Alu Elements
Repetitive Sequences, Nucleic Acid
Long Interspersed Nucleotide Elements
Short Interspersed Nucleotide Elements
DNA Transposable Elements
Genome, Human
Base Sequence
Molecular Sequence Data
Retroelements
Strepsirhini
Sequence Homology, Nucleic Acid
Exons
3' Flanking Region
Hominidae
Response Elements
Cercopithecidae
Introns
RNA Editing
Promoter Regions, Genetic
Pan troglodytes
Enhancer Elements, Genetic
Evolution, Molecular
Transcription, Genetic
DNA
RNA Polymerase III
Mutagenesis, Insertional
Genes, Neurofibromatosis 1
Gorilla gorilla
Regulatory Sequences, Nucleic Acid
Gene Conversion
Inosine
Sequence Alignment
Gene Expression Regulation
Polymerase Chain Reaction
Sequence Analysis, DNA
Chromosome Breakage
Consensus Sequence
CpG Islands
HeLa Cells
Cloning, Molecular
Terminal Repeat Sequences
RNA, Messenger
Restriction Mapping
Chromosome Mapping
Binding Sites
Gene Rearrangement
Computational Biology
Hereditary desmoid disease in a family with a germline Alu I repeat mutation of the APC gene. (1/466)
Two families with autosomal dominantly inherited desmoid tumors have recently been shown to have germline mutations at the 3' end of the APC gene. We subsequently identified an Amish family with autosomal dominantly inherited desmoid tumors. Genetic analysis performed on one family member, a 47-year-old man with multiple desmoid tumors and no colon polyps, revealed a protein truncating mutation in the middle of the APC gene. The truncating mutation is the result of a 337-bp insertion of an Alu I sequence into codon 1526 of the APC gene. The presence of a poly(A) tail at the 3' end of the insertion suggests that the Alu I sequence was inserted by a retrotranspositional event. Germline insertions of Alu I sequences have occasionally been reported to cause other genetic diseases including type I neurofibromatosis, hereditary site-specific breast cancer (BRCA2), and hemophilia B. However, this is the first report of a germline mutation of the APC gene resulting from an Alu I insertion. (+info)A novel human DNA-binding protein with sequence similarity to a subfamily of redox proteins which is able to repress RNA-polymerase-III-driven transcription of the Alu-family retroposons in vitro. (2/466)
In this study we identified a novel protein which may contribute to the transcriptional inactivity of Alu retroposons in vivo. A human cDNA clone encoding this protein (ACR1) was isolated from a human expression library using South-western screening with an Alu subfragment, implicated in the regulation of Alu in vitro transcription and interacting with a HeLa nuclear protein down-regulated in adenovirus-infected cells. Bacterially expressed ACR1 is demonstrated to inhibit RNA polymerase III (Pol III)-dependent Alu transcription in vitro but showed no repression of transcription of a tRNA gene or of a reporter gene under control of a Pol II promoter. ACR1 mRNA is also found to be down-regulated in adenovirus-infected HeLa cells, consistent with a possible repressor function of the protein in vivo. ACR1 is mainly (but not exclusively) located in cytoplasm and appears to be a member of a weakly characterized redox protein family having a central, highly conserved sequence motif, PGAFTPXCXXXXLP. One member of the family identified earlier as peroxisomal membrane protein (PMP)20 is known to interact in a sequence-specific manner with a yeast homolog of mammalian cyclosporin-A-binding protein cyclophilin, and mammalian cyclophilin A (an abundant ubiquitously expressed protein) is known to interact with human transcriptional repressor YY1, which is a major sequence-specific Alu-binding protein in human cells. It appears, therefore, that transcriptional silencing of Alu in vivo is a result of complex interactions of many proteins which bind to its Pol III promoter. (+info)Translational control of specific genes during differentiation of HL-60 cells. (3/466)
Eukaryotic gene expression can be regulated through selective translation of specific mRNA species. Nevertheless, the limited number of known examples hampers the identification of common mechanisms that regulate translation of specific groups of genes in mammalian cells. We developed a method to identify translationally regulated genes. This method was used to examine the regulation of protein synthesis in HL-60 cells undergoing monocytic differentiation. A partial screening of cellular mRNAs identified five mRNAs whose translation was specifically inhibited and five others that were activated as was indicated by their mobilization onto polysomes. The specifically inhibited mRNAs encoded ribosomal proteins, identified as members of the 5'-terminal oligopyrimidine tract mRNA family. Most of the activated transcripts represented uncharacterized genes. The most actively mobilized transcript (termed TA-40) was an untranslated 1.3-kilobase polyadenylated RNA with unusual structural features, including two Alu-like elements. Following differentiation, a significant change in the cytoplasmic distribution of Alu-containing mRNAs was observed, namely, the enhancement of Alu-containing mRNAs in the polysomes. Our findings support the notion that protein synthesis is regulated during differentiation of HL-60 cells by both global and gene-specific mechanisms and that Alu-like sequences within cytoplasmic mRNAs are involved in such specific regulation. (+info)Human-specific insertion/deletion polymorphisms in Indian populations and their possible evolutionary implications. (4/466)
DNA samples from 396 unrelated individuals belonging to 14 ethnic populations of India, inhabiting various geographical locations and occupying various positions in the socio-cultural hierarchy, were analysed in respect of 8 human-specific polymorphic insertion/deletion loci. All loci, except Alu CD4, were found to be highly polymorphic in all populations. The levels of average heterozygosities were found to be very high in all populations and, in most populations, also higher than those predicted by the island model of population structure. The coefficient of gene differentiation among Indian populations was found to be higher than populations in most other global regions, except Africa. These results are discussed in the light of two possible scenarios of evolution of Indian populations in the broader context of human evolution. (+info)Y chromosomal polymorphisms reveal founding lineages in the Finns and the Saami. (5/466)
Y chromosomal polymorphisms were studied in 502 males from 16 Eurasian ethnic groups including the Finns, Saami (Inari Lake area and Skolt Saami), Karelians, Mari, Mokshas, Erzas, Hungarians (Budapest area and Csangos), Khanty, Mansi, Yakuts, Koryaks, Nivkhs, Mongolians, and Latvians. The samples were analysed for polymorphisms in the Y chromosome specific Alu insertion (YAP) and six microsatellites (DYS19, DYS389-I and II, DYS390, DYS392, DYS393). The populations were also screened for the recently described Tat polymorphism. The incidence of YAP+ type was highest in the Csangos and in other Hungarians (37.5% and 17.5%, respectively). In the Karelians and the Latvians it was present at approximately the same level as commonly found in other European populations, whilst absent in our further samples of Eurasian populations, including the Finns and the Saami. Aside from the Hungarians, the C allele of the Tat polymorphism was common in all the Finno-Ugric speaking populations (from 8.2% to 63.2%), with highest incidence in the Ob-Ugrian Khanty. The C allele was also found in the Latvians (29.4%). The haplotypes found associated with the Tat C allele showed consistently lower density than those associated with the T allele, indicating that the T allele is the original form. The computation of the age of the Tat C suggested that the mutation might be a relatively recent event giving a maximum likelihood estimate of 4440 years (95% confidence interval about 3140-6200 years). The distribution patterns of the 222 haplotypes found varied considerably among the populations. In the Finns a majority of the haplotypes could be assigned to two distinct groups, one of which harboured the C allele of the Tat polymorphism, indicating dichotomous primary source of genetic variation among Finnish males. The presence of a bottleneck or founding effect in the male lineages of some of the populations, namely in the Finns and the Saami, would appear to be one likely interpretation for these findings. (+info)Molecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) in human lymphoma. (6/466)
A region of 150 kb has been analysed around a previously isolated, lymphoma associated, translocation breakpoint located at chromosome band 11q23. This balanced and reciprocal translocation, t(11;14)(q32;q23), has been shown to result in the fusion between chromosome 11 specific sequence and the switch gamma4 region of the IGH locus. The LPC gene, encoding a novel proprotein convertase belonging to the furin family, has been identified in this region. In order to characterize further the region surrounding the translocation, we have determined the detailed structure of LPC. Here we show that LPC consists of at least 16 exons covering 25 kb, and that there is a partial duplication, involving mobile genetic elements and containing LPC exons 13-17 in a tail-tail configuration at 65 kb downstream. Since the chromosomal breakpoint lay between these two structures, the intervening region was further analysed and shown to contain at least two unrelated genes. The previously known SM22 gene was localized close to the 3' tail of LPC. Furthermore, we identified the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) at the chromosomal breakpoint. The position of another previously identified breakpoint was also located to within the first intron of this gene. Altogether, our results give evidence of a genomic instability of this area of 11q23 and show that Pafah1a2 and not LPC is the gene disrupted by the translocation, suggesting that deregulated Pafah1a2 may have a role in lymphomagenesis. (+info)Concerted evolution of the tandem array encoding primate U2 snRNA (the RNU2 locus) is accompanied by dramatic remodeling of the junctions with flanking chromosomal sequences. (7/466)
The genes encoding primate U2 snRNA are organized as a nearly perfect tandem array (the RNU2 locus) that has been evolving concertedly for >35 Myr since the divergence of baboons and humans. Thus the repeat units of the tandem array are essentially identical within each species, but differ between species. Homogeneity is maintained because any change in one repeat unit is purged from the array or fixed in all other repeats. Intriguingly, the cytological location of RNU2 has remained unchanged despite concerted evolution of the tandem array. We had found previously that junction sequences between the U2 tandem array and flanking DNA were subject to remodeling over a region of 200-300 bp during the past 5 Myr in the hominid lineage. Here we show that the junctions between the U2 tandem array and flanking DNA have undergone dramatic rearrangements over a region of 1 to >10 kbp in the 35 Myr since divergence of the Old World Monkey and hominid lineages. We argue that these rearrangements reflect the high level of genetic activity required to sustain concerted evolution, and propose a model to explain why maintenance of homogeneity within a tandemly repeated multigene family would lead to junctional diversity. (+info)Expressed sequence tag (EST) phenotyping of HT-29 cells: cloning of ser/thr protein kinase EMK1, kinesin KIF3B, and of transcripts that include Alu repeated elements. (8/466)
To study the mechanisms that control epithelial commitment and differentiation we have used undifferentiated HT-29 colon cancer cells and a subpopulation of mucus secreting cells obtained by selection of HT-29 cells in 10-6 M methotrexate (M6 cells) as experimental models. We isolated cDNAs encoding transcripts overexpressed in early confluent M6 cells regarding steady-state levels in HT-29 cells by subtractive hybridisation. Fifty-one cDNA clones, corresponding to 34 independent transcripts, were isolated, partially sequenced by their 5' end, and classified into four groups according to their identity: transcripts that included a repeated sequence of the Alu family (10 clones, among them those encoding ribonucleoprotein RNP-L and E-cadherin), transcripts encoded by the mitochondrial genome (nine clones), transcripts encoding components of the protein synthesis machinery (23 clones, including the human ribosomal protein L38 not previously cloned in humans) and nine additional cDNAs that could not be classified in the previous groups. These last included ferritin, cytokeratin 18, translationally controlled human tumour protein (TCHTP), mt-aldehyde dehydrogenase, as well as unknown transcripts (three clones), and the human homologues of the molecular motor kinesin KIF3B and of the ser/thr protein kinase EMK1. Spot dot and Northern blot analyses showed that ser/thr protein kinase EMK1 was differentially expressed in M6 cells when compared with parental HT-29 cells. Steady-state levels of EMK1 were higher in proliferating, preconfluent, M6 and HT-29 cells than in 2 days post confluence (dpc) and 8dpc M6 and HT-29 cells. Transcripts that included an Alu repeat were also shown to be differentially expressed and accumulated in differentiating M6 cells when analysed by Northern blot. The significance of the transcripts cloned is discussed in the context of the commitment and differentiation of the M6 cells to the mucus secreting lineage of epithelial cells. (+info)When a chromosome breaks, it can lead to genetic instability and potentially contribute to the development of diseases such as cancer. Chromosome breakage can also result in the loss or gain of genetic material, which can further disrupt normal cellular function and increase the risk of disease.
There are several types of chromosome breakage, including:
1. Chromosomal aberrations: These occur when there is a change in the number or structure of the chromosomes, such as an extra copy of a chromosome (aneuploidy) or a break in a chromosome.
2. Genomic instability: This refers to the presence of errors in the genetic material that can lead to changes in the function of cells and tissues.
3. Chromosomal fragile sites: These are specific regions of the chromosomes that are more prone to breakage than other regions.
4. Telomere shortening: Telomeres are the protective caps at the ends of the chromosomes, and their shortening can lead to chromosome breakage and genetic instability.
Chromosome breakage can be detected through cytogenetic analysis, which involves staining the cells with dyes to visualize the chromosomes and look for any abnormalities. The detection of chromosome breakage can help diagnose certain diseases, such as cancer, and can also provide information about the risk of disease progression.
In summary, chromosome breakage is a type of genetic alteration that can occur as a result of various factors, including exposure to radiation or chemicals, errors during cell division, or aging. It can lead to genetic instability and increase the risk of diseases such as cancer. Detection of chromosome breakage through cytogenetic analysis can help diagnose certain diseases and provide information about the risk of disease progression.
Alu element
Retrotransposon marker
Short interspersed nuclear element
ARMH3
Mutation
Pseudogene
Jerzy Jurka
Retrotransposon
Transposable element
Barbary macaque
HSD17B1
Exon shuffling
A. Thomas Look
Azaras's capuchin
Genome
Circular RNA
Feng's classification
BC200 lncRNA
Evolution of biological complexity
CpG site
Non-coding DNA
Genome survey sequence
Kronos (computer)
Repeated sequence (DNA)
Signal recognition particle RNA
Microprocessor
Proopiomelanocortin
Paisa (region)
Gene polymorphism
Maria Beckley Kahea
Anthony Luvera
List of cults of personality
Buddha in Africa
PDP-8
LDL receptor
Heart Gear
Românul
Intel 4004
BCL2L13
Steam juicer
Xerox Alto
Prostatic acid phosphatase
Rangana Premaratne
Dicer
National List for Intangible Cultural Heritage
Ilham Shahmuradov
Urartian language
MicroRNA
One Big Union (concept)
Old Assyrian period
Microcode
MHC class III
Music of Hawaii
Shortland Island
Diana Mulili
DeCS - Termos Novos
Innovations - Urban GmbH & Co. Maschinenbau KG
A Couple of Tasty Morsels - Reasons to Believe
Mutations primarily alter the inclusion of alternatively spliced exons | eLife
Publications | www.ibmc.up.pt
Frontiers | Dynamic expression of long noncoding RNAs and repeat elements in synaptic plasticity
Alexander Eckehart Urban's Profile | Stanford Profiles
Roll insulation - All architecture and design manufacturers
NIOSHTIC-2 Search Results - Full View
The Tribune, Chandigarh, India - Real Estate
Impact of polymorphic transposable elements on transcription in lymphoblastoid cell lines from public data | BMC Bioinformatics...
SciELO - Genetics and Molecular Biology, Volume: 32, Issue: 1, Published: 2009
HESX1 gene: MedlinePlus Genetics
LED MODEA - Table and floor lamps
DeCS
Quickly parsing eight digits - Daniel Lemire's blog
lawcareer Archives - ALU.edu
Products grid - Shop Personalized & Unique Gift Items Online with Fast Gift Delivery - FundayGift
Decor: 446 Alu Brushed Steeltone - Homapal
Alu profil 45 x 45 , U10 - OPL d.o.o.
Búsqueda | BVS CLAP/SMR-OPS/OMS
The coevolution between APOBEC3 and retrotransposons in primates | Mobile DNA | Full Text
BTM100A/DB Angular Contact Ball Bearing 100x150x45mm
Gibson Knob 1-1/4' Brushed Gold Elements 105-BG - Builders Surplus
DNA methylation of individual repetitive elements in hepatitis C virus infection-induced hepatocellular carcinoma. | Scholars...
ARB Fridge Solid Mount Kit Element 63Q
- Off Road Tents
DeCS - Termos Novos
DeCS - Termos Novos
Transposable elements8
- Here, we present a mechanism for protecting the human transcriptome from the aberrant exonization of transposable elements . (bvsalud.org)
- 18. A Maximum-Likelihood Approach to Estimating the Insertion Frequencies of Transposable Elements from Population Sequencing Data. (nih.gov)
- This class of junk DNA belongs to a category of sequences known as transposable elements -pieces of DNA that jump around the genome, or transpose. (reasons.org)
- In the process of moving around the genome, some transposable elements make additional copies of themselves, and therefore increase in number when they transpose. (reasons.org)
- SINES belong to a subclass of transposable elements, called retrotransposons . (reasons.org)
- Paired-end mapping is also a critical component of advanced RNA-Seq approaches, mapping of transposable elements and the study of long-range chromatin interactions using the HiC method. (stanford.edu)
- Transposable elements (TEs) are DNA sequences able to mobilize themselves and to increase their copy-number in the host genome. (biomedcentral.com)
- Transposable elements (TEs) are genomic sequences able to move from one location to another within the genome [ 1 ]. (biomedcentral.com)
Genomic4
- 14. Analysis of genomic variation in non-coding elements using population-scale sequencing data from the 1000 Genomes Project. (nih.gov)
- 20. Recently integrated Alu elements and human genomic diversity. (nih.gov)
- Alu-PCR is a relatively simple technique that can be used to investigate genomic instability in cancer. (scielo.br)
- The Alu sequence is approximately 300 bp in length and is found commonly in introns, 3' untranslated regions of genes, and intergenic genomic regions. (nih.gov)
Sequences4
- In primates, the most common SINES are the so-called Alu sequences . (reasons.org)
- Alu sequences contain a segment that the cell's machinery can use to produce an RNA message. (reasons.org)
- Because introns interrupt coding sequences of DNA and are excised by the cell's machinery, many scientists view these elements as junk DNA. (reasons.org)
- It is therefore likely that throughout human evolution different TE-derived sequences have been co-opted into diverse classes of functional elements [ 12 , 23 ]. (biomedcentral.com)
Sequence4
- The Alu sequence family (named for the restriction endonuclease cleavage enzyme Alu I) is the most highly repeated interspersed repeat element in humans (over a million copies). (nih.gov)
- Almost 1 million copies of the Alu sequence are estimated to be present, making it the most abundant mobile element. (nih.gov)
- The Alu sequence is so named because of the presence of a recognition site for the AluI endonuclease in the middle of the Alu sequence. (nih.gov)
- The Alu universal primer sequence is as follows: 5'-GTG GAT CAC CTG AGG TCA GGA GTT TC-3' (26-mer). (nih.gov)
Copies2
- In fact, there are about 1.1 million Alu copies in the human genome (roughly 12% of the human genome). (reasons.org)
- The Alu repeat family comprises short interspersed elements (SINES) present in multiple copies in the genomes of humans and other primates. (nih.gov)
Retroelements2
- The overall goal of this funding opportunity announcement (FOA) is to encourage applications to investigate mechanisms regulating the expression and activity of mobile genetic elements, including long terminal repeat (LTR) and non-LTR retroelements, in cancer. (nih.gov)
- For example, although long interspersed element-1 (LINE-1 or L1) retroelements are active in many cancers whether somatic L1 insertions lead to cancer cell heterogeneity and/or adaptive phenotypes that confer growth or survival advantages during cancer evolution or response to therapy is not clear. (nih.gov)
Genes2
- Transposition of this element into coding and regulatory regions of genes is responsible for many heritable diseases. (nih.gov)
- La transposición de este elemento en regiones codificadoras y reguladoras de genes es la responsable de muchas enfermedades hereditarias. (bvsalud.org)
Mutations2
- Minigene experiments explain disease -associated mutations in Alu elements that hamper hnRNP C binding. (bvsalud.org)
- 2012). Alu elements mediate large SPG11 gene rearrangements: Further spatacsin mutations . (up.pt)
Primates1
- Exaptation of an ancient Alu short interspersed element provides a highly conserved vitamin D-mediated innate immune response in humans and primates. (oregonstate.edu)
Transcript2
- Loss of hnRNP C leads to formation of previously suppressed Alu exons , which severely disrupt transcript function. (bvsalud.org)
- Alu insertion variants alter gene transcript levels. (nih.gov)
Identifies1
- 4. Mobile element scanning (ME-Scan) identifies thousands of novel Alu insertions in diverse human populations. (nih.gov)
Insertion4
- 1. A comprehensive map of mobile element insertion polymorphisms in humans. (nih.gov)
- 2. Tangram: a comprehensive toolbox for mobile element insertion detection. (nih.gov)
- 8. Toolbox for mobile-element insertion detection on cancer genomes. (nih.gov)
- 12. In Silico identification of a common mobile element insertion in exon 4 of RP1. (nih.gov)
Genomes1
- 7. Characterizing mobile element insertions in 5675 genomes. (nih.gov)
Gene1
- These experiments reveal a hitherto unknown complexity of gene expression in long-term synaptic plasticity involving the dynamic regulation of lncRNAs and repeat elements. (frontiersin.org)
Methylation6
- We estimated changes in repetitive element DNA methylation associated with ambient particles (particulate matter ≤ 2.5 µm in aerodynamic diameter), black carbon (BC), and sulfates (SO₄), with mixed models. (nih.gov)
- Methylation of Alu and long interspersed nucleotide elements (LINE-1) is a well-established measure of DNA methylation often used in epidemiologic studies. (cdc.gov)
- Yet, few studies have examined the effects of host factors on LINE-1 and Alu methylation in children. (cdc.gov)
- We measured Alu and LINE-1 methylation by pyrosequencing bisulfite-treated DNA isolated from whole blood samples collected from newborns and nine-year old children (n=358). (cdc.gov)
- Higher prenatal DDT/E exposure was associated with lower Alu methylation at birth, particularly after adjusting for cell type composition (P=0.02 for o,p' -DDT). (cdc.gov)
- Our data suggest that repeat element methylation can be an informative marker of epigenetic differences by age and sex and that prenatal exposure to POPs may be linked to hypomethylation in fetal blood. (cdc.gov)
Aluminum1
- The ALU 320 + PFA is our stable, extendible aluminum probe with PFA assembly system. (ortovox.com)
Human5
- There are ~650,000 Alu elements in transcribed regions of the human genome . (bvsalud.org)
- 3. Evidence for positive selection on recent human transposable element insertions. (nih.gov)
- 5. Mobile elements create structural variation: analysis of a complete human genome. (nih.gov)
- 11. [Evolutionary recent insertions of mobile elements and their contribution to the structure of human genome]. (nih.gov)
- They are mobile elements and are present in the human genome in extremely high copy number. (nih.gov)
Aluminium1
- An automatic logistics system for elements made from aluminium. (u-r-b-a-n.com)
Long1
- It has the same features as our ALU 240 PFA probe, but is 320cm long and extendible. (ortovox.com)
Repeat1
- In light of observations suggesting a role for retrotransposons in brain function, we examined the expression of various classes of repeat elements. (frontiersin.org)
Cell1
- In an effort to address this knowledge gap, this FOA invites research proposals that specifically investigate mechanisms regulating the expression and activity of mobile genetic elements in the context of cell transformation and assess the impact of their activity on tumor heterogeneity, cancer evolution, and response to therapy. (nih.gov)
Mobile4
- 6. The Mobile Element Locator Tool (MELT): population-scale mobile element discovery and biology. (nih.gov)
- 10. Mobile element insertions are frequent in oesophageal adenocarcinomas and can mislead paired-end sequencing analysis. (nih.gov)
- 13. The Simons Genome Diversity Project: A Global Analysis of Mobile Element Diversity. (nih.gov)
- 16. Identification of novel exonic mobile element insertions in epithelial ovarian cancers. (nih.gov)
Constant1
- These elements contain cryptic splice sites , so they are in constant danger of aberrant incorporation into mature transcripts. (bvsalud.org)
Sites1
- Indeed, a substantial portion of 3′-UTR-located Alu elements is believed to be at the basis of regulatory modules that, throughout primate evolution, stabilized their presence in the genome as miRNA binding sites [ 18 ]. (biomedcentral.com)
Health1
- A larger theme is that translational fidelity via tRNAs meeting mRNA demands is a key element of health and disease. (nih.gov)
System1
- Thanks to the optimized PFA system, the ALU 320 + PFA is now MORE COMPACT while also offering better handling. (ortovox.com)
TECHNIQUE1
- Methods 70XX) is an alternate analytical technique for many of these elements. (cdc.gov)
Analysis1
- manufacturer for analysis of elements of 5. (cdc.gov)
Role1
- Thus, by preventing U2AF65 binding to Alu elements , hnRNP C plays a critical role as a genome -wide sentinel protecting the transcriptome . (bvsalud.org)
Move1
- Molecular biologists believe that these DNA elements duplicate and move around the genome through an RNA intermediate and the activity of reverse transcriptase . (reasons.org)