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Next Generation DNA sequencing of telomere fusion events isolated from HCT116 LIG3-/-:mL3, HCT116 LIG4-/-, WT HCT116 and MRC5HPVE6E7 cells

ABSTRACT: Next Generation DNA sequencing of telomere fusion events isolated from HCT116 LIG3-/-:mL3, HCT116 LIG4-/-, WT HCT116 and MRC5HPVE6E7 cells

PROVIDER: PRJEB6772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR567599_1.fastq.gz	Fastqsanger.gz
	ERR567599_2.fastq.gz	Fastqsanger.gz
	ERR567600_1.fastq.gz	Fastqsanger.gz
	ERR567600_2.fastq.gz	Fastqsanger.gz
	ERR567601_1.fastq.gz	Fastqsanger.gz

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Next Generation DNA sequencing of telomere fusion events isolated from HCT116 LIG3-/-:mL3, HCT116 LIG4-/-, WT HCT116 and MRC5HPVE6E7 cells

Project description:We characterized the DNA sequences spanning telomere fusion junctions focusing on XpYp:17p inter-chromosomal events in HCT116 LIG3-/-:mL3, HCT116 LIG4-/-, WT HCT116 and MRC5HPVE6E7 cells.

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Telomere dysfunction and fusion during the progression of chronic lymphocytic leukaemia: evidence for a telomere crisis

Project description:We performed single-molecule telomere length and telomere fusion analysis in patients at different stages of chronic lymphocytic leukaemia (CLL). Our work identified the shortest telomeres ever recorded in primary human tissue reinforcing the concept that there is significant cell division in CLL. Furthermore, we provide direct evidence that critical telomere shortening, dysfunction and fusion contribute to disease progression. The frequency of short telomeres and fusion events increased with advanced disease, but importantly these were also found in a subset of early-stage patient samples indicating that these events can precede disease progression. Sequence analysis of fusion events isolated from individuals with the shortest telomeres revealed limited numbers of repeats at the breakpoint, sub-telomeric deletion and microhomology. Array-CGH analysis of individuals displaying evidence of telomere dysfunction revealed large-scale genomic rearrangements that were concentrated in the telomeric regions; this was not observed in samples with longer telomeres. Array CGH was undertaken on six individuals (five CLL stage C and one stage A) that displayed evidence of telomere dysfunction, and four (three CLL stage A and one stage B) that displayed longer and apparently stable telomeres.

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Project description:Studies of fusion genes have mainly focused on the formation of fusions that result in the production of hybrid proteins or, alternatively, on promoter-switching events that put a gene under the control of aberrant signals. However, gene fusions may also disrupt the transcriptional control of genes that are encoded in introns downstream of the breakpoint. By ignoring structural constraints of the transcribed fusions, we highlight the importance of a largely unexplored function of fusion genes. Using breast cancer as an example, we show that miRNA host genes are specifically enriched in fusion genes and that many different, low-frequency, 5' partners may deregulate the same miRNA irrespective of the coding potential of the fusion transcript. These results indicate that the concept of recurrence, defined by the rate of functionally important aberrations, needs to be revised to encompass convergent fusions that affect a miRNA independently of transcript structure and protein-coding potential.

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