Browse
Submit Data
Databases
API
Help

Dataset Information

9 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fitness costs linked to dinitroaniline resistance mutation in Setaria.

ABSTRACT: A mutant Thr-239-Ileu at the α2-tubulin gene was found to confer resistance to dinitroanilines, a family of mitosis-disrupting herbicides. However, mutations affecting microtubule polymerization and cell division are expected to impact growth and reproduction, that is, the fitness of a resistant weed or the yield of a tolerant crop, although it has not been demonstrated yet. This study was designed to test this hypothesis for the growth and reproduction of near-isogenic resistant and susceptible materials that were created in F(2) and F(3) generations after a Setaria viridis x S. italica cross. Differential growth was noticeable at the very onset of seedling growth. The homozygous resistant plants, grown both in a greenhouse cabinet and in the field, were smaller and had lower 1000-grain weight and therefore a lower yield. This fitness penalty is certainly due to modified cell division kinetics. Although the presence of the mutant allele accounted for 20% yield losses, there were also measurable benefits of dinitroaniline resistance, and these benefits are discussed.

SUBMITTER: Darmency H

PROVIDER: S-EPMC3186120 | biostudies-other | 2011 Jul

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Insecticide resistance fitness costs in D. simulans

Project description:Fitness effects for Ace insecticide resistance mutations are determined by ambient temperature

| PRJEB39894 | ENA

The fitness costs of antibiotic resistance mutations.

Project description: Not available

| S-EPMC4380921 | biostudies-literature

Resource misallocation as a mediator of fitness costs in antibiotic resistance

Project description:Antimicrobial resistance (AMR) poses a threat to global health and the economy. Rifampicin resistant Mycobacterium tuberculosis accounts for a third of the global AMR burden. Gaining the upper hand on AMR requires a deeper understanding of the physiology of resistance. AMR often results in the erosion of normal cell function: a fitness cost. Identifying intervention points in the mechanisms underpinning the cost of resistance in M. tuberculosis could play a pivotal role in strengthening future treatment regimens. We used a collection of M. tuberculosis strains providing an evolutionary and phylogenetic snapshot of rifampicin resistance and subjected them to genome-wide transcriptomic and proteomic profiling to identify key perturbations of normal physiology. We found that a rifampicin resistance-conferring mutation in RpoB imparts considerable gene expression changes, many of which are mitigated by a compensatory mutation in RpoC. However, our data also provide evidence for pervasive epistasis: the same resistance mutation imposed a different fitness cost and functionally unrelated changes to gene expression in clinical strains from unrelated genetic backgrounds. Rather than functional changes in specific pathways, our data suggest that the fitness cost of rifampicin resistance stems from a misallocation of resources: the greater the departure from the wild type baseline proteome investment, the greater the fitness cost of rifampicin resistance in a given strain. We summarize these observations in the “Burden of Expression” hypothesis of fitness cost and provide evidence that it can be used for suppressing the emergence of rifampicin resistance.

2021-03-12 | PXD011568 | Pride

Compensation of fitness costs and reversibility of antibiotic resistance mutations.

Project description: Not available

| S-EPMC2863634 | biostudies-literature

Compensating the fitness costs of synonymous mutations

Project description:Synonymous mutations do not change the sequence of the polypeptide but they may still influence fitness. We investigated in Salmonella enterica how four synonymous mutations in the rpsT gene (encoding ribosomal protein S20) reduce fitness (i.e. growth rate) and the mechanisms by which this cost can be genetically compensated. The reduced growth rates of the synonymous mutants were correlated with reduced levels of the rpsT transcript and S20 protein. In an adaptive evolution experiment these fitness impairments could be compensated by mutations that either caused up-regulation of S20 through increased gene dosage (due to duplications), increased transcription of the rpsT gene (due to an rpoD mutation or mutations in rpsT), or increased translation from the rpsT transcript (due to rpsT mutations). We suggest that the reduced levels of S20 in the synonymous mutants result in production of a defective subpopulation of 30S subunits lacking S20 that reduce protein synthesis and bacterial growth and that the compensatory mutations restore S20 levels and the number of functional ribosomes. Our results demonstrate how specific synonymous mutations can cause substantial fitness reductions and that many different types intra- and extragenic compensatory mutations can efficiently restore fitness. Furthermore, our study highlights that also synonymous sites can be under strong selection, which may have implications for the use of dN/dS ratios as signature for selection.

2016-03-11 | PXD003495 | Pride

uORF-mediated translation allows engineered plant disease resistance without fitness costs.

Project description: Not available

| S-EPMC5532539 | biostudies-literature

Expression Dysregulation as a Mediator of Fitness Costs in Antibiotic Resistance.

Project description: Not available

| S-EPMC8370218 | biostudies-literature

In vitro and in vivo fitness costs associated with Mycobacterium tuberculosis RpoB mutation H526D.

Project description: Not available

| S-EPMC5506874 | biostudies-other

Phenotypic and transcriptional profiling in Entamoeba histolytica reveal costs to fitness and adaptive responses associated with metronidazole resistance

Project description:In vitro studies have described metronidazole (MTZ) resistance and the potential mechanisms involved. Costs to fitness and adaptive responses associated with resistance, however, have not been investigated. In this study we generated an HM-1-derived strain resistant to 12 µM MTZ (MTZR). We examined its phenotypic and transcriptional profile to determine the consequences and mRNA level changes associated with MTZ resistance. The expression profile of 9,230 genes in wild-type and metronidazole-resistant strains was compared. Transcriptome analysis revealed 142 differentially expressed genes in MTZR. In contrast to other MTZ-resistant parasites, MTZR did not down-regulate pyruvate:ferredoxin oxidoreductase, but showed increased expression of genes for a hypothetical protein (HP1) and several iron-sulfur flavoproteins, and the downregulation of genes for leucin-rich proteins. Overexpression of HP1-HA did not confer MTZR level of resistance, but provided a slight advantage in cell survival. Fisher's exact test showed 24 significantly enriched GO terms in MTZR, and a 3-way comparison of modulated genes with MTZR cultured without MTZ and HM-1 cultured with MTZ showed that 88 genes were specific to MTZR. Wild-type and the MTZ-resistant strain MTZR were cultured either in the presence or absence of MTZ. 2 biological replicates per strain/condition.

2012-02-22 | E-GEOD-35990 | biostudies-arrayexpress

An X-linked meiotic drive allele has strong, recessive fitness costs in female Drosophila pseudoobscura.

Project description: Not available

| S-EPMC6939274 | biostudies-literature