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Inversion frequencies in Pool-Seq data

ABSTRACT: Inference of chromosomal inversion dynamics from Pool-Seq data in natural and laboratory populations of Drosophila melanogaster

PROVIDER: PRJEB4952 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR368828.fastq.gz	Fastqsanger.gz
	ERR368828_1.fastq.gz	Fastqsanger.gz
	ERR368828_2.fastq.gz	Fastqsanger.gz
	ERR368829.fastq.gz	Fastqsanger.gz
	ERR368829_1.fastq.gz	Fastqsanger.gz

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Project description:Aging is a time-dependent biological phenomenon governed by complex networks of regulatory components and their transitions over lifetime. Yet, there have been limited efforts to pin down age-associated networks and map their dynamic characteristics onto aging phenotypes. Here, we built time-course genetic regulatory networks of NAM/ATAF/CUC (NAC) transcription factors during the course of leaf aging in Arabidopsis, using causal regulatory relationships among NACs identified from mutants of 49 aging-associated NACs. These temporal networks revealed a regulatory inversion from activating to repressive regulatory modes at a pre-senescent stage. The inversion was governed by three hub NACs, and their mutants conferred earlier aging with altered expression of reactive oxygen species and salicylic acid response genes. Overexpression of the hub NACs delayed the regulatory inversion, rendering delayed age-dependent cell death. We conclude that the regulatory inversion in NAC networks at a pre-senescent stage directs when age-dependent cell death should proceed in plants.

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brine pool

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FBXO9 in Murine Inversion 16 AML

Project description:The hematopoietic system is maintained throughout life by hematopoietic stem cells that are capable of differentiation to all hematopoietic lineages. An intimate balance between self-renewal, differentiation, and quiescence is required to maintain hematopoiesis. Disruption of this balance can result in hematopoietic malignancy, including acute myeloid leukemia (AML). FBXO9, from the F-box ubiquitin E3 ligases, is down-regulated in patients with AML compared to normal bone marrow. FBXO9 is a substrate recognition component of the Skp1-Cullin-F-box (SCF)-type E3 ligase complex. FBXO9 is highly expressed in hematopoietic stem and progenitor populations, which contain the tumor-initiating population in AML. In AML patients, decrease in FBXO9 expression is most pronounced in patients with the inversion of chromosome 16 (Inv(16)), a rearrangement that generates the transcription factor fusion gene, CBFB-MYH11. To study FBXO9 in malignant hematopoiesis, we generated a conditional knockout mouse model using a novel CRISPR/Cas9 strategy. Our data shows that deletion of Fbxo9 in mice expressing Cbfb-MYH11 leads to markedly accelerated and aggressive leukemia development. In addition, we find loss of FBXO9 leads to increased proteasome expression and tumors are more sensitive to bortezomib suggesting that FBXO9 expression may predict patient response to bortezomib treatment.

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