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Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox and AB42 overexpression versus control

ABSTRACT: Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox and AB42 overexpression versus control

PROVIDER: PRJEB87284 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14758500_1.fastq.gz	Fastqsanger.gz
	ERR14758500_2.fastq.gz	Fastqsanger.gz
	ERR14758501_1.fastq.gz	Fastqsanger.gz
	ERR14758501_2.fastq.gz	Fastqsanger.gz
	ERR14758502_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox and AB42 overexpression versus control

Project description:Neuronal Wwox overexpression using CRISPRa in Drosophila melanogaster also expressing human AB42 can rescue amyloid related phenotypes. To understand how this may occur we performed bulk transcriptomics on day 14 heads from the same genotypes: 1) Control gRNA + lacZ expression control, 2) Control gRNA + amyloid, 3) Wwox gRNA + LacZ control, 4) Wwox gRNA + amyloid.

2025-04-18 | E-MTAB-14949 | biostudies-arrayexpress

Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox knockdown and AB42 overexpression versus control

Project description:Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox knockdown and AB42 overexpression versus control

| PRJEB87283 | ENA

Bulk RNA-Seq of Drosophila melanogaster heads after neuronal Wwox knockdown and AB42 overexpression versus control

Project description:Wwox knockdown in Drosophila melanogaster neurons (elav-GAL4) also expressing human AB42 worsens lifespan and climbing as well as increasing AB42 load. To understand these effects further we performed transcriptomics on the same genotypes. Neurons expressing RNAi Control and a LacZ control, RNAi Control and AB42, Wwox RNAi and LacZ control or Wwox RNAi and AB42. This design allowed us to pull apart the effects of knockdown, amyloid and the interaction between the two.

2025-04-18 | E-MTAB-14948 | biostudies-arrayexpress

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Project description:Expression profile comparison of the heads of females of D. melanogaster, D. simulans and their hybrid. Keywords: other

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Diverse effect of WWOX overexpression in SW480 colon cancer cell line.

Project description:The WWOX gene is a tumor suppressor probably involved in regulation of cell cycle and apoptosis and downregulated in variety of cancer types.However, its role in colon cancerogenesis is unknown. The aim of this study was to characterize how WWOX may be involved in colon cancerogenesis or cancer progression, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in HT29 colon cancer cell line increased expression of WWOX may result in transition of cancer cells into more normal- like colon epithelium phenotype, on the other hand in SW480 WWOX revealed the well-known tumour suppressor properties. However, as the colon cancer is very heterogeneous disease, obtained discrepancies may reflect the known differences between cell lines and cancerogenesis pathway, which they undergone.

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Diverse effect of WWOX overexpression in HT29 colon cancer cell line.

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Diverse effect of WWOX overexpression in HT29 colon cancer cell line.

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Diverse effect of WWOX overexpression in SW480 colon cancer cell line.

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WWOX P47T loss-of-function mutation induces epilepsy, progressive neuroinflammation, and cerebellar degeneration

Project description:WWOX gene loss-of-function (LoF) has been associated with neuropathologies resulting in developmental, epileptic, and ataxic phenotypes of varying severity based on the level of WWOX dysfunction. WWOX gene biallelic germline variant p.Pro47Thr (P47T) has been causally associated with a new form of autosomal recessive cerebellar ataxia with epilepsy and intellectual disability (SCAR12). This mutation affects the WW1 protein binding domain of WWOX, impairing its ability to interact with canonical proline-proline-X-tyrosine motifs in partner proteins. We generated a mutant knock-in mouse model of Wwox P47T that phenocopies SCAR12. WwoxP47T/P47T mice displayed epilepsy, profound social behavior and cognition deficits, and poor motor coordination. These deficits progressed with age, and mice became practically immobile, suggesting severe cerebellar dysfunction. WwoxP47T/P47T mice exhibited signs of progressive neuroinflammation with elevated astro-microgliosis that increased with age. The cerebellar cortex displayed significantly reduced molecular and granular layer thickness and a strikingly reduced number of Purkinje cells with degenerated dendrites. Transcriptome profiling from various brain regions from these Wwox LoF mice highlighted widespread changes in neuronal and glial pathways, enrichment of bioprocesses related to neuroinflammation and severe cerebellar dysfunction, activation of pathways compatible with compensatory neurogenesis along with major suppression of gene networks associated with neuronal cell differentiation and brain development. Our results show significant pathobiological effects and potential mechanisms through which Wwox LoF leads to cerebellar neurodegeneration, neuroinflammation, and ataxia.

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