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Evolution experiment tub2T238A

ABSTRACT: Laboratory evolution experiments of yeast cells impaired for microtubule dynamics. The sequencing was done at two time-points, early and late, to identify compensatory mutations. For details see Macaluso et al, Cell Reports, 2025.

INSTRUMENT(S): NextSeq 550

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Data Submission IFOM ETS

PROVIDER: E-MTAB-14739 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Evolution experiment tub2T238A

Project description:Evolution experiment tub2T238A

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The life history of retrocopies illuminates the evolution of new mammalian genes

Project description:New genes contribute substantially to adaptive evolutionary innovation, but the functional evolution of new mammalian genes has been little explored at a broad scale. Previous work established mRNA-derived gene duplicates, known as retrocopies, as useful models for the study of new gene origination. Here we combine extensive mammalian transcriptomic and epigenomic data to unveil the processes underlying the evolution of stripped-down retrocopies into complex new genes. We show that although some robustly expressed retrocopies are transcribed from preexisting promoters, the majority evolved new promoters from scratch or recruited proto-promoters in their genomic vicinity. In particular, many retrocopy promoters emerged from ancestral enhancers or bivalent regulatory elements, as well as from CpG islands not associated to other genes. Altogether, these mechanisms facilitated the birth of up to 280 retrogenes in each therian species. Furthermore, the regulatory evolution of the originally monoexonic retrocopies was frequently accompanied by exon gain, which facilitated the cooption of distant promoters and in many cases allowed the expression of alternative isoforms. While young retrogenes are often initially expressed in the testis, increased regulatory and structural complexities allowed retrogenes to functionally diversify and evolve somatic organ functions, sometimes as complex as those of their parents. Thus, some retrogenes evolved the capacity to temporarily substitute their parents during the process of male (meiotic) X inactivation, while others even rendered parental functions completely superfluous, allowing for parental gene loss. Overall, our reconstruction of the complete â??life historyâ?? of mammalian retrogenes highlights the usefulness of retroposition as a general model for understanding new gene birth and functional evolution. Assembly and expression of vertebrate retrogene transcripts

2015-12-16 | E-GEOD-72236 | biostudies-arrayexpress

Single-cell mRNAseq human pulmonary arterial endothelial cells in healthy and pulmonary arterial hypertension

Project description:We report the single cell transcriptomic profiles of isolated and cultured human pulmonary arterial endothelial cells. Details were published in Scientifc Reports | (2021) 11:14714

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Comamonas sp. 7D-2evo2 isolate:Compensatory evolution

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Comamonas sp. 7D-2evo1 isolate:Compensatory evolution

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Comamonas sp. 7D-2evo1 isolate:Compensatory evolution

Project description:Comamonas sp. 7D-2evo1 isolate:Compensatory evolution Genome sequencing

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Mutation Order Affects Tumor Evolution and Clinical Course of Disease

Project description:Background: Cancers result from accumulation of somatic mutations and their properties are thought to reflect the sum of these mutations. However, little is known about the consequences of altering the order of mutation acquisition. Methods: Mutation order was determined in myeloproliferative neoplasm patients by genotyping hematopoietic colonies or next generation sequencing. Stem and progenitor cells were isolated to study the effect of mutation order on mature and immature hematopoietic cells. Results: Age of presentation, acquisition of JAK2V617F homozygosity and the balance of immature progenitors were all influenced by mutation order. Compared to TET2-first patients, JAK2-first patients had an increased likelihood of presenting with polycythemia vera than essential thrombocythemia, an increased risk of thrombosis and an increased sensitivity of JAK2-mutant progenitors to ruxolitinib in vitro. In studies of single hematopoietic stem and progenitor cells (HSPCs), mutation order influenced the proliferative response to JAK2V617F and the capacity of double-mutant HSPCs to generate colony-forming cells. Moreover the HSPC compartment was dominated by TET2 single-mutant cells in TET2-first patients but by JAK2/TET2 double-mutant cells in JAK2-first patients. Prior mutation of TET2 altered the transcriptional consequences of JAK2V617F in a cell-intrinsic manner, and prevented JAK2V617F from up-regulating genes associated with proliferation. These data demonstrate that mutation order influences progenitor proliferation and terminal cell expansion, thus influencing clinical presentation, thrombosis risk and progenitor response to targeted therapy. Conclusions: The order in which JAK2 and TET2 mutations are acquired influences clinical features, stem/progenitor cell biology and clonal evolution in patients with myeloproliferative neoplasms.

2014-11-17 | E-MTAB-3086 | biostudies-arrayexpress

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2006-08-04 | GSE5419 | GEO

gNOMO: an pipeline to integrate meta-omics data analisys of non-model organisms

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2021-09-09 | PXD018642 | Pride

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