Dataset Information

Interactions with a Complex Microbiota Mediate a Trade-Off between the Host Development Rate and Heat Stress Resistance.

ABSTRACT: Animals and plants host diverse communities of microorganisms, and these microbiotas have been shown to influence host life history traits. Much has been said about the benefits that host-associated microbiotas bestow on the host. However, life history traits often demonstrate tradeoffs among one another. Raising Caenorhabditis elegans nematodes in compost microcosms emulating their natural environment, we examined how complex microbiotas affect host life history traits. We show that soil microbes usually increase the host development rate but decrease host resistance to heat stress, suggesting that interactions with complex microbiotas may mediate a tradeoff between host development and stress resistance. What element in these interactions is responsible for these effects is yet unknown, but experiments with live versus dead bacteria suggest that such effects may depend on bacterially provided signals.

SUBMITTER: Slowinski S

PROVIDER: S-EPMC7697855 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Interactions with a Complex Microbiota Mediate a Trade-Off between the Host Development Rate and Heat Stress Resistance.

Slowinski Samuel S Ramirez Isabella I Narayan Vivek V Somayaji Medha M Para Maya M Pi Sarah S Jadeja Niharika N Karimzadegan Siavash S Pees Barbara B Shapira Michael M

Microorganisms 20201113 11

Animals and plants host diverse communities of microorganisms, and these microbiotas have been shown to influence host life history traits. Much has been said about the benefits that host-associated microbiotas bestow on the host. However, life history traits often demonstrate tradeoffs among one another. Raising <i>Caenorhabditis elegans</i> nematodes in compost microcosms emulating their natural environment, we examined how complex microbiotas affect host life history traits. We show that soil ...[more]

PMID: 33202910

Similar Datasets

Project description:Lethal mutagenesis is a broad-spectrum antiviral strategy that employs mutagenic nucleoside analogs to exploit the high mutation rate and low mutational tolerance of many RNA viruses. Studies of mutagen-resistant viruses have identified determinants of replicative fidelity and the importance of mutation rate to viral population dynamics. We have previously demonstrated the effective lethal mutagenesis of influenza A virus using three nucleoside analogs as well as the virus's high genetic barrier to mutagen resistance. Here, we investigate the mutagen-resistant phenotypes of mutations that were enriched in drug-treated populations. We find that PB1 T123A has higher replicative fitness than the wild type, PR8, and maintains its level of genome production during 5-fluorouracil (2,4-dihydroxy-5-fluoropyrimidine) treatment. Surprisingly, this mutagen-resistant variant also has an increased baseline rate of C-to-U and G-to-A mutations. A second drug-selected mutation, PA T97I, interacts epistatically with PB1 T123A to mediate high-level mutagen resistance, predominantly by limiting the inhibitory effect of nucleosides on polymerase activity. Consistent with the importance of epistatic interactions in the influenza virus polymerase, our data suggest that nucleoside analog resistance and replication fidelity are strain dependent. Two previously identified ribavirin {1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-1H-1,2,4-triazole-3-carboxamide} resistance mutations, PB1 V43I and PB1 D27N, do not confer drug resistance in the PR8 background, and the PR8-PB1 V43I polymerase exhibits a normal baseline mutation rate. Our results highlight the genetic complexity of the influenza A virus polymerase and demonstrate that increased replicative capacity is a mechanism by which an RNA virus can counter the negative effects of elevated mutation rates. IMPORTANCE RNA viruses exist as genetically diverse populations. This standing genetic diversity gives them the potential to adapt rapidly, evolve resistance to antiviral therapeutics, and evade immune responses. Viral mutants with altered mutation rates or mutational tolerance have provided insights into how genetic diversity arises and how it affects the behavior of RNA viruses. To this end, we identified variants within the polymerase complex of influenza virus that are able to tolerate drug-mediated increases in viral mutation rates. We find that drug resistance is highly dependent on interactions among mutations in the polymerase complex. In contrast to other viruses, influenza virus counters the effect of higher mutation rates primarily by maintaining high levels of genome replication. These findings suggest the importance of maintaining large population sizes for viruses with high mutation rates and show that multiple proteins can affect both mutation rate and genome synthesis.

Dataset Information

Interactions with a Complex Microbiota Mediate a Trade-Off between the Host Development Rate and Heat Stress Resistance.

Publications

Interactions with a Complex Microbiota Mediate a Trade-Off between the Host Development Rate and Heat Stress Resistance.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets