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Pseudogene repair driven by selection pressure applied in experimental evolution

ABSTRACT: Pseudogene repair driven by selection pressure applied in experimental evolution

PROVIDER: PRJNA506264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8218070_1.fastq.gz	Fastqsanger.gz
	SRR8218070_2.fastq.gz	Fastqsanger.gz
	SRR8218071_1.fastq.gz	Fastqsanger.gz
	SRR8218071_2.fastq.gz	Fastqsanger.gz
	SRR8218072_1.fastq.gz	Fastqsanger.gz

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Pseudogene repair driven by selection pressure applied in experimental evolution

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Phenotypic selection during laboratory evolution of yeast populations leads to a genome-wide sustainable chromatin compaction shift

Project description:Based on inheritance of acquired characteristics, Lamarckian theory of evolution explains the evolution of biological systems through epigenetics. In a previous study, we have shown how microbial evolution has resulted in a persistent reduction in expression after repeatedly selecting for the lowest PGAL1-YFP-expressing cells. Applying the ATAC-seq assay on samples collected from this 28-days evolution experiment, here we show how genome-wide chromatin compaction change during evolution under selection pressure. We found that the chromatin compaction was altered not only on GAL network genes directly impacted by the selection pressure, showing an example of non-genetic memory, but also at the whole genome level. The GAL network genes experienced chromatin compaction accompanying the reduction in PGAL1-YFP reporter expression; strikingly, the fraction of global genes with differentially compacted chromatin states accounted for about a quarter of the total genome. Moreover, some of the ATAC-seq peaks followed well-defined temporal dynamics. Comparing the peak’s intensity in consecutive days, we found most of the differential compaction to occur between days 0 and 3 when the selection pressure was first applied, and between days 7 and 10 when the pressure was lifted. Among the gene sets enriched for the differential compaction events, some had increased chromatin availability once selection pressure was applied and decreased availability after the pressure was lifted (or vice versa). These results intriguingly show that, despite the lack of targeted selection, transcriptional availability of a large fraction of the genome change in a very diverse manner during evolution and these changes can occur in a relatively short number of generations.

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Project description:Purpose Despite advances and significant improvement in survival, multiple myeloma (MM) remains incurable and nearly all patients relapse after treatment. Previous studies have shown a complex spectrum of diverse genetic alterations in almost all patients, but evolution of genomic rearrangements throughout myeloma life cycle has not been investigated. Patients and Methods We performed genomic analysis integrating copy number, allele specific copy number, allele ratio calculations, breakpoint sequencing and rearrangement PCR genotyping on matched diagnosis and relapse samples from 24 MM patients either treated with proteasome inhibitor (bortezomib)-based induction regimen or conventional chemotherapeutic agents. Results All relapse samples have a clear relationship to the diagnosis clone with significant increase of copy number abnormalities (CNAs). Despite a wide diversity of CNAs acquired at relapse, regulators of NF-kB activity were targeted in 25% of the patients. Relapse-associated lesions either appeared as new acquisition or were selected from minor subpopulations at diagnosis. In one third of the patients, we found loss of abnormities containing loss of heterozygosity (LOH) providing evidence that the relapse clone derived from an ancestral clone shared with the dominant diagnosis clone. Remarkably, re-emergence of ancestral clones was almost exclusively found in patients treated with bortezomib, attested to a remarkable adaptability of myeloma cells under targeted drug selection pressure. Conclusion These data suggest that genomic instability and clonal selection are the main forces that drive adaptive changes in MM under drug selection pressure, and they support the proposal to combine several anti-myeloma drugs upfront in order to obtain long-term remissions. [SNP genotyping] 24 myeloma patients at diagnosis and relapse examined with high resolution genome-wide chip

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Genetic adaptability of cancer cells under treatment selection pressure in multiple myeloma patients.

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