De novo activation of the transposable element Tam2 of Antirrhinum majus

1987 ◽  
Vol 207 (1) ◽  
pp. 54-59 ◽  
Author(s):  
Andrew Hudson ◽  
Rosemary Carpenter ◽  
Enrico S. Coen
Keyword(s):  
Transposable Element ◽  
De Novo ◽  
Antirrhinum Majus

Curation Guidelines for de novo Generated Transposable Element Families

2021 ◽  
Vol 1 (6) ◽  
Author(s):  
Jessica M. Storer ◽  
Robert Hubley ◽  
Jeb Rosen ◽  
Arian F. A. Smit
Keyword(s):  
Transposable Element ◽  
De Novo

The transposable element Tam1 of Antirrhinum majus is 17 kb long

1984 ◽  
Vol 194 (1-2) ◽  
pp. 138-143 ◽  
Author(s):  
Ulla Bonas ◽  
Hans Sommer ◽  
Brian J. Harrison ◽  
Heinz Saedler
Keyword(s):  
Transposable Element ◽  
Antirrhinum Majus

scholarly journals Contingency in the convergent evolution of a regulatory network: Dosage compensation in Drosophila

2018 ◽  
Author(s):  
Doris Bachtrog ◽  
Chris Ellison
Keyword(s):  
Transposable Element ◽  
Dosage Compensation ◽  
Sex Chromosomes ◽  
Binding Sites ◽  
Evolutionary Biology ◽  
De Novo ◽  
Binding Motif ◽  
Sequence Motif ◽  
X Chromosomes ◽  
Msl Complex

The repeatability or predictability of evolution is a central question in evolutionary biology, and most often addressed in experimental evolution studies. Here, we infer how genetically heterogeneous natural systems acquire the same molecular changes, to address how genomic background affects adaptation in natural populations. In particular, we take advantage of independently formed neo-sex chromosomes in Drosophila species that have evolved dosage compensation by co-opting the dosage compensation (MSL) complex, to study the mutational paths that have led to the acquisition of 100s of novel binding sites for the MSL complex in different species. This complex recognizes a conserved 21-bp GA-rich sequence motif that is enriched on the X chromosome, and newly formed X chromosomes recruit the MSL complex by de novo acquisition of this binding motif. We identify recently formed sex chromosomes in the Drosophila repleta and robusta species groups by genome sequencing, and generate genomic occupancy maps of the MSL complex to infer the location of novel binding sites. We find that diverse mutational paths were utilized in each species to evolve 100s of de novo binding motifs along the neo-X, including expansions of microsatellites and transposable element insertions. However, the propensity to utilize a particular mutational path differs between independently formed X chromosomes, and appears to be contingent on genomic properties of that species, such as simple repeat or transposable element density. This establishes the “genomic environment” as an important determinant in predicting the outcome of evolutionary adaptations.

scholarly journals Synaptonemal complex-deficient Drosophila melanogaster females exhibit rare DSB repair events, recurrent copy number variation, and an increased rate of de novo transposable element movement

2019 ◽  
Author(s):  
Danny E. Miller
Keyword(s):  
Drosophila Melanogaster ◽  
Copy Number Variation ◽  
Transposable Element ◽  
Synaptonemal Complex ◽  
Copy Number ◽  
De Novo ◽  
Wild Type ◽  
Dsb Repair ◽  
Number Variation ◽  
Element Movement

ABSTRACTGenetic stability depends on the maintenance of a variety of chromosome structures and the precise repair of DNA breaks. During meiosis, programmed double-strand breaks (DSBs) made in prophase I are normally repaired as gene conversions or crossovers. Additionally, DSBs are made by the movement of transposable elements (TEs), which must also be resolved. Incorrect repair of these DNA lesions can lead to mutations, copy number variations, translocations, and/or aneuploid gametes. In Drosophila melanogaster, as in most organisms, meiotic DSB repair occurs in the presence of a rapidly evolving multiprotein structure called the synaptonemal complex (SC). Here, whole-genome sequencing is used to investigate the fate of meiotic DSBs in D. melanogaster mutant females lacking functional SC, to assay for de novo CNV formation, and to examine the role of the SC in transposable element movement in flies. The data indicate that, in the absence of SC, copy number variation still occurs but meiotic DSB repair by gene conversion may occur only rarely. Remarkably, an 856-kilobase de novo CNV was observed in two unrelated individuals of different genetic backgrounds and was identical to a CNV recovered in a previous wild-type study, suggesting that recurrent formation of large CNVs occurs in Drosophila. In addition, the rate of novel TE insertion was markedly higher than wild type in one of two SC mutants tested, suggesting that SC proteins may contribute to the regulation of TE movement and insertion in the genome. Overall, this study provides novel insight into the role that the SC plays in genome stability and provides clues as to why SC proteins are among the most rapidly evolving in any organism.

scholarly journals Synaptonemal Complex-Deficient Drosophila melanogaster Females Exhibit Rare DSB Repair Events, Recurrent Copy-Number Variation, and an Increased Rate of de Novo Transposable Element Movement

2019 ◽  
Vol 10 (2) ◽  
pp. 525-537 ◽  
Author(s):  
Danny E. Miller
Keyword(s):  
Drosophila Melanogaster ◽  
Copy Number Variation ◽  
Transposable Element ◽  
Synaptonemal Complex ◽  
Copy Number ◽  
De Novo ◽  
Wild Type ◽  
Dsb Repair ◽  
Number Variation ◽  
Element Movement

Genetic stability depends on the maintenance of a variety of chromosome structures and the precise repair of DNA breaks. During meiosis, programmed double-strand breaks (DSBs) made in prophase I are normally repaired as gene conversions or crossovers. DSBs can also be made by other mechanisms, such as the movement of transposable elements (TEs), which must also be resolved. Incorrect repair of these DNA lesions can lead to mutations, copy-number changes, translocations, and/or aneuploid gametes. In Drosophila melanogaster, as in most organisms, meiotic DSB repair occurs in the presence of a rapidly evolving multiprotein structure called the synaptonemal complex (SC). Here, whole-genome sequencing is used to investigate the fate of meiotic DSBs in D. melanogaster mutant females lacking functional SC, to assay for de novo CNV formation, and to examine the role of the SC in transposable element movement in flies. The data indicate that, in the absence of SC, copy-number variation still occurs and meiotic DSB repair by gene conversion occurs infrequently. Remarkably, an 856-kilobase de novo CNV was observed in two unrelated individuals of different genetic backgrounds and was identical to a CNV recovered in a previous wild-type study, suggesting that recurrent formation of large CNVs occurs in Drosophila. In addition, the rate of novel TE insertion was markedly higher than wild type in one of two SC mutants tested, suggesting that SC proteins may contribute to the regulation of TE movement and insertion in the genome. Overall, this study provides novel insight into the role that the SC plays in genome stability and provides clues as to why the sequence, but not structure, of SC proteins is rapidly evolving.

scholarly journals De novo synthesis of an intron by the maize transposable element Dissociation.

1994 ◽  
Vol 91 (25) ◽  
pp. 12150-12154 ◽  
Author(s):  
M. J. Giroux ◽  
M. Clancy ◽  
J. Baier ◽  
L. Ingham ◽  
D. McCarty ◽  
...  
Keyword(s):  
Transposable Element ◽  
De Novo ◽  
De Novo Synthesis ◽  
Maize Transposable Element

scholarly journals Resistance to Gap Repair of the Transposon Tam3 in Antirrhinum majus: A Role of the End Regions

Genetics ◽  
1999 ◽  
Vol 153 (4) ◽  
pp. 1899-1908 ◽  
Author(s):  
Shiko Yamashita ◽  
Toshiyuki Takano-Shimizu ◽  
Ken Kitamura ◽  
Tetsuo Mikami ◽  
Yuji Kishima
Keyword(s):  
Phylogenetic Analysis ◽  
De Novo ◽  
Secondary Structures ◽  
Sharp Contrast ◽  
Hairpin Structure ◽  
Antirrhinum Majus ◽  
Free Energies ◽  
Structural Homogeneity ◽  
Hairpin Structures

Abstract The extremely homogeneous organization of the transposon family Tam3 in Antirrhinum majus is in sharp contrast to the heterogeneity of the copies constituting many other transposon families. To address the issue of the Tam3 structural uniformity, we examined two possibilities: (1) recent invasion of Tam3 and (2) failure of gap repair, which is involved in conversion from autonomous forms to defective forms. The phylogenetic analysis of 17 Tam3 copies suggested that the invasion of Tam3 into the Antirrhinum genome occurred at least 5 mya, which is sufficiently long ago to have produced many aberrant copies by gap repair. Thus, we investigated gap repair events at the nivearecurrens:Tam3 (nivrec::Tam3) allele, where Tam3 is actively excised. We show here that the gap repair of de novo somatic Tam3 excision was arrested immediately after initiation of the process. All of the identified gap repair products were short stretches, no longer than 150 bp from the ends. The Tam3 ends have hairpin structures with low free energies. We observed that the gap repair halted within the hairpin structure regions. Such small gap repair products appear to be distributed in the Antirrhinum genome, but are unlikely to be active. Our data strongly suggest that the structural homogeneity of Tam3 was caused by immunity to gap repair at the hairpins in both of the end regions. The frequency of extensive gap repair of de novo excision products in eukaryotic transposons was found to be correlated with the free energies of the secondary structures in the end regions. This fact suggests that the fates of transposon families might depend on the structures of their ends.

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