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General Information
Symbol
P-element
Species
D. melanogaster
Feature type
natural_transposable_element
FlyBase ID
FBte0000037
Sequences and Components
Complete element (bp)
Terminal repeat (bp)
31
Component genes
Sequence Accessions
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
Sequence Ontology (SO)
Insertions and Copy Number
Copy number and comments
0-50
Zero in euchromatin of Release 3 genome annotation (strain chosen to sequence was one lacking P-elements).
Target Site Duplication
Orthologs
Curated drosophilid orthologs
Comments
The density of insertions of P-element transgenic constructs is significantly lower in underreplicated regions of the genome (URs) compared to neighboring regions or the genomic average. Testis-specific genes have a low frequency of insertions of P-element transgenic constructs.
Hybrid dysgenesis is repressed much more strongly by TP (telomeric P-elements) - M' combinations than by TP or M' P-elements by themselves, indicating that telomeric P-elements interact with other P-elements to create the strong system of repression that is referred to as the P cytotype.
Guanosin triphosphate acts as a cofactor to promote protein-DNA assembly during transposition and is involved in the first detectable noncovalent procleavage synaptic complex.
It is suggested that the P-element transposition mechanism has a two fold dyad symmetry and recognises a structural feature at insertion sites, rather than a sequence specific motif.
P-element movement in somatic cells significantly reduces fitness. The mating activity of males with somatically active P-elements is significantly reduced and they have a significantly lower locomotion activity.
Transposase production and transpositional activation of the M-type element is limited to Dhel\P-element and P-element, M-type elements have become immobile in Dbif\P-element.
Examination of the P-element phylogeny in light of the species phylogeny suggests that additional horizontal transfers may have occurred at various times in the past and may explain the overall structure of the P-element phylogeny in Sophophora.
Correlations between the rate of transposition and TE copy number are determined for P-elements and are found to be negative.
The regulation, transposition and deleterious effects of the P-element are formalised and integrated in a global model to produce a simulation program that simulates a P-element invasion. The simulation demonstrates that present knowledge of the P-element can explain its behaviour in the Drosophila genus. Results suggest success of a P-element invasion into a new species greatly depends on its ability to produce dysgenic crosses.
Naturally occurring regulatory P-elements inserted at the telomere of the X chromosome have been isolated in a genomic context devoid of other P-elements. One or two copies of autonomous P-elements at this site (1A) are sufficient to elicit a strong P repression in the germline. Regulatory properties of the P-elements at 1A are strongly impaired by mutation of Su(var)205.
Based on data of P-element copy number and average level of P-element sensitivity the Altai population of D.melanogaster is assigned M-type.
The combination of a right-end and a left-end deleted P-element can lead to high levels of male recombination (FBrf0080429). This strongly suggests that P-element ends from different chromosomes can become associated, followed by 'pseudo-excision'. Two different processes are involved in resolving the pseudo-excision event: Hybrid Element Insertion (HEI) and Hybrid Excision and Repair (HER). HEI involves the excised P-element ends functioning as a single unit and inserting at a nearby site in the chromosome or into the element itself.
Ten lines of D.simulans have been investigated with respect to P activity, P susceptibility and the number and structure of their P-element copies, eight years after transformation with P{π25.1}. All the lines have reached a steady state. They exhibit varying levels of P activity (from 0 to 96% GD sterility) and are not P-susceptible (with the exception of one line). In contrast to P-element behaviour in D.melanogaster, no relationship is found between the molecular pattern of P-element copies in a line and its ability to induce or repress P expression in D.simulans, peculiar P-element derivatives are observed in D.simulans and the average number of P-element copies per genome is half that of D.melanogaster.
Study of TE distribution (P-element, hobo, I-element, copia, mdg1, mdg3, 412, 297 and roo) along chromosome arms shows no global tendency for the TE site occupancy frequency to negatively follow the recombination rate, except for the 3L arm. The tendency for TE insertion number to increase from base to tip of some chromosome arms is simply explicable by a positive relationship with DNA content along the chromosomes. So for all TEs, except hobo, there is no relationship between distribution of TE insertion numbers weighted by DNA content and recombination rate. hobo insertion site number is positively correlated with recombination rate.
Rearrangements involving repeated sequences within a P-element preferentially occur between units close to the transposon extremities.
The great majority of P-element induced recombination sites occur within 2kb on either side of the mobile P-element. Most male recombination events are not due to the random P\T cuts, approximately two thirds of the recombinants carry a flanking duplication or deletion and the remaining third are simple crossovers. Results suggest that most male recombination events occur by an aberrant transposition process, 'hybrid element insertion', as opposed to double-strand break repair.
Most P-element induced recombinants in germline mitotic cells retain a mobile P-element at the site of recombination, usually with either a deletion or a duplication immediately adjacent to the P-end at which the crossover occurred. These structures fit the 'hybrid element insertion' (HEI) model of male recombination in which two P-element copies on sister chromatids combine to form a hybrid element whose termini insert into a nearby position on the homologue. P-element induced recombination can be used as an efficient means of generating flanking deletions in the vicinity of existing P-elements and retention of a mobile P-element allows extension of the deletion or generate additional variability at the site by subsequent rounds of recombination.
Complete maternally inherited P repression in the germline (P cytotype) can be elicited by only two autonomous P-elements at 1A, and a single element at this position has only partial regulatory properties. Surrounding chromosomal regions include TAS sequences and the regulatory properties of P-elements at 1A are affected by mutants at Su(var)205.
Experimental results from expressing sense and antisense constructs from an Hsp70 promoter suggests that in nature P-element activity could be regulated by P-encoded polypeptides and by antisense P-element RNAs although evidence for naturally occurring antisense P-element RNA has not yet been obtained.
The P-Q-M latitudinal step-cline described in 1983-1986 populations from eastern Australia is still evident in 1991-1994 populations. Full size (highest frequency in the north) and KP elements (highest frequency in south) vary in frequency per genome reciprocally with latitude.
A series of 48 single-P-element lines reveal statistically significant heterogeneity in both longevity and fecundity. Longevity and early fecundity are only weakly correlated. Both the pooled sample and 30 of the individual lines exhibit a leveling of age-specific mortality at advanced ages, in opposition to the classical demographic models.
A series of metabolic characters are quantified in lines bearing single P-element insertions. Data indicates that the distribution of mutational effects is leptokurtic, so that, relative to Guassian distribution there is an excess of mutations of large effect. Pleiotropic effects, quantified by correlations of effects of P-element insertions, appear to differ in pattern both from spontaneous mutational effects and correlations in a natural population.
A phylogenetic survey has identified four major P-element subfamilies in the saltans and willistoni species groups of Drosophila.
Ancient repeated P elements, termed the 'archaeo-P' family, have been identified using a montium species-subgroup P element as a probe, in several true M strains of D.melanogaster.
The distribution of transposable elements within heterochromatin indicates that they are major structural components of the heterochromatin.
Biochemical evidence demonstrates that somatic inhibition of P-element IVS3 splicing requires Psi. Soma specific expression of Psi may be sufficient to explain why P-element transposition occurs in the germ line.
mus309 may act to preserve P-element ends when transposition produces a double strand gap. This allows the terminus to serve as a template upon which DNA synthesis can act to repair the gap.
The combination of P-elements that are deficient for the same P-end produce very little recombination. The combination of a right-end and a left-end element can generate recombination values higher than that given by two complete P-elements at homologous sites. This strongly suggests that 'hybrid' P-elements containing ends from two different elements can be recognised by P\T protein. Combination of a complete element and an end deficient element yields reasonably high levels of recombination; the majority of events derive from the association of complementary ends from the same element.
The activity of a single P-element in somatic cells may reduce lifespan. The P-element effect on lifespan can be reduced by a P-element repressor and the frequency of somatic genetic damage, as measured by chromosome breakage, is significantly increased in flies with active P-elements.
The mode of action of pteridines is two fold. Pteridines may be mutagenic agents which disturb mitotic and meiotic recombination and pteridines disturb the system regulating the mobility and insertion of P-elements.
The distribution of P-elements across the chromosomes has been analysed in individuals from a natural population of D.melanogaster.
The number of P-elements present in lines originating from an M' natural population (containing many, mostly defective P-elements) has been studied over many generations. These lines vary for their cytotype (P or M). P cytotype lines maintained the same copy number of P-elements over time, with a very low rate, if any, of transposition. M cytotype lines accumulated P-element insertions until they reached a plateau of P-element copy number at which insertion and excision rates were equal.
P-element sequences from nine Dipteran species, including D.melanogaster, have been compared. The P-element phylogeny contradicts the phylogeny of the species, suggesting that horizontal transfer of P-elements may have occurred.
It is proposed that ageing is induced by somatic replication of transposable elements (TEs). Most TEs replicate using the enzyme reverse transcriptase. Drugs (PFA and ddI) that inhibit reverse transcriptase were shown to slow aging, prolonging life span, when administered in the first half of adult life by inhibition of TE replication.
Δ2-3-induced transposition of P{FRT(whs)} most frequently causes two copies of the element at or near the original site of insertion. Rearrangements induced in such chromosome with Scer\FLP1hs.PG depend on the relative orientations of the two P{FRT(whs)} elements. When the elements lay in the same orientation deficiencies and duplications are produced, when the elements are inverted, dicentric chromosomes and acentric fragments form as a result of unequal sister chromatid exchange.
Meiotic gene conversion and P element induced gap repair are distinct processes defined by different parameters and, possibly, mechanisms.
Patterns of P-element establishment and evolution have been compared in populations of D.melanogaster and D.simulans (D.simulans does not naturally contain P-elements, and the flies used in this study are transgenic, carrying P-element copies introduced by microinjection).
P and Q strains derived from Japanese natural populations are analysed to study the relationship between the structure and activity of their P-elements.
P-elements transposing from a donor site at the cact gene were found to show nearly a three fold preference for transposition to a region of the homologous chromosome containing the cact locus and extending over two or three number divisions. This preferential transposition is likely to result from a physical proximity of homologous chromosomal regions in the nuclei of germline cells.
The transposition behaviour of P-elements has been analysed in two laboratory strains.
The distribution and copy number of P-elements and hobos has been studied in long-term D.melanogaster cage populations kept under different culture conditions.
Single P-element insertions can be efficiently isolated throughout the heterochromatin by suppressing position effects genetically.
Transient expression P-element excision assays in embryos indicate that somatic expression of the complete transposase transcription unit, as well as the presence of excess numbers of P-element termini, both result in the repression of P-element mobility.
The splicing of the third intron of the P element was assayed in pole cells: not all pole cells were capable of splicing the third intron. Almost all pole cells that have the splicing activity penetrate the gonad and differentiate into primordial germ cells. The splicing of the third intron of the P-element was assayed in pole Almost all pole cells that have the splicing activity penetrate the gonad and differentiate into primordial germ cells.
In a cross screen that was well defined with respect to its P-element components and specifically designed to mobilise and recover P-element insertion mutations the study instead mobilised hobos and hobo insertion mutations are isolated instead.
P-element constructs containing a functional gene (Adh) are capable of rapid dispersal through an experimental population. The inserted gene retains its ability to code for a protein with enzymatic activity. The rate of dispersal is comparable to the rate of dispersal exhibited by unmodified elements.
P-element mobilization has been to study the repair of double strand breaks in the w locus in premeiotic germ cells: distribution of conversion tracts is unaffected by changes in the length of sequence homology between the broken ends of the template, indicating that only a short match is required, and frequency of repair is highly sensitive to single base mismatches in the homologous region.
The wasp L.boulardi, which parasitizes Drosophila larvae, failed to incorporate P-element sequences from its victim, even though the Drosophila carried in excess of 30 genomic copies of the P-element.
Zygotes produced by a P cytotype mother and that have not received maternal P-elements do show evidence of having received a maternal component, a pre-P cytotype. This extra-chromosomal state strongly promotes determination of P cytotype in zygotes into which regulatory P-elements have been paternally introduced. The determinants of the pre-P cytotype cannot persist for even one generation in an individual devoid of P-elements so therefore are not auto-replicative.
P-element and hobo enhancer trap constructs insert into the genome with different patterns of insertions. hobos may be used effectively for enhancer trap mutagenesis into genes that are resistant to P-element inserts.
P-elements preferentially transpose into genomic regions close to their starting sites.
Three Harwich P sublines have been used to investigate the influence of P-derived chromosomes on snw mutability and suppression of vg21-3. Destabilisation of the snw allele and suppression of vg21-3 is correlated with the number of complete P-elements (for chromosome 3).
P-elements located at several different sites preferentially transpose locally. More local insertions are observed in the progeny of mutagenized females than of mutagenized males, and most occur in a preferred orientation with respect to the starting element.
Polymorphism of transposable elements in inbred lines has been examined: P-element, gypsy, jockey, I-element, mdg1, 412, mdg3 and 297 sites are largely stable, whereas roo and copia sites are polymorphic.
There are significant differences in P-element insertion density between inverted and standard chromosome arms. The minority of rearrangements carry the highest density of P-elements.
P-elements from a wild type inbred strain were used as P-element donors to study the frequency and distribution of male recombination events generated on recipient chromosomes that were originally devoid of P-elements. The majority of male recombination breakpoints were associated with either unsuccessful P-element insertion or with the action of P\T attracted by newly inserted P-elements elsewhere on the recipient chromosome. Male recombination breakpoints effectively seem to be distributed at random along the recipient chromosomes.
Development of the P-M system of transposable elements shows interesting correlations with the distribution of Sigma rhabdovirus in D.melanogaster populations.
Superunstable mutations at oc, sn, w, y, psb, ctw and psc were generated in crosses of π2 strain to a wa strain or its derivatives. Each superunstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression. Mutations with the same phenotype often differ in the specificity of their potential for further mutation. Each superunstable mutation is associated with a specific reversible mutation. Active transposase encoded by the P-element is necessary to maintain superinstability.
One KP element at 47D1 is correlated with ability to regulate/suppress P element dysgenic activity. Effect acts through repression of P element transcription.
P-element insertions reduce heterozygous and homozygous viability compared to wild-type in lines containing P-element insertions on the third chromosome.
P-elements from the strong P strain π2 have been cloned and analysed and their cytological location determined. The distribution and structures of the elements demonstrates that some P-element encoded proteins affect transcription from the P-element promoter while others affect the tactivity of the transposase. The activity of the elements is highly dependent on their location, so the properties of a strain reflects the number and type of P-element and their location in the genome.
Biochemical experiments support a mechanism for somatic inhibition of P-element intron 3 (IVS3) splicing in which the binding of a U1snRNP and multiprotein complexes to two exon pseudo 5' splice sites (F1 and F2) prevents U1snRNP binding to the accurate 5' splice site. Somatic cell extracts inhibit binding of U1snRNP to the accurate 5' splice site, and mutations in the exon pseudo 5' splice sites activate IVS3 splicing. A 97kD protein, Psi, contacts P-element RNA upstream of the exon pseudo 5' splice sites, these bases are critical fr RNA-protein complex formation. A 50kD protein, Hrb27C contacts the F2 5' splice site.
Transposition and excision of a P-element at the molecular level has been analysed using a highly transposable P-element insertion (P{hsneo}). Precise excision of the P-element is a rare event. Target-site duplication at the original insertion site does not play a role in forward excision and transposition. Extra sequences that cannot be accounted for by the double-strand gap repair model are often found after excision. A model that could account for these extra sequences is discussed.
D.yakuba, a member of melanogaster subgroup being free of P-element, can be transformed with the P-element at a frequency comparable to that of D.melanogaster. Furthermore, the occurance of 8 base pair duplications upon the insertion of the element suggests that the P-element can be inserted into the genome in the same manner as in D.melanogaster. No consensus for preferential insertion is evident, as in D.melanogaster. However, a series of short palindromic stretches is common around the insertion sites in both species, suggesting that a structural feature of DNA plays a role as a landmark for P-element insertion.
Transposition of P-elements has produced new additive genetic variance at a rate which is more than 30 times greater that the rate expected from spontaneous mutation.
Effect of P-element movement in somatic cells on adult life span has been studied. Lifespan is significantly reduced in males containing P{Δ2-3} element and 17, 4, and 3 but not just a single P-element. Direct correlation between the number of transposing P-elements and the amount of lifespan reduction has been observed. Significant increase in recessive sex-linked lethal mutations in the same males that have reduced life span correlates with previous observation of chromosome breakage in somatic cells of similar males.
The reduced recovery of chromosomes undergoing P-element transposition in flies mutant for either of two genes involved in postreplication repair (mei-41 and mus302) suggests that P-element induced lesions are repaired by a postreplication pathway of DNA repair in Drosophila.
The relationship between the number of complete P-elements and P-element insertion mutagenesis has been studied in several MR (P) strains.
P-element mobilisation is shown to induce quantitative variation for inebriation time.
The repression of P-element mediated hybrid dysgenesis has been studied in twelve inbred lines derived from an M' strain of D.melanogaster. The lines initially differed in their ability to repress gonadal dysgenesis, this ability was highly correlated with the ability to repress snw hypermutability. Most of the lines with low or intermediate repression potential evolved to a state of higher repression potential.
Two sublines B-202 and B-207 are found to cause a new type of gonadal dysgenic sterility, designated as GD-3. It is caused, at a frequency close to 100%, in dysgenic offspring reared above 25oC only. The temperature sensitive period of GD-3 sterility is estimated to the prepupal stage by shift-down experiments.
Samples of the semiparasitic mite Proctolaelaps regalis that have been in contact with P-strains of D.melanogaster contain P-element sequences.
Interspecific crosses carried out between P-element transformed strains of D.simulans and a strain of D.mauritiana, devoid of P-elements, conclude that some of the P-elements can transpose into the D.mauritiana genome.
The ability to repress P-element induced gonadal dysgenesis has been studied in 14 wild-type D.melanogaster strains derived from populations in the central and eastern United States. Repression ability is determined by a complex mixture of chromosomal and cytoplasmic factors.
P{hsneo} is used to study mobilisation of an insertion following introduction of a stable transposase source. A strain carrying a 26bp tandem repeat at the end of the original P{hsneo} insertion exhibits reduced frequency of excision, although frequency of transposition is not altered. Results indicate independence of transposition from excision and the importance of terminal repeats in excision.
An extensive survey of the occurrence of P-element homologous sequences in the genus Drosophila has been carried out by Southern blot analysis. The strongest hybridisation of P-element probes occurs in species from the closely related willistoni and saltans groups.
No correspondence between P-element mobilisation events and recombination in males is found. Definition of 2 adjacent short genetic and molecular regions, one devoid of male recombination and the other acting as a 'hot spot' for exchange in the absence of supporting P-element insertion and excision activity, suggests that transposase may be active at non-P-element sites and that the genome may harbour sequences ranging from highly responsive to completely unresponsive to transposase action.
The rate of precise P-element loss under a variety of genetic conditions has been studied, to investigate the mechanism of P-element transposition. Very high rates of excision can occur, but depend on the presence of a homolog with wild-type sequence at the site of P-element insertion.
Comparison of the Dbif\P-element with the D.melanogaster P-element and the Dneb\P-element shows that the two latter sequences are more similar ro each other than either is to the Dbif\P-element. This contradicts the phylogenetic relationship of the species, and suggests that recent horizontal transfer of P-elements from a relative of D.bifasciata to D.melanogaster has occurred.
The distribution of a number of transposable elements, including P-elements, in a D.melanogaster laboratory strain with a high frequency of spontaneous mutations and its derivatives, has been studied. No P-element sequences have been found in this strain.
The ability of the P-M system of hybrid dysgenesis to generate mutations affecting quantitative characters is tested by measuring the de novo production of variation for two bristle traits between X chromosomes of inbred P and M strains passed through a single dysgenic or nondysgenic cross, in a common autosomal background. Dysgenic crosses are capable of inducing polygenic mutational variance at levels equivalent to heritabilities of these traits from natural levels.
An unusually high level of P-M hybrid dysgenesis is characteristic of hybrid offspring originating from Harwich P strain crosses. The high thermosensitive sterility, low fecundity and premature aging of the male germ line are greatly exacerbated when males are deficient either in excision repair (mei-9 mutation) or in post-replication repair (mei-41 mutation). These findings demonstrate that both DNA repair pathways are essential for the repair of lesions induced by P-element transposition and support the hypothesis that P-element induced chromosome breaks are responsible for the virtual abolition of the germ line.
P{π25.1} has been introduced into the germline of D.simulans and the invasion kinetics of P-elements have been studied in 7 independent lines over 60 generations. Some of the main phenotypic and molecular characteristics of P-M hybrid dysgenesis have been observed, for example, gonadal dysgenesis (GD sterility), chromosome rearrangements, and the occurrence of degenerate P-elements. At least 4 lines reached a steady state with complete or nearly complete P-element regulation, but with a moderate number of P-elements (10-24 per haploid genome) and P activity (10-35% GD sterility).
By controlling the amount of transposase produced by complete P-elements and controlling the amount and effectiveness of different types of repressors, the contribution of the number and distribution of P-elements in the genome to the phenomena of hybrid dysgenesis is studied. A quantitative relationship between P-element number and the incidence of gonadal dysgenesis could not be found probably reflecting the complex etiology of the trait.
The mechanism of P-element transposition, its genetic control and tissue specificity has been determined by the use of biochemical and genetic experiments.
Biochemical assays for RNA binding protein detect a 97kD protein, Psi, that interacts specifically with P-element 5' exon sequences previously implicated in the control of intron 3 (IVS3) splicing in vivo. Inhibition of IVS3 splicing in vivo can be correlated with binding of the 97kD protein to the 5' exon sequence as it preferentially interact with IVS3 and RNA that binds with the 97kD protein relieves inhibition of IVS3 splicing. IVS3 is not spliced in somatic Drosophila splicing extracts, but is accurately spliced in human cell extracts and when microinjected in Xenopus oocytes.
Inbred lines from a strain called Sexi are analysed for their abilities to repress P-element-mediated gonadal sterility.
P-elements insert at random, but their distribution is not uniform. There is a strong preference for euchromatin and the 5' untranslated regions of genes. They also tend to insert adjacent to other P-elements and have a slight preference for target sequences resembling GGCCAGAC. Precise insertional hotspots have been seen in several genes, suggesting that there are additional specificities not yet characterized (O'Hare and Rubin, 1983; Engels). P strains and M' strains have relatively little transposition and excision activity and several regulatory mechanisms are thought to be involved. One of these, called the P 'cytotype,' is found only in P strains and has a partial maternal inheritance resulting in relative stability in P-elements in the progeny of P strain females crossed to M strain males. However, the elements are active in progeny from the reciprocal cross. Certain defective P-elements have been shown to encode a negative regulator of P-element activity. hybrid dysgenesis; Mobilization of P-elements results in a syndrome of abnormal traits called hybrid dysgenesis (Kidwell et al., 1977; Engels et al., 1987). This syndrome includes high frequencies of chromosome rearrangements and male recombination, both of which occur preferentially at the insertion sites of P-elements (Engels and Preston, 1984; Sved et al., 1990). Elevated mutation rates result from insertion mutations and other genomic changes. At high temperatures there is considerable cell death either in the germ-line or in somatic tissues depending on the transposase source (Simmons et al., 1987; Engels et al.). use as transformation vectors: When P-elements are injected into M strain embryos in the presence of transposase, they will jump from the injected DNA into chromosomal locations, carrying along any sequence that has been inserted into the internal portion of the element (Rubin and Spradling, 1982). Genes transformed in this way usually display approximately normal expression and regulation. However, there is usually some position effect, the degree of which depends on the particular transformed sequence. The transposase source can be a gene coinjected with the P vector such as the 'wings clipped' element (Karess and Rubin, 1984) or a stable genomic source such as P{ry+Δ2-3}99B (Robertson et al.). use in mutagenesis: Selecting P-element insertion mutations is useful for cloning genes through 'transposon tagging' and for generating variability. The most effective approach is to mobilize defective elements with an immobile transposase source (Robertson et al., 1988). The mobilized elements can be either naturally occurring defective P-elements or marked elements introduced by transformation (Cooley et al., 1988). use as 'enhancer traps' (O'Kane and Gehring,1987): Genes with specific expression patterns can be identified by mobilization of a P-element carrying the β-galactosidase gene fused to the transposase promoter. The spatial and developmental pattern of β-galactosidase expression appears to depend on the surrounding sequences.
The P-element is a transposable element characteristic of P strains, that produce dysgenic progeny when crossed to M strains in the direction P males to M females, but not vice versa. The older laboratory strains, dating from 1950 or earlier, are M and have no P homologous sequences. Most natural populations in North and South America and Africa are called P strains, meaning they have multiple copies of both complete and defective P-elements in scattered and highly variable genomic positions. The total copy number is usually 30-50. Most European and Asian populations are called M' strains, meaning that they have mostly defective P-elements and a different kind of regulation. The total copy number tends to be less than P strains. Australia has both P and M' strains.
Other Information
Etymology
External Crossreferences and Linkouts ( 24 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
TF
  • R03080
  • R03081
Synonyms and Secondary IDs (6)
References (8,249)