into subfamilies of distinctive evolutionary ages in conjunction with examination of Alu sequences in several primate genomes has revealed a more detailed temporal image of the Alu amplification pattern in primates (6,12,27,47,57,64,78). Alu proliferation in prosimian primates appears to have occurred in that isolated lineage since (i) galago (prosimian) Alu sequences are diagnostically different from anthropoid Alus (12) and (ii) individual Alu repeats common to anthropoid genomes cannot be found at the orthologous loci in prosimians (55,57,59).…”

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“…In early primates, Alu monomers underwent modest divergence from 7SL and were remodeled into a dimeric element of great transpositional potential while preserving 7SL RNA secondary structures in each monomer (26,31,56,62). However, although the dimeric Alu structure appeared in the earliest primates, its amplification rate has been significantly lower in prosimians than in simians (anthropoids) (11,12). Furthermore, while rodent and prosimian genomes amplified 7SL-related SINEs in addition to tRNA-related SINEs, simian genomes expanded only one dominant SINE, i.e., Alu (3,11,13).…”

mentioning

confidence: 99%

“…Classification of Alu repeats into subfamilies of distinctive evolutionary ages in conjunction with examination of Alu sequences in several primate genomes has revealed a more detailed temporal image of the Alu amplification pattern in primates (6,12,27,47,57,64,78). Alu proliferation in prosimian primates appears to have occurred in that isolated lineage since (i) galago (prosimian) Alu sequences are diagnostically different from anthropoid Alus (12) and (ii) individual Alu repeats common to anthropoid genomes cannot be found at the orthologous loci in prosimians (55,57,59).…”

mentioning

confidence: 99%

“…Alu proliferation in prosimian primates appears to have occurred in that isolated lineage since (i) galago (prosimian) Alu sequences are diagnostically different from anthropoid Alus (12) and (ii) individual Alu repeats common to anthropoid genomes cannot be found at the orthologous loci in prosimians (55,57,59). These studies indicate that a dimeric founder Alu existed in the earliest primate genome but that it subsequently amplified to different extents and evolved along different pathways in prosimian and simian genomes.…”

mentioning

confidence: 99%

“…In the simian lineage, Alu elements underwent a concentrated amplification that was specific to early anthropoids. Thus, by 30 to 50 million years ago, the great majority of Alu repeats to be ultimately inherited by the human genome were amplified de novo in early anthropoid DNA, and the rate of amplification slowed dramatically thereafter (5)(6)(7)12; reviewed in references 57 and 59).…”

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confidence: 99%

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A Trinucleotide Repeat-Associated Increase in the Level of Alu RNA-Binding Protein Occurred during the Same Period as the Major Alu Amplification That Accompanied Anthropoid Evolution

Chang

Sasaki-Tozawa

Green

et al. 1995

Molecular and Cellular Biology

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Nearly 1 million Alu elements in human DNA were inserted by an RNA-mediated retroposition-amplification process that clearly decelerated about 30 million years ago. Since then, Alu sequences have proliferated at a lower rate, including within the human genome, in which Alu mobility continues to generate genetic variability. Initially derived from 7SL RNA of the signal recognition particle (SRP), Alu became a dominant retroposon while retaining secondary structures found in 7SL RNA. We previously identified a human Alu RNA-binding protein as a homolog of the 14-kDa Alu-specific protein of SRP and have shown that its expression is associated with accumulation of 3-processed Alu RNA. Here, we show that in early anthropoids, the gene encoding SRP14 Alu RNA-binding protein was duplicated and that SRP14-homologous sequences currently reside on different human chromosomes. In anthropoids, the active SRP14 gene acquired a GCA trinucleotide repeat in its 3-coding region that produces SRP14 polypeptides with extended C-terminal tails. A C3G substitution in this region converted the mouse sequence CCA GCA to GCA GCA in prosimians, which presumably predisposed this locus to GCA expansion in anthropoids and provides a model for other triplet expansions. Moreover, the presence of the trinucleotide repeat in SRP14 DNA and the corresponding C-terminal tail in SRP14 are associated with a significant increase in SRP14 polypeptide and Alu RNA-binding activity. These genetic events occurred during the period in which an acceleration in Alu retroposition was followed by a sharp deceleration, suggesting that Alu repeats coevolved with C-terminal variants of SRP14 in higher primates.Ample evidence indicates that amplification of short interspersed elements (SINEs) occurred via reverse transcription of small RNA intermediaries in a process termed retroposition (52). The SINEs of many organisms are related to one or another tRNA, and these have been found widely distributed in nature, including in plants, fish, and mammals (see references 13, 43, and 44 and references therein). The Alu family of SINEs was derived from the terminal portions of the 7SL RNA component of the signal recognition particle (SRP), a small ribonucleoprotein involved in intracellular protein trafficking (6,24,27,70,71,74,77). In contrast to tRNA-like SINEs, and despite the ubiquity of 7SL SRP RNAs, Alu-related SINEs are for unknown reasons mostly limited to rodents and primates (for a recent review, see reference 13).Evolution of Alu-related SINEs apparently occurred in two major phases: an ancient period during which Alu sequences emerged as monomeric elements followed by a period of remodelling and proliferation (see reference 50 and references therein). The discovery of fossil Alu sequences provided evidence that an Alu monomer originated in an ancestor common to rodents and primates (50). The monomeric Alu-equivalent SINE referred to as B1 has since undergone substantial divergence from 7SL during its amplification to ϳ50,000 to 80,000 copies per haploid genom...

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confidence: 99%

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confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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A Trinucleotide Repeat-Associated Increase in the Level of Alu RNA-Binding Protein Occurred during the Same Period as the Major Alu Amplification That Accompanied Anthropoid Evolution

Chang

Sasaki-Tozawa

Green

et al. 1995

Molecular and Cellular Biology

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Alu-polymerase chain reaction genomic fingerprinting technique identifies multiple genetic loci associated with pancreatic tumourigenesis

McKie

Iwamura

Leung

et al. 1997

Genes Chromosom. Cancer

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DNA fingerprinting can be used to detect genetic rearrangements in cancer that may be associated with activation of oncogenes and inactivation of tumour suppressor genes. We have developed a fingerprinting strategy based on polymerase chain reaction (PCR) amplification of genomic DNA with primers specific for the Alu repeat sequences, which are highly abundant in the human genome. This has been applied to DNA from pancreatic cancer and paired normal samples to isolate and identify fragments of genomic DNA rearranged in the malignant cells. These fragments have been sequenced and used as probes to isolate hybridising clones from gridded bacteriophage PI, phage artificial chromosome, and cosmid libraries for fluorescent in situ hybridisation mapping and the identification of expressed sequences. Further characterisation has identified a putative novel gene (ART1) that is up‐regulated specifically in pancreatic cancer as well as another sequence with similarity to genes involved in differentiation (POU domains). In conclusion, we suggest that Alu‐PCR fingerprinting may be a useful technique for the identification of genes involved in tumourigenesis. Genes Chromosom. Cancer 18:30–41, 1997. © 1997 Wiley‐Liss, Inc.

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Alu‐polymerase chain reaction genomic fingerprinting technique identifies multiple genetic loci associated with pancreatic tumourigenesis

McKie¹,

Iwanamura²,

Leung³

et al. 1997

Genes Chromosomes & Cancer

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Species-specific homogeneity of the primate Alu family of repeated DNA sequences

Cited by 51 publications

References 31 publications

A Trinucleotide Repeat-Associated Increase in the Level of Alu RNA-Binding Protein Occurred during the Same Period as the Major Alu Amplification That Accompanied Anthropoid Evolution

A Trinucleotide Repeat-Associated Increase in the Level of Alu RNA-Binding Protein Occurred during the Same Period as the Major Alu Amplification That Accompanied Anthropoid Evolution

Alu-polymerase chain reaction genomic fingerprinting technique identifies multiple genetic loci associated with pancreatic tumourigenesis

Alu‐polymerase chain reaction genomic fingerprinting technique identifies multiple genetic loci associated with pancreatic tumourigenesis

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