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001-es BibID:BIBFORM119263
035-os BibID:(WoS)001177370100001 (Scopus)85186911726
Első szerző:Székvölgyi Lóránt (biofizikus, biokémikus, sejtbiológus)
Cím:Chromosomal R-loops : who R they? / Lóránt Székvölgyi
Dátum:2024
ISSN:2676-8615 2676-8607
Megjegyzések:R-loops, composed of DNA-RNA hybrids and displaced single-stranded DNA, are known to pose a severe threat to genome integrity. Therefore, extensive research has focused on identifying regulatory proteins involved in controlling R-loop levels. These proteins play critical roles in preventing R-loop accumulation and associated genome instability. Herein I summarize recent knowledge on R-loop regulators affecting R-loop homeostasis, involving a wide array of R-loop screening methods that have enabled their characterization, from forward genetic and siRNA-based screens to proximity labeling and machine learning. These approaches not only deepen our understanding on R-loop formation processes, but also hold promise to find new targets in R-loop dysregulation associated with human pathologies.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
R-hurok, kromatinszerkezet
Megjelenés:Biologia Futura. - 3 (2024), p. 1-8. -
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM106110
035-os BibID:(Scopus)85144296158
Első szerző:Tóth András (Budapest)
Cím:The genome loading model for the origin and maintenance of sex in eukaryotes / Tóth András, Székvölgyi Lóránt, Vellai Tibor
Dátum:2022
ISSN:2676-8615 2676-8607
Megjegyzések:Understanding why sexual reproduction-which involves syngamy (union of gametes) and meiosis-emerged and how it has subsisted for millions of years remains a fundamental problem in biology. Considered as the essence of sex, meiotic recombination is initiated by a DNA double-strand break (DSB) that forms on one of the pairing homologous chromosomes. This DNA lesion is subsequently repaired by gene conversion, the non-reciprocal transfer of genetic information from the intact homolog. A major issue is which of the pairing homologs undergoes DSB formation. Accumulating evidence shows that chromosomal sites where the pairing homologs locally differ in size, i.e., are heterozygous for an insertion or deletion, often display disparity in gene conversion. Biased conversion tends to duplicate insertions and lose deletions. This suggests that DSB is preferentially formed on the "shorter" homologous region, which thereby acts as the recipient for DNA transfer. Thus, sex primarily functions as a genome (re)loading mechanism. It ensures the restoration of formerly lost DNA sequences (deletions) and allows the efficient copying and, mainly in eukaryotes, subsequent spreading of newly emerged sequences (insertions) arising initially in an individual genome, even if they confer no advantage to the host. In this way, sex simultaneously repairs deletions and increases genetic variability underlying adaptation. The model explains a remarkable increase in DNA content during the evolution of eukaryotic genomes.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Adaptive gene combination
Biased gene conversion
Crossover
DNA double-strand break
Deletion
Genome size
Group selection
Individual advantage
Insertion
Meiotic recombination
Origin of sex
Selfish DNA
Megjelenés:Biologia Futura. - 12 (2022), p. 1-20. -
További szerzők:Székvölgyi Lóránt (1977-) (biofizikus, biokémikus, sejtbiológus) Vellai Tibor
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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