Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA97559 | ENA |
REPOSITORIES: ENA
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Project description:The kep1 gene encodes an RNA-binding protein containing a single maxi-KH domain. We have previously demonstrated that loss of the kep1 gene results in Drosophila females displaying a reduction in fertility and wished to further characterize the kep1 mutation in Drosophila males. Wild-type females mated to homozygous kep1- males resulted in 6% of the eggs laid hatching. This reduced reproductive success is due in part to a meiosis defect during spermatogenesis with approximately 10 % of sperm demonstrating a defect in cytokinesis. Utilizing indirect immunohistochemistry we found that the Kep1 protein is present in the nucleus of adult brain neuronal cells, suggesting a behavioural component contributing to the almost complete male sterility phenotype. We report that homozygote kep1- males display almost no courtship behaviour with a measured median courtship index of 0.005 relative to a median index of 0.77 for OreR wild-type controls. In order to better understand the behavioural role of kep1, we carried out gene profiling experiments to identify transcripts whose steady-state levels are altered in the kep1- homozygote males. Our gene profiling studies identified 61 transcripts whose steady-state levels are altered by at least 2 fold or more comparing RNA isolated from w1118 and kep1-/kep1- male heads. A large percentage of transcripts identified whose steady-state expression levels are depleted in kep1-/kep1- heads (10 out of 44) encode for proteins involved in some aspect of proteolysis. Our results show that the Kep1 protein has a pleiotropic effect in Drosophila males leading to cytokinesis defects and behavioural abnormalities. RNA was isolated from heads of 3-4 day old wild-type or homozygote mutant males. Three indepentent RNA samples were utilized to complete experiment.
2010-06-10 | E-GEOD-6086 | biostudies-arrayexpress
Project description:The kep1 gene encodes an RNA-binding protein containing a single maxi-KH domain. We have previously demonstrated that loss of the kep1 gene results in Drosophila females displaying a reduction in fertility and wished to further characterize the kep1 mutation in Drosophila males. Wild-type females mated to homozygous kep1- males resulted in 6% of the eggs laid hatching. This reduced reproductive success is due in part to a meiosis defect during spermatogenesis with approximately 10 % of sperm demonstrating a defect in cytokinesis. Utilizing indirect immunohistochemistry we found that the Kep1 protein is present in the nucleus of adult brain neuronal cells, suggesting a behavioural component contributing to the almost complete male sterility phenotype. We report that homozygote kep1- males display almost no courtship behaviour with a measured median courtship index of 0.005 relative to a median index of 0.77 for OreR wild-type controls. In order to better understand the behavioural role of kep1, we carried out gene profiling experiments to identify transcripts whose steady-state levels are altered in the kep1- homozygote males. Our gene profiling studies identified 61 transcripts whose steady-state levels are altered by at least 2 fold or more comparing RNA isolated from w1118 and kep1-/kep1- male heads. A large percentage of transcripts identified whose steady-state expression levels are depleted in kep1-/kep1- heads (10 out of 44) encode for proteins involved in some aspect of proteolysis. Our results show that the Kep1 protein has a pleiotropic effect in Drosophila males leading to cytokinesis defects and behavioural abnormalities. Keywords: Mutant vs wild-type compairson
2006-10-21 | GSE6086 | GEO
Project description:Gestational and perinatal disruption of neural development increases the risk of developing schizophrenia (SCZ) later in life. Embryonic day 17 (E17) methylazoxymethanol (MAM) treatment leads to histological, physiological and behavioural abnormalities in post-puberty rats resembling those described in SCZ patients. However, the validity of E17 MAM-exposed mice as a SCZ model has not been explored. Here we treated E17 C57BL/6 mouse dams with various dosages of MAM. We found that this mouse strain was more vulnerable to MAM treatment than rats and there were gender difference in behavioural abnormalities, histological changes and prefrontal cortical gene expression profiles in MAM (7.5 mg/kg)-exposed mice. Both male and female MAM-exposed mice had deficits in prepulse inhibition but were normal in social interaction and novel object recognition tasks. Female MAM-exposed mice were hyperactive in spontaneous locomotion while male mice were normal. Consistently, only female MAM-exposed mice exhibited reduced brain weight, decreased size of prefrontal cortex (PFC) and enlarged lateral ventricles. Transcriptome analysis of the PFC revealed that there were more differentially expressed genes in female MAM-exposed mice than those in male mice. Moreover, expression of Pvalb, Arc and genes in their association networks were downregulated in the PFC of female MAM-exposed mice. These results show that E17 MAM-exposure in C57BL/6 mice leads to behavioural changes that mimic positive symptoms and sensorimotor gating deficits associated with SCZ. MAM-exposed female mice may be used to study gene expression changes, inhibitory neural circuit dysfunction and glutamatergic synaptic plasticity deficits related to SCZ.
2019-01-09 | GSE108925 | GEO
Project description:Seminal fluid plays an essential role in promoting male reproductive success and modulating female physiology and behaviour. In the fruit fly, Drosophila melanogaster, Sex Peptide (SP) is the best-characterised protein mediator of these effects. It is secreted from the paired male accessory glands (AGs), which, like the mammalian prostate and seminal vesicles, generate most of the seminal fluid contents. After mating, SP binds to spermatozoa and is retained in the female sperm storage organs. It is gradually released by proteolytic cleavage and induces several long-term post-mating responses including increased ovulation, elevated feeding and reduced receptivity to remating, primarily signalling through the SP receptor (SPR). We demonstrate a previously unsuspected SPR-independent function for SP. We show that, in the AG lumen, SP and secreted proteins with membrane-binding anchors are carried on abundant, large neutral lipid-containing microcarriers, also found in other SP-expressing Drosophila species. These microcarriers are transferred to females during mating, where they rapidly disassemble. Remarkably, SP is a key microcarrier assembly and disassembly factor. Its absence leads to major changes in the seminal proteome transferred to females upon mating. Males expressing non-functional SP mutant proteins that affect SP binding to and release from sperm in females also do not produce normal microcarriers, suggesting that this male-specific defect contributes to the resulting widespread abnormalities in ejaculate function. Our data reveal a novel role for SP in formation of seminal macromolecular assemblies, which may explain the presence of SP in Drosophila species that lack the signalling functions seen in D. melanogaster. In this experiment we assessed the effect of SP loss-of-function on the transferred seminal proteome.
2021-01-26 | PXD021897 | Pride
Project description:We performed neuron and glia specific knockdown of PIG-A in Drosophila to understand the molecular defects that occur with loss of GPI anchored proteins. PIG-A encodes an enzyme responsible for the first step in GPI anchor biosynthesis. Loss of PIG-A in neurons and glia results in different neurological defects.
2023-10-31 | GSE241512 | GEO
Project description:ITRAQ Phosphoproteomics revealed proteins associated with spermatogenesis in Wolbachia-Infected Male Drosophila Melanogaster
2024-09-29 | PXD026049 | Pride
Project description:Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development
| PRJNA356839 | ENA
Project description:UPF1 is a well-conserved RNA helicase in eukaryotes, involved in nuclear and cytoplasmic processes of gene expression. This study presents ChIP-seq evidence for its RNA-dependent association with mtDNA transcription sites in Drosophila S2 cells, and RNA-seq data indicating its requirement for the correct expression of mtDNA genes. UPF1 localisation in mitochondria was observed by immunostaining and GFP-tagging in different fly tissues and cell types. During spermatogenesis, depletion of UPF1 but not of other NMD factors, resulted in major defects in meiosis and cytokinesis, leading to complete sterility. Notably, the few spermatids produced show abnormalities in the formation of the nebenkern and, unlike the wild type, retain the mtDNA.
2024-05-10 | GSE266138 | GEO
Project description:Cytokinesis is a key step in the later stage of cell division to partition cellular contents into daughter cells, which undergoes precise regulation in temporal and spatial. However, the underlying mechanisms are still unclear. Here, we show that Hsp90 cochaperone, NudCL2 (NudC-like protein 2), is required for cytokinesis in mammalian cells. NudCL2 localizes to midbody during cytokinesis. Knockout (KO) of NudCL2 using CRISPR/Cas9-based genome editing causes cytokinesis failure and leads to the accumulation of multinucleated cells. To investigate the potential regulator involved in NudCL2-mediated cytokinesis regulation, we performed isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomic analysis in WT and NudCL2 KO cells and found hundreds of differentially expressed proteins (KO/WT fold change > 1.2 or < 0.83, p < 0.05) in NudCL2 KO cells. We found that the protein level of RCC2 (a midbody-associated protein) is obviously decrease in NudCL2 KO cells. Further studies display that knockout of NudCL2 induces an increase in RCC2 protein instability and degradation. Our data show that depletion of RCC2 leads to the similar defects as NudCL2 KO. Ectopic expression of RCC2 effectively rescues the cytokinesis failure caused by the loss of NudCL2. Interestingly, our data reveals that Hsp90 localizes to midbody in cytokinesis, and interacts with NudCL2 and RCC2. Inhibition of Hsp90 ATPase activity also causes the RCC2 instability and cytokinesis failure as NudCL2 KO. Moreover, the abnormal phenotypes induced by NudCL2 KO are able to rescue by the ectopic expression of Hsp90, but not vice versa. Taken together, our data suggest that NudCL2 is required to cytokinesis by stabilizing RCC2 at midbody through the Hsp90 pathway, providing a hitherto unrecognized mechanism crucial for cytokinesis regulation.
2024-03-21 | PXD043570 | Pride
Project description:SAGA is a highly conserved transcriptional co-activator complex involved in multiple steps of transcription with activities that function both pre and post initiation. Loss of individual subunits results in developmental defects, suggesting a role in development. In particular, SAGA contains a ubiquitin protease activity involved in the transition from transcription initiation to elongation. Loss of the Sgf11 SAGA subunit causes loss of deubiquitination activity, and leads to defects in axon targeting and embryonic lethality. To better understand the roles of SAGA functions in developmental gene expression we examined its composition, binding profile, and the effects of subunit loss on gene expression in two distinct cell types in late stage Drosophila embryos: muscle and neurons.
2011-08-22 | GSE29525 | GEO