DNMT3.1 controls life span and trade-off between growth and fecundity under the starved condition in the cladoceran crustacean Daphnia magna
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ABSTRACT:
PROVIDER: PRJNA664094 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12660004_1.fastq.gz | Fastqsanger.gz | |||
| SRR12660004_2.fastq.gz | Fastqsanger.gz | |||
| SRR12660005_1.fastq.gz | Fastqsanger.gz | |||
| SRR12660005_2.fastq.gz | Fastqsanger.gz | |||
| SRR12660006_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: We aim to clarify the physiological function of DNMT3.1 in extending longevity and energy allocation to reproduction under starved condition. In this study, we introduced a mutation into DNMT3.1 and analyzed the transcriptional changes, corresponded to phenotypic changes, of the mutant compared to wild type under starved condition. Methods: Whole body mRNA profiles of 12 days old daphnids from wild type (WT) and mutant (MT) cultured in nutrient rich (HF) and starved (LF) conditions were proceeded by using Illumina sequencing (provided by Novogene). Data analysis was performed by using CLC Genomics Workbench 12 (Qiagen) software. Results: In nutrient rich and starved conditions, numbers of differentially expressed genes were 220 and 2770 respectively, between wild type and mutant. Conclusions: Consistent with the DNMT3.1 mutant phenotypes, the starved condition led to larger difference of transcriptome between the mutant and wild type. This findind reveal how energy allocation is implemented by selective expression of a DNMT3 ortholog.
2020-09-18 | GSE158129 | GEO
Project description:crustacean metagenome Raw sequence reads
| PRJNA330760 | ENA
Project description:crustacean metagenome Raw sequence reads
| PRJNA533204 | ENA
Project description:crustacean metagenome Raw sequence reads
| PRJNA322089 | ENA
Project description:The cladoceran crustacean Daphnia has long been a model of energy allocation studies due to its important position in the trophic cascade of freshwater ecosystems. However, the loci for controlling energy allocation between life history traits still remain unknown. Here, we report CRISPR/Cas-mediated target mutagenesis of DNA methyltransferase 3.1 (DNMT3.1) that is upregulated in response to caloric restriction in Daphnia magna. The resulting biallelic mutant is viable and did not show any change in growth rate, reproduction, and longevity under nutrient rich conditions. In contrast, under starved conditions, the growth rate of this DNMT3.1 mutant was increased but its reproduction was reciprocally reduced compared to the wild type when the growth and reproduction activities competed during a period from instar 4 to 8. The life span of this mutant was significantly shorter than that of the wild type. We also compared transcriptomes between DNMT3.1 mutant and wild type under nutrient-rich and starved conditions. Consistent with the DNMT3.1 mutant phenotypes, the starved condition led to changes in the transcriptomes of the mutant including differential expression of vitellogenin genes. In addition, we found upregulation of the I am not dead yet (INDY) ortholog, which has been known to shorten the life span in Drosophila, explaining the shorter life span of the DNMT3.1 mutant. These results establish DNMT3.1 as a key regulator for life span and energy allocation between growth and reproduction during caloric restriction. Our findings reveal how energy allocation is implemented by selective expression of a DNMT3 ortholog that is widely distributed among animals. We also infer a previously unidentified adaptation of Daphnia that invests more energy for reproduction than growth under starved conditions.
| S-EPMC8016896 | biostudies-literature
Project description:ABSTRACT MAGWIRE, MICHAEL MAHLON. 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 Dunnett’s 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 Dunnett’s, 70 lines increased in life span, while 270 decreased in life span. An additional 48 increased longevity lines were close enough to meeting Dunnett’s 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. Keywords: Genetic (P-element insertion) modification and comparison to control line
2008-08-01 | GSE8775 | GEO