Ontology highlight
ABSTRACT:
PROVIDER: PRJNA588020 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR10403900_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR10403601_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR10403901_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR10403602_subreads.fastq.gz | Fastqsanger.gz |
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Project description:The abundance of transposable elements and DNA repeat sequences in mammalian genomes raises the question whether such insertions represent passive evolutionary baggage or may influence the expression of complex traits. We addressed this question in Drosophila melanogaster where the effects of single transposable elements on complex traits can be assessed in genetically identical individuals reared in controlled environments. Here we demonstrate that single P-element insertions in the intergenic region between the Gustatory receptor 5a (Gr5a) and Trapped in endoderm 1 (Tre1), which encodes an orphan receptor, exert complex pleiotropic effects on fitness traits, including selective nutrient intake, resistance to starvation and heat stress, and life span. Mutations in this region interact epistatically with downstream components of the insulin signaling pathway. Transposon-induced sex-specific and sex-antagonistic effects further accentuate the complex influences intergenic transposable elements can contribute to complex phenotypes. Keywords: Transcriptional profiles of P-element insertion lines in the Tre1/GR5a region of Drosophila
2006-05-31 | GSE4789 | GEO
Project description:A transposable element insertion in APOB causes cholesterol deficiency in Holstein cattle
| PRJEB11963 | ENA
Project description:A transposable element insertion in APOB causes cholesterol deficiency in Holstein cattle
| PRJEB11965 | ENA
Project description:Mutations Increasing Drosophila melanogaster; Life Span. (Under the direction of Trudy F. C. Mackay.); Better living conditions and advances in medicine have made it possible for; humans to live considerably longer than before. This has uncovered many; health problems associated with age. By identifying genes involved in the; limitation of life span, we may better understand the processes that lead to aging. In model organisms, we can use mutagenesis to discover mutations that; increase life span, and hence infer that the wild-type allele limits life span by some means. We have assessed longevity in a collection of 1332 co-isogenic gene-trap; P-element insertion lines and determined changes in life span of each insert line relative to the corresponding control line. Significant lines were determined via two different methods of analysis: A 95% confidence interval was established based on deviations of the mutant life spans from the controls and Dunnettâs two tailed t-tests were used to examine differences between mutant and control in each individual block. Based on the 95% confidence interval, 139 inserts displayed an increase in life span and 194 inserts a decrease. Using Dunnettâs, 70 lines increased in life span, while 270 decreased in life span. An additional 48 increased longevity lines were close enough to meeting Dunnettâs criteria to be considered for additional investigation. Combining these two analyses, we chose 83 inserts associated with increased life span for a secondary screen using an; additional twelve replicates. 58 of these lines remained significant. We have; determined the P-element insertion site for 50 of these lines. Starvation resistance, chill coma recovery time and climbing activity were; measured on the lines remaining significant after the the secondary screen to identify pleiotropic effects. A positive correlation was found for males between life span and starvation resistance as well as between life span and chill coma recovery. Females only displayed a correlation between life span and chill coma recovery, which was negative. None of the lines indicated increased fitness for all phenotypes, indicating there may be some type of trade-off. There also appears to be a lot of pleiotropic variation depending on background and sex. Ten of the lines, all with the same parental background, were chosen for a; half-diallel cross to identify epistasis between the mutants. There were; substantial epistatic interactions between all ten lines. Furthermore, males and females displayed vastly different patterns of epistasis, again indicating major differences in life span regulation between the sexes. Finally, a subset of seven of the lines used in the epistatic study, in; addition to the corresponding parental control, were chosen for microarray; analysis to look for possible pathways and novel genes involved in increasing life span. 1,996 probe sets were significant at a false discovery rate q-value; threshold of q < 0.0001. Tukeys tests were carried out for these probe sets to determine how each of the seven mutant backgrounds differed compared to the control and each other. In addition, each mutant background was compared individually with the control to identify any changes in expression. Gene ontologies were determined for each of the lines to identify over-represented biological functions which would indicate possible longevity pathways. Dozens of pathways were suggested, including several novel pathways. Experiment Overall Design: We used seven mutant lines homozygous for a P-element insertion and a control line. All lines were isogenic other than the P-element insert. Males and females were done separately with two replicates for a total of 32 arrays.
2008-10-18 | E-GEOD-8775 | biostudies-arrayexpress