Sentences with phrase «dna gain and loss»

Although DNA gain and loss in human occurred mostly in different regions, they both tended to impact on the same biological processes, while in mouse DNA loss was enriched for developmental genes and DNA gain did not associate with any particular biological process.
To understand the evolutionary impacts and trajectories of DNA gain and loss dynamics we analysed their genomic distributions in the context of various genomic features and biological processes.
Therefore, the role of genome structure on widespread DNA gain and loss and its subsequent impact on lineage - specific species evolution remains unknown.
To understand the relationship between both the spatial and temporal dynamics of DNA gain and loss, we analysed the genomic distribution of DNA gain and loss events that occurred between each divergence event.
We also investigated various groups of transposons whose genomic distributions have been previously characterised and used to investigate genome - wide DNA gain and loss rates.
Using our identified DNA gain and loss events it is possible to characterise genome - wide patterns of DNA gain and loss and to begin to determine how DNA turnover may impact on mammalian genome evolution.
This makes it possible to compare them to a wide variety of outgroup species and detect genomic features that associate with DNA gain and loss.
For our analysis, we detected DNA gain and loss events using two distinct, yet complementary, methods from which we characterised DNA gain and loss hotspots.
Importantly, our understanding of DNA gain and loss stems from genome - wide estimates rather than detection of individual events.
Citation: Buckley RM, Kortschak RD, Adelson DL (2018) Divergent genome evolution caused by regional variation in DNA gain and loss between human and mouse.
In addition, we also measured how gene in DNA gain and loss hotspots associate with gene regulatory blocks (GRBs), genomic regions preserved between mammals and birds that are enriched for highly conserved elements [72].
Collectively, these results demonstrate that it is possible to identify locations for the majority of DNA gain and loss events since human and mouse divergence.
However in contrast to hg19, older mm10 DNA gain and loss events show strong negative associations with each other (Fig 8).
Consistent between both methods is size distribution difference between DNA gain and loss.
To better characterise the molecular drivers and evolutionary impacts of DNA gain and loss, we calculated lineage - specific gain and loss rates across the human and mouse genomes.
Thus, regional / species specific variation in DNA gain and loss are primarily driven by clade specific / recent transposons interacting with open chromatin either in the male germ line, female germ line or early embryo.
This is consistent with a model in which DNA gain and loss results in turnover or «churning» in regulatory element dense regions of open chromatin, where interruption of regulatory elements is selected against.
Our results showed that both hg19 and mm10 underwent similar temporal patterns of DNA gain and loss.
It indicates that the recent transposon method is a reasonably effective method in identifying DNA gain and loss in species where it is difficult to detect ancestral elements.
First, we identified DNA gain and loss hotspots using the hotspot identification procedure described in the methods section.
Next, the genomic distribution for each set of time - specific DNA gain and loss hotspots were then compared by performing Fisher's exact test based on their overlap, hotspot overlaps were considered significant if their FDR was < 0.05.
Bins with less than 150 kb of DNA not belonging to RBH nets were removed and our tallies were normalised to reflect DNA gain and loss amounts per 200 kb.
To better understand the spatio - temporal dynamics of DNA gain and loss, we dated individual DNA gain or loss events using a series of ingroup species that each mark specific divergence events between either human or mouse (Methods).
Fourth, the observed autosomal divergence of gain and loss hotspot patterns in proximity to genes supports a model in which developmental / regulatory mechanisms (based on GO term results) are robust to large amounts of transposon driven DNA gain and loss.
Focusing on the distribution of DNA gains and losses, relationships to important structural features and potential impact on biological processes, we found that in autosomes, DNA gains and losses both followed separate lineage - specific accumulation patterns.
Our results revealed that DNA gains and losses occur in different regions across autosomes, while DNA gains from both species are particularly enriched on the X chromosome where they overlap.
This creates a synthetic genome consisting of DNA gains and losses that occurred across both the reference and query lineages.
This suggests that for the most part the accumulation of DNA gains and losses have had little impact on phenotypic change.
Interestingly, Human DNA gains and losses and mouse DNA losses all occurred near genes involved in fundamental cellular / metabolic processes.
Because DNA loss is caused by repair of DNA Double Stranded Breaks (DSB)[81], this means that L1 ORF2p activity can both cause DNA gains and losses as a cause of DSB.
First, hot spots for DNA gains and losses occur in different compartments; loss hot spots in open chromatin / regulatory regions and gain hot spots in heterochromatin.
Collectively, our results show that the regional distribution of DNA gains and losses over time have been highly dynamic and most likely the result of complex interactions between genome organisation, genome biology and transposon activity.

Not exact matches

«Our study shows that epigenetic drift, which is characterized by gains and losses in DNA methylation in the genome over time, occurs more rapidly in mice than in monkeys and more rapidly in monkeys than in humans,» explains Jean - Pierre Issa, MD, Director of the Fels Institute for Cancer Research at LKSOM, and senior investigator on the new study.
DNA gain events generally associate with L1 accumulation and DNA loss occurs in regions associated with biological activity such as transcription and regulation.
These non-aligning reference sequences are absent from the query and are either the result of DNA gain in the reference or DNA loss in the query.
However, the high level of consistency for both methods in identifying hg19 DNA gain and mm10 DNA loss where there is good support for outgroup species is highly encouraging.
To determine whether or not increased DNA gain or loss likely had an evolutionary impact we compared human and mouse gene expression divergence.
They performed testing for IDH1 R132H and ATRX by immunohistochemistry (IHC); 1p / 19q deletion, 7p gain, and 10q loss by DNA array; and IDH 1 and 2 and H3.3 K27M by sequencing.
The resulting DNA copy number variation and patterns of chromosome loss and gain are tumor - type specific, suggesting differential selective pressures on the two tumor cell types.
For this study, researchers conducted genome - wide sampling of methylation, gene expression and DNA structural abnormalities, including the gain or loss of DNA.
Through DNA testing we analyze genetic markers known to impact weight gain or loss, metabolism, exercise, and energy use within the human body.
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