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Chapter 21 : P Transposable Elements in Drosophila melanogaster

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Abstract:

P transposable elements are one of the best studied eukaryotic mobile DNA elements in metazoans. This chapter focuses on the more recent developments in understanding the mechanism and specificity of P element transposition through detailed biochemical and genetic experiments. With the use of P element transformation to introduce the yeast site-specific Flip recombinase (FLP) and the Flip recombinase target (FRT) recombination sites into the genome, it was shown that the FLP recombinase could catalyze DNA strand exchange between FRT sites. Subsequently, it was shown that strand exchange could occur between FRT sites on different chromosomes or sister chromatids. With the development of efficient single P element mutagenesis strategies, many laboratories have undertaken large-scale P element insertional mutation screens. The ability to stimulate recombination at P element sites has had several useful applications in genetics. A system for purifying the P element transposase protein from tissue culture cell nuclear extracts was developed by using a combination of conventional and affinity chromotography methods. It will be extremely important and interesting for the future to understand how P element mobility might be linked to the cell cycle and DNA repair checkpoints and how P element transposition might be influenced by extracellular stimuli.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21

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Figures

Image of Figure 1
Figure 1

The genetics and symptoms of hybrid dysgenesis. The reciprocal crosses of hybrid dysgenesis are shown. Only when P strain males are mated toMstrain females is germ line development abnormal, because of high rates of P element transposition. Progeny from reciprocal M male by P female, P× P or M × M crosses are normal. M females give rise to eggs with a state permissive for P element transposition (M cytotype), whereas P females give rise to eggs with a state restrictive for P element transposition (P cytotype).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 2
Figure 2

Features of the complete 2.9-kb P element. (A) Sequence features of the 2.9-kb P element. The four coding exons (ORF0, 1, 2, and 3) are indicated by boxes with nucleotide numbers shown. The positions of the three introns (IVS1, 2, 3) are indicated below. The DNA sequences of the terminal inverted 31-bp repeats and the internal 11-bp inverted repeats are shown, with corresponding nucleotide numbers shown above. The 8-bp duplications (dup) of target site DNA are shown by boxes at the ends of the element. (B) cis-acting elements of P element transposition. Key sequence features of the left (5′) and right (3′) end are indicated. The terminal 31-bp inverted repeats and the 11-bp internal inverted repeats are indicated by arrows. The transposase binding sites and 8-bp target site duplications are indicated by boxes. The distinct spacer lengths between the 31-bp repeats and the transposase binding sites, 21 bp at the 5′ end and 9 bp at the 3′ end, are indicated above.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 3
Figure 3

P element mRNAs and proteins. The 2.9-kb P element and four exons (ORF0, 1, 2, and 3) are shown at the top. The germ line mRNA, in which all three introns are removed, encodes the 87-kDa transposase mRNA. The somatic mRNA, from which only the first two introns are removed (and which is also expressed in germ line and somatic cells), encodes the 66-kDa repressor mRNA. Shown at the bottom is a KP element, which contains an internal deletion. This truncated element encodes a 24-kDa repressor protein.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 4
Figure 4

P element-mediated germ line transformation. Outline of the method for germ line transformation of Drosophila with P element vectors. Two plasmids, one encoding the P element transposase protein but lacking P element ends and the second plasmid carrying a foreign DNA segment and an eye color marker gene (wor ry) within P element ends, are injected into the posterior pole of preblastoderm embryos. The transposase plasmid enters nuclei of presumptive germ line cells, is expressed, and leads to transposition of the P element from the second plasmid into Drosophila germ line chromosomes. After development of the injected embryos (G generation), the surviving adults are mated to w or ry flies (G generation), and the progeny from this cross (G generation) are scored for restoration of wild-type eye color. The transformation frequency is typically ∼20% of the fertile G adults.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 5
Figure 5

Features of the P element transposase protein. The N-terminal region contains a C2HC motif and basic region involved in site-specific DNA binding. Adjacent to this region are consensus sites for phosphorylation by the ATM family of DNA repair-checkpoint PI-related protein kinases. These sites, when mutated, affect transposase activity in vivo (Beall et al., unpublished). There are two dimerization regions adjacent to the N-terminal DNA binding domain: dimerization region I is a leucine zipper motif and dimerization region II is C-terminal to the leucine zipper but does not resemble any known motif. The central part of the protein contains a GTP binding region, with some sequence motifs found in the GTPase superfamily ( ). The C-terminal region is highly acidic and contains four acidic residues (D444, D528, E531, and D545) that, when mutated, block transposase activity in vivo and in vitro (Ahrens et al., unpublished).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 6
Figure 6

Amino acid sequences of the P element transposase and 66-kDa repressor protein. Single letter code for the 751-aminoacid and 576-amino-acid transposase and 66-kDa proteins. The alternative C terminus of the 66-kDa protein (GMTNLKECVNKVIP) encoded by sequences from IVS is indicated below the corresponding transposase residues (amino acids 562 to 576). The C2HC DNA binding motif is indicated by boxed shadowed letters. The leucine zipper motif is indicated by boxed, outlined L residues. The three GTP binding region homologies are indicated by white letters on a black background. Potential phosphorylation sites for the ATM family of DNA repair-checkpoint PI3 protein kinases (S/TQ or QS/T) are indicated by white letters on a black background. Potential phosphorylation sites for cdc2 (TPHL and TPLQ) are indicated by highlighting and underlining. Acidic residues at the C terminus are underlined, and the four acidic residues that, when mutated, inactivate the protein for catalysis in vivo and in vitro are boxed and highlighted.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 7
Figure 7

Similarities between P element transposase and GTPase superfamily members. Alignments of regions of P element transposase that bear some resemblance to known G proteins. The conserved motifs for phosphoryl binding and guanine specificity are indicated at the top. Amino acid numbers are given below for ras, T antigen, and P element transposase. The residue D379 that when changed to N switched the specificity from guanosine to xanthosine in P element transposase is indicated at the bottom. Reprinted from reference 139 with permission.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 8
Figure 8

Binding sites for transposase on P element DNA. DNA sequences from the 5′ end (nt 48 to 68) and from the 3′ end (nt 2855 to 2871) that are protected from DNase I cleavage by P element transposase. Distance of the beginning of the 10-bp core sequence from the corresponding 31-bp terminal repeat is indicated at the right. A consensus site derived by comparing the two protected regions is shown at the bottom.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 9
Figure 9

Pathway of DNA cleavage and joining during P element transposition. Shown at the top is the P element donor site with the target site duplications, 31-bp inverted repeats, and the 5′ and 3′ cleavage sites indicated. In the first step of transposition, donor cleavage, both ends of the P element are cleaved. The novel cleavage results in a 17-nt single-strand extension on the P element ends and leaves 17 nt from each P element inverted repeat attached to the donor DNA cleavage site. Once transposon excision occurs, the donor site can be repaired via an NHEJ pathway (shown to the right) or via an SDSA gap repair pathway (not shown) (142). The excised P element then selects a target site and, upon strand transfer, integrates into the donor site, generating a gapped intermediate, which upon repair completes integration, creating an 8-bp duplication of target DNA (bottom). Reprinted from reference 10 with permission.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 11
Figure 11

DNA repair pathways used at the donor site after transposase-mediated P element excision. After cleavage of P element DNA by transposase, the Drosophila Ku subunits may associate with the single-strand extensions. These cleaved termini can undergo two fates. One involves NHEJ where the cleaved termini are brought together and after DNA polymerase, ligase, and possibly nuclease action rejoining occurs with the P element sequences and target site duplications present ( ). The second pathway involves gap repair via the SDSA pathway. Either with or without resection, these single-stranded 3′ extensions find homologous DNA sequences to use as templates for DNA repair synthesis. Copying can occur from either P element or flanking Drosophila genomic sequences as templates ( ).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 10
Figure 10

Model for gap repair after P element excision. Homologous chromosomes or sister chromatids, which after undergoing P element excision leave a double-strand gap at the donor site. The homologous sequence then serves as a template for SDSA synthesis ( ). Completion of repair replaces the original P element with a newly synthesized copy. If this gap repair process were incomplete, internal deletions of the P element would result.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 12
Figure 12

Molecular mechanisms for repression of P element transposition. Two effects of repressor proteins can affect repression: transcriptional (left) and posttranscriptional (right). (Left) The binding of repressor to a transposase site at the 5′ P element end blocks transcription from the P element promoter, reducing transposase mRNA synthesis. (Right) The binding of repressor to the transposase sites occludes transposase-DNA interactions required to initiate P element transposition.

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Image of Figure 13
Figure 13

Model for P element trans-silencing. Telomeric P element insertions in TAS repeats interact with heterochromatin proteins. After mating, the euchromatic lacZ reporter P element transgene can form a paired complexwith the P element at the telomere (bottom). This association results in transcriptional repression of the reporter, hence the term “trans-silencing.”

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Figure 14

Model for P cytotype regulation. Maternal P cytotype provides several components to control P element activity. Maternal deposition of repressor protein or RNA leads to reduction of P element pre-mRNA synthesis, altering the ratio of repressor and transposase mRNAs, resulting in an autoregulatory loop ( ). The maternal genome contains some P elements that acquire a maternal imprint of heterochromatin proteins (clustered grey circles) that, in the zygote, can lead to trans-silencing of certain P element insertions. Production and binding of the repressor to P element DNA can inhibit transposase RNA synthesis (left) and block transposase binding to P element DNA (right).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Figure 15

Alternative splicing of the P element third intron (IVS3). (A) Diagram of two IVS3 splicing patterns observed in vivo. The 5′ exon (ORF2), 3′ exon (ORF3), and intron (IVS3) elements are shown schematically. The negative regulatory elements in the 5′ exon (F1 and F2) are indicated. The accurate 5′ (1947) and 3′ (2138) splice sites are shown. The minor alternative D2 5′ (2048) splice site and alternative 3′ splice site (2017) with the flanking microexon is indicated below ( ). (B) RNA sequence of the IVS3 region in the P element. The accurate 5′ and 3′ splice sites are indicated, as is the intron branchpoint (BP). Also underlined are the internal (D1, D2, D3, and D4) and upstream (F1 and F2) 5′ splice site-like (pseudo) sequences ( Table 2 ) ( ). (C) The 5′ exon negative regulatory element and mutations that activate IVS3 splicing. Sequence of the P element 5′ exon. The F1 and F2 sites (labeled brackets) and the accurate 5′ splice site (arrowhead) are shown. Below is shown a reiterated sequence (PyAGNUUAAG) present overlapping the F1 and F2 sites. Below are shown 5′ exon mutations that activate IVS3 splicing in vitro ( ) or in vivo ( ).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Figure 16

Model for somatic inhibition of IVS splicing. U1 snRNP usually interacts with the IVS3 5′ splice site during the early steps of intron recognition and spliceosome assembly. In somatic cells (and in vitro) this site is blocked ( ). Mutations in the upstream negative regulatory element lead to activation of IVS3 splicing in vivo ( ) and in vitro ( ). The F1 site binds U1 snRNP ( ) and the F2 site binds the hnRNP protein, hrp48 ( ). An RNA-binding protein containing four KH domains that is expressed highly in somatic cells, called PSI, has also been implicated in IVS3 splicing control ( ). Several other uncharacterized proteins from Drosophila extracts have been identified by UV cross-linking to the IVS3 5′ exon ( ).

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Tables

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Table 1

Genetic assays for P cytotype repression

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21
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Table 2

Sequences of 5′ splice sites

Citation: Rio D. 2002. P Transposable Elements in Drosophila melanogaster, p 484-518. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch21

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