Background: Kinetoplastids are a flagellated group of protists, including some parasites, such as and species, that can cause diseases in humans and other animals. The genomes of these species enclose a fraction of retrotransposons including and , two poorly studied transposable elements that encode a tyrosine recombinase (YR) and were previously classified as DIRS elements. This study investigated the distribution and evolution of and in kinetoplastids to understand the relationships of these elements with other retrotransposons.
Results: We observed that and have a discontinuous distribution among Trypanosomatidae, with several events of loss and degeneration occurring during a vertical transfer evolution. We were able to identify the terminal repeats of these elements for the first time, and we showed that these elements are potentially active in some species, including copies of . We found that and are strictly related elements, which were named in this study as . The reverse transcriptase (RT) tree presented a low resolution, and the origin and relationships among YR groups remain uncertain. Conversely, for RH, grouped with , whereas for YR, sequences constituted two different clades that are closely allied to . Distinct topologies among RT, RH and YR trees suggest ancient rearrangements/exchanges in domains and a modular pattern of evolution with putative independent origins for each ORF.
Conclusions: Due to the presence of both elements in a nontrypanosomatid species, we suggested that and have survived and remained active for more than 400 million years or were reactivated during the evolution of the host species. We did not find clear evidence of independent origins of from the other YR retroelements, supporting the maintenance of the DIRS group of retrotransposons. Nevertheless, according to phylogenetic findings and sequence structure obtained by this study and other works, we proposed separating DIRS elements into four subgroups: and
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6681497 | PMC |
| http://dx.doi.org/10.1186/s13100-019-0175-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Protein and DNA Conformational Changes Contribute to Specificity of Cre Recombinase.
bioRxiv
December 2024
Department of Chemistry and Biochemistry, The Ohio State University, Columbus, Ohio.3.
Cre, a conservative site-specific tyrosine recombinase, is a powerful gene editing tool in the laboratory. Expanded applications in human health are hindered by lack of understanding of the mechanism by which Cre selectively binds and recombines its cognate sequences. This knowledge is essential for retargeting the enzyme to new sites and for mitigating effects of off-target recombination.
View Article and Find Full Text PDFThe recombination efficiency of the bacterial integron depends on the mechanical stability of the synaptic complex.
Sci Adv
December 2024
B CUBE, TU Dresden, Tatzberg 41, 01307 Dresden, Germany.
Multiple antibiotic resistances are a major global health threat. The predominant tool for adaptation in Gram-negative bacteria is the integron. Under stress, it rearranges gene cassettes to offer an escape using the tyrosine recombinase IntI, recognizing folded DNA hairpins, the sites.
View Article and Find Full Text PDFUnlabelled: Focal adhesion kinase (FAK) functions as a signaling and scaffolding protein within endothelial cells (ECs) impacting blood vessel function and tumor growth. Interpretations of EC FAK-null phenotypes are complicated by related PYK2 (protein tyrosine kinase 2) expression, and to test this, we created PYK2 FAK mice with tamoxifen-inducible EC-specific Cre recombinase expression. At 11 weeks of age, EC FAK inactivation resulted in increased heart and lung mass and vascular leakage only on a PYK2 background.
View Article and Find Full Text PDFIn vivo models of subclonal oncogenesis and dependency in hematopoietic malignancy.
Cancer Cell
November 2024
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address:
Cancer evolution is a multifaceted process leading to dysregulation of cellular expansion and differentiation through somatic mutations and epigenetic dysfunction. Clonal expansion and evolution is driven by cell-intrinsic and -extrinsic selective pressures, which can be captured with increasing resolution by single-cell and bulk DNA sequencing. Despite the extensive genomic alterations revealed in profiling studies, there remain limited experimental systems to model and perturb evolutionary processes.
View Article and Find Full Text PDFConditional Activation of c-MYC in Distinct Catecholaminergic Cells Drives Development of Neuroblastoma or Somatostatinoma.
Cancer Res
November 2024
St. Jude Children's Research Hospital, Memphis, TN, United States.
Article Synopsis
- c-MYC is a crucial factor in the development of high-risk neuroblastoma, and the lack of mouse models has limited research on its mechanisms and therapy development.
- Inducing c-MYC through different promoters showed varied tumor types: using a tyrosine hydroxylase promoter led to pancreatic tumors, while a dopamine β-hydroxylase promoter resulted in neuroblastoma.
- The neuroblastoma tumors in mice exhibited similar characteristics to human neuroblastoma and responded to existing treatments, highlighting the importance of these models for testing new therapies.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!