Ontology highlight
ABSTRACT:
PROVIDER: PRJNA293974 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3099554_1.fastq.gz | Fastqsanger.gz | |||
| SRR3099554_2.fastq.gz | Fastqsanger.gz | |||
| SRR3130625_1.fastq.gz | Fastqsanger.gz | |||
| SRR3130625_2.fastq.gz | Fastqsanger.gz | |||
| SRR3130998_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 22 |
Similar Datasets
Project description:Maleae genomics: selection following recent whole genome duplication
| PRJNA293976 | ENA
Project description:This a model from the article:
Increased glycolytic flux as an outcome of whole-genome duplication in yeast.
Conant GC, Wolfe KH Mol. Syst. Biol.
[2007 ; Volume: 3 (Issue: )]: 129 17667951
,
Abstract:
After whole-genome duplication (WGD), deletions return most loci to single copy. However, duplicate loci may survive through selection for increased dosage. Here, we show how the WGD increased copy number of some glycolytic genes could have conferred an almost immediate selective advantage to an ancestor of Saccharomyces cerevisiae, providing a rationale for the success of the WGD. We propose that the loss of other redundant genes throughout the genome resulted in incremental dosage increases for the surviving duplicated glycolytic genes. This increase gave post-WGD yeasts a growth advantage through rapid glucose fermentation; one of this lineage's many adaptations to glucose-rich environments. Our hypothesis is supported by data from enzyme kinetics and comparative genomics. Because changes in gene dosage follow directly from post-WGD deletions, dosage selection can confer an almost instantaneous benefit after WGD, unlike neofunctionalization or subfunctionalization, which require specific mutations. We also show theoretically that increased fermentative capacity is of greatest advantage when glucose resources are both large and dense, an observation potentially related to the appearance of angiosperms around the time of WGD.
This model reproduces fig. 2C from the corrigendum
to the publication
The parameter Vmax_PDH
was corrected by a factor 60 from 6.32 mM/min in the publication to 379.2 mM/min in accordance with the authors.
see the corrigendum
at msb or its pubmed entry (pmid:18594520)
This model comprises the glycolysis model from Pritchard and Kell (2002) with an extension for the metabolisation of pyruvate in the mitochondria by pyruvate dehydrogenase and an additional parameter, WGD_E
, to adjust for the differing enzyme concentrations before the whole genome duplication (WGD).
To switch off transport of pyruvate to the mitochondria, set the parameter t_m
= 0.
Figure 2C from the article can be reproduced by manually changing the value of parameter WGD_E
in the range between 0.65 and 1.0 and calculating the ratios of ratio of PDC/PDH
fluxes in the altered model to the one of the model with WGD_E
= 1. This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2012 The BioModels.net Team.
For more information see the terms of use
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000177 | BioModels
Project description:This a model from the article:
Increased glycolytic flux as an outcome of whole-genome duplication in yeast.
Conant GC, Wolfe KH Mol. Syst. Biol.
[2007 ; Volume: 3 (Issue: )]: 129 17667951
,
Abstract:
After whole-genome duplication (WGD), deletions return most loci to single copy. However, duplicate loci may survive through selection for increased dosage. Here, we show how the WGD increased copy number of some glycolytic genes could have conferred an almost immediate selective advantage to an ancestor of Saccharomyces cerevisiae, providing a rationale for the success of the WGD. We propose that the loss of other redundant genes throughout the genome resulted in incremental dosage increases for the surviving duplicated glycolytic genes. This increase gave post-WGD yeasts a growth advantage through rapid glucose fermentation; one of this lineage's many adaptations to glucose-rich environments. Our hypothesis is supported by data from enzyme kinetics and comparative genomics. Because changes in gene dosage follow directly from post-WGD deletions, dosage selection can confer an almost instantaneous benefit after WGD, unlike neofunctionalization or subfunctionalization, which require specific mutations. We also show theoretically that increased fermentative capacity is of greatest advantage when glucose resources are both large and dense, an observation potentially related to the appearance of angiosperms around the time of WGD.
The original model submitted by the authors was slightly altered and now comprises the models originally submitted as MODEL2426780967, MODEL2427021978, MODEL2427095802. It reproduces figures 2A,3A and 3B from the publication.
This model uses the glycolysis model from Pritchard and Kell (2002) with an additional parameter, WGD_E
, to adjust for the differing enzyme conzentrations before the whole genome duplication (WGD) and parameters fV_xxx
that adjust the Vmax
of the different reactions (xxx eg. HXT or PYK).
Figure 3A from the article can be reproduced by changing the value of the parameters fV_xxx
to 0.9 indiviually, with xxx signifying the different enzymes (HXT, HXK ...)
Figure 3B from the publication can be reproduced by setting the parameter WGD_E
to 0.75 and individually setting the parameters fV_xxx
to 1.333.
To reproduce figure 2A from the article change the parameter WGD_E
in the range between 0.65 and 1.0.
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2012 The BioModels.net Team.
For more information see the terms of use
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000176 | BioModels
Project description:Venoms and the toxins they contain represent molecular adaptations that have evolved on numerous occasions throughout the animal kingdom. However, the processes that shape venom protein evolution are poorly understood because of the scarcity of whole genome data available for comparative analyses of venomous species. Here, we perform a broad comparative toxicogenomic analysis to gain insight into the genomic mechanisms of venom evolution in robber flies (Asilidae). We first sequenced a high-quality draft genome of the hymenopteran hunting robber fly Dasypogon diadema, and analysed its venom by a combined proteotranscriptomic approach, and compared our results to recently described robber fly venoms to assess the general composition and major components of asilid venom. We then applied a comparative genomics approach, based on one additional asilid genome, ten high-quality dipteran genomes, and two lepidopteran outgroup-genomes, to reveal the evolutionary mechanisms and origins of identified venom proteins in robber flies. While some venom proteins were identified in the non-asilid genomes, several of the identified highly expressed venom proteins appear to be unique to robber flies. Our results reveal that the venom of D. diadema likely evolves in a multimodal fashion comprising 1) neofunctionalization after gene duplication, 2) expression-dependent co-option of proteins and 3) asilid lineage-specific orphan genes with enigmatic origin. The role of such orphan genes is currently being disputed in evolutionary genomics, but has not yet discussed in the context of toxin evolution. Our results display an unexpected dynamic venom evolution in asilid insects, which contrasts the findings of the only other insect toxicogenomic evolutionary analysis, in parasitoid wasps (Hymenoptera), were toxin evolution is dominated by single gene co-option.
2019-06-13 | PXD013358 | Pride
Project description:Transcriptomic changes following recent natural hybridization and allopolyploidy in the salt marsh species Spartina x townsendii and Spartina anglica (Poaceae) Allopolyploidy results from two events: the merger of divergent genomes and genome duplication. Both events have important functional consequences for the evolution and adaption of newly formed allopolyploid species. In spite of significant progress made the last years, a few studies have decoupled the effects of hybridization from genome duplication in the observed patterns of expression changes accompanying allopolyploidy in natural conditions. We used Agilent Rice oligo-microarrays to explore gene expression changes following allopolyploidy in Spartina that includes a classical example of recent allopolyploid speciation, S. anglica formed during the 19th century following genome duplication of the hybrid S. x townsendii. Our data indicate important, thought different effects of hybridization and genome duplication in the expression patterns of the hybrid and allopolyploid. Deviation from parental additivity was most important following hybridization and was accompanied by maternal expression dominance, although transgressively expressed genes were also encountered. Maternal dominance is attenuated following genome duplication in S. anglica while this species exhibits an increased number of transgressively over expressed genes. These results reflect the decoupled effects of the “genomic shock” following hybridization and genome redundancy, on the genetic, epigenetic and regulatory mechanisms characterizing transcriptomic evolution in allopolyploids.
2010-11-10 | GSE18961 | GEO
Project description:ADARp150 prohibits whole genome duplication
| PRJNA1090949 | ENA
Project description:The genome of the western honey bee (Apis mellifera) harbours ten different major royal jelly protein genes (mrjp1-10) which originate from a single-copy precursor via gene duplication. The evolutionary fate of duplicated genes is eventually determined over time as to result in loss due to pseudogenization, or in preservation due to neo- or sub-functionalization. Both fates were already observed in the mrjp gene cluster, as only mrjp1 - 9 are expressed, whereas mrjp10 was pseudogenized and represents an incomplete gene copy. In contrast, MRJP1 underwent neofunctionalization and developed an essential function within the food jelly of queen larvae, to guaranty the survival of the whole colony. We here show combining quantitative real time PCR with quantitative mass spectrometry that expression of most mrjps (mrjp1-5 and 7) shows an age dependent pattern in worker hypopharyngeal glands as well as in brains. Expression increases after hatching until the nurse bee period and is followed by a decrease in older workers that forage for different plant products. Mrjp6 expression deviates considerably from the expression profiles of the other mrjps and transcript abundance does not correlate with protein amount. Thus, either mrjp6 does fulfil a total different function or it might be on its way to pseudogenization. Furthermore, a tissue-specific function of the proteins MRJP8 and 9 in the hypopharyngeal glands and the brain can be excluded, suggesting a more general physiological than a nutritive function for both gene products.
2019-07-18 | PXD012618 | Pride
Project description:An overall goal of functional genomics has been to measure the impact of variants on molecular endophenotypes (e.g. gene expression levels or the degree of TF binding) and relate this to organismal traits and disease phenotypes. However, all the experiments to date have been described relative to a generic reference genome, significantly hobbling their interpretation. Here, we describe a strategy for finding significant relationships between disease variation and genomic annotation via personal functional genomics, by performing personal genome sequencing and paired functional genomics experiments, on the same individual.
2024-05-22 | PXD022787 | Pride