KAS-seq: genome-wide sequencing of single-stranded DNA by N3-kethoxal–assisted labeling

2022 ◽  
Author(s):  
Ruitu Lyu ◽  
Tong Wu ◽  
Allen C. Zhu ◽  
Diana C. West-Szymanski ◽  
Xiaocheng Weng ◽  
...  
2008 ◽  
Vol 83 (6) ◽  
pp. 2697-2707 ◽  
Author(s):  
P. Lefeuvre ◽  
J.-M. Lett ◽  
A. Varsani ◽  
D. P. Martin

ABSTRACT The combinatorial nature of genetic recombination can potentially provide organisms with immediate access to many more positions in sequence space than can be reached by mutation alone. Recombination features particularly prominently in the evolution of a diverse range of viruses. Despite rapid progress having been made in the characterization of discrete recombination events for many species, little is currently known about either gross patterns of recombination across related virus families or the underlying processes that determine genome-wide recombination breakpoint distributions observable in nature. It has been hypothesized that the networks of coevolved molecular interactions that define the epistatic architectures of virus genomes might be damaged by recombination and therefore that selection strongly influences observable recombination patterns. For recombinants to thrive in nature, it is probably important that the portions of their genomes that they have inherited from different parents work well together. Here we describe a comparative analysis of recombination breakpoint distributions within the genomes of diverse single-stranded DNA (ssDNA) virus families. We show that whereas nonrandom breakpoint distributions in ssDNA virus genomes are partially attributable to mechanistic aspects of the recombination process, there is also a significant tendency for recombination breakpoints to fall either outside or on the peripheries of genes. In particular, we found significantly fewer recombination breakpoints within structural protein genes than within other gene types. Collectively, these results imply that natural selection acting against viruses expressing recombinant proteins is a major determinant of nonrandom recombination breakpoint distributions observable in most ssDNA virus families.


2018 ◽  
Vol 7 (7) ◽  
Author(s):  
Vasishta Somayaji ◽  
Dale DeNardo ◽  
Melissa A. Wilson Sayres ◽  
Mellecha Blake ◽  
Kara Waits ◽  
...  

The Gila monster (Heloderma suspectum) is native to the Sonoran Desert. Metagenomic analyses of a Gila monster fecal sample revealed the presence of a small, circular, single-stranded DNA virus that is most closely related to a gemykrogvirus (family Genomoviridae) genome from caribou feces sharing 88% genome-wide pairwise identity.


2021 ◽  
Author(s):  
Jennifer L. McCann ◽  
Agnese Cristini ◽  
Emily K. Law ◽  
Seo Yun Lee ◽  
Michael Tellier ◽  
...  

AbstractThe single-stranded DNA cytosine-to-uracil deaminase APOBEC3B is an antiviral protein implicated in cancer. However, its substrates in cells are not fully delineated. Here, APOBEC3B proteomics reveal interactions with a surprising number of R-loop factors. Biochemical experiments show APOBEC3B binding to R-loops in human cells and in vitro. Genetic experiments demonstrate R-loop increases in cells lacking APOBEC3B and decreases in cells overexpressing APOBEC3B. Genome-wide analyses show major changes in the overall landscape of physiological and stimulus-induced R-loops with thousands of differentially altered regions as well as binding of APOBEC3B to many of these sites. APOBEC3 mutagenesis impacts overexpressed genes and splice factor mutant tumors preferentially, and APOBEC3-attributed kataegis are enriched in RTCW consistent with APOBEC3B deamination. Taken together with the fact that APOBEC3B binds single-stranded DNA and RNA and preferentially deaminates DNA, these results support a mechanism in which APOBEC3B mediates R-loop homeostasis and contributes to R-loop mutagenesis in cancer.HighlightsUnbiased proteomics link antiviral APOBEC3B to R-loop regulationSystematic alterations of APOBEC3B levels trigger corresponding changes in R-loopsAPOBEC3B binds R-loops in living cells and in vitroBioinformatics analyses support an R-loop deamination and mutation model


2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
D Ubmann ◽  
B Göricke ◽  
L Fichtner ◽  
I Panou ◽  
G.H Braus ◽  
...  
Keyword(s):  

2009 ◽  
Vol 42 (05) ◽  
Author(s):  
B Konte ◽  
I Giegling ◽  
AM Hartmann ◽  
H Konnerth ◽  
P Muglia ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document