<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Scheuring I</submitter><funding>Ministry of Science and Technology of China</funding><funding>Chinese Academy of Sciences</funding><funding>University of East Anglia</funding><funding>UK Natural Environment Research Council</funding><funding>Kunming Institute of Zoology</funding><funding>Medical Research Council</funding><funding>European Science Foundation/European Collaborative Research</funding><funding>National Natural Science Foundation of China</funding><funding>Natural Environment Research Council</funding><pagination>1300-1307</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3507015</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(11)</volume><pubmed_abstract>There is great interest in explaining how beneficial microbiomes are assembled. Antibiotic-producing microbiomes are arguably the most abundant class of beneficial microbiome in nature, having been found on corals, arthropods, molluscs, vertebrates and plant rhizospheres. An exemplar is the attine ants, which cultivate a fungus for food and host a cuticular microbiome that releases antibiotics to defend the fungus from parasites. One explanation posits long-term vertical transmission of Pseudonocardia bacteria, which (somehow) evolve new compounds in arms-race fashion against parasites. Alternatively, attines (somehow) selectively recruit multiple, non-coevolved actinobacterial genera from the soil, enabling a 'multi-drug' strategy against parasites. We reconcile the models by showing that when hosts fuel interference competition by providing abundant resources, the interference competition favours the recruitment of antibiotic-producing (and -resistant) bacteria. This partner-choice mechanism is more effective when at least one actinobacterial symbiont is vertically transmitted or has a high immigration rate, as in disease-suppressive soils.</pubmed_abstract><journal>Ecology letters</journal><pubmed_title>How to assemble a beneficial microbiome in three easy steps.</pubmed_title><pmcid>PMC3507015</pmcid><funding_grant_id>20080A001</funding_grant_id><funding_grant_id>0902281081</funding_grant_id><funding_grant_id>2012FY110800</funding_grant_id><funding_grant_id>NE/J01074X/1</funding_grant_id><funding_grant_id>K 100299</funding_grant_id><funding_grant_id>G0801721</funding_grant_id><funding_grant_id>31170498</funding_grant_id><pubmed_authors>Scheuring I</pubmed_authors><pubmed_authors>Yu DW</pubmed_authors></additional><is_claimable>false</is_claimable><name>How to assemble a beneficial microbiome in three easy steps.</name><description>There is great interest in explaining how beneficial microbiomes are assembled. Antibiotic-producing microbiomes are arguably the most abundant class of beneficial microbiome in nature, having been found on corals, arthropods, molluscs, vertebrates and plant rhizospheres. An exemplar is the attine ants, which cultivate a fungus for food and host a cuticular microbiome that releases antibiotics to defend the fungus from parasites. One explanation posits long-term vertical transmission of Pseudonocardia bacteria, which (somehow) evolve new compounds in arms-race fashion against parasites. Alternatively, attines (somehow) selectively recruit multiple, non-coevolved actinobacterial genera from the soil, enabling a 'multi-drug' strategy against parasites. We reconcile the models by showing that when hosts fuel interference competition by providing abundant resources, the interference competition favours the recruitment of antibiotic-producing (and -resistant) bacteria. This partner-choice mechanism is more effective when at least one actinobacterial symbiont is vertically transmitted or has a high immigration rate, as in disease-suppressive soils.</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Nov</publication><modification>2024-10-18T16:21:55.463Z</modification><creation>2019-03-27T01:01:00Z</creation></dates><accession>S-EPMC3507015</accession><cross_references><pubmed>22913725</pubmed><doi>10.1111/j.1461-0248.2012.01853.x</doi></cross_references></HashMap>