<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14(1)</volume><submitter>Gu X</submitter><pubmed_abstract>Recurrent heat stress and pathogen invasion seriously threaten crop production, and abiotic stress often antagonizes biotic stress response against pathogens. However, the molecular mechanisms of trade-offs between thermotolerance and defense remain obscure. Here, we identify a rice thermo-sensitive mutant that displays a defect in floret development under high temperature with a mutation in SUPPRESSOR OF GENE SILENCING 3a (OsSGS3a). OsSGS3a interacts with its homolog OsSGS3b and modulates the biogenesis of trans-acting small interfering RNA (tasiRNA) targeting AUXIN RESPONSE FACTORS (ARFs). We find that OsSGS3a/b positively, while OsARF3a/b and OsARF3la/lb negatively modulate thermotolerance. Moreover, OsSGS3a negatively, while OsARF3a/b and OsARF3la/lb positively regulate disease resistance to the bacterial pathogen Xanthomonas oryzae pv. oryzae (Xoo) and the fungal pathogen Magnaporthe oryzae (M. oryzae). Taken together, our study uncovers a previously unknown trade-off mechanism that regulates distinct immunity and thermotolerance through the OsSGS3-tasiRNA-OsARF3 module, highlighting the regulation of abiotic-biotic stress response trade-off in plants.</pubmed_abstract><journal>Nature communications</journal><pagination>4441</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10366173</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The OsSGS3-tasiRNA-OsARF3 module orchestrates abiotic-biotic stress response trade-off in rice.</pubmed_title><pmcid>PMC10366173</pmcid><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Gu X</pubmed_authors><pubmed_authors>Feng Z</pubmed_authors><pubmed_authors>Wu XN</pubmed_authors><pubmed_authors>Yang C</pubmed_authors><pubmed_authors>Li L</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors><pubmed_authors>Liang D</pubmed_authors><pubmed_authors>Tang J</pubmed_authors><pubmed_authors>Feng L</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Cao X</pubmed_authors><pubmed_authors>Li T</pubmed_authors><pubmed_authors>He Z</pubmed_authors><pubmed_authors>Yang P</pubmed_authors><pubmed_authors>Wan J</pubmed_authors><pubmed_authors>Liu JY</pubmed_authors><pubmed_authors>Si F</pubmed_authors><pubmed_authors>Yan B</pubmed_authors><pubmed_authors>Song X</pubmed_authors><pubmed_authors>Zhou J</pubmed_authors><pubmed_authors>Deng Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>The OsSGS3-tasiRNA-OsARF3 module orchestrates abiotic-biotic stress response trade-off in rice.</name><description>Recurrent heat stress and pathogen invasion seriously threaten crop production, and abiotic stress often antagonizes biotic stress response against pathogens. However, the molecular mechanisms of trade-offs between thermotolerance and defense remain obscure. Here, we identify a rice thermo-sensitive mutant that displays a defect in floret development under high temperature with a mutation in SUPPRESSOR OF GENE SILENCING 3a (OsSGS3a). OsSGS3a interacts with its homolog OsSGS3b and modulates the biogenesis of trans-acting small interfering RNA (tasiRNA) targeting AUXIN RESPONSE FACTORS (ARFs). We find that OsSGS3a/b positively, while OsARF3a/b and OsARF3la/lb negatively modulate thermotolerance. Moreover, OsSGS3a negatively, while OsARF3a/b and OsARF3la/lb positively regulate disease resistance to the bacterial pathogen Xanthomonas oryzae pv. oryzae (Xoo) and the fungal pathogen Magnaporthe oryzae (M. oryzae). Taken together, our study uncovers a previously unknown trade-off mechanism that regulates distinct immunity and thermotolerance through the OsSGS3-tasiRNA-OsARF3 module, highlighting the regulation of abiotic-biotic stress response trade-off in plants.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jul</publication><modification>2025-04-05T12:34:19.221Z</modification><creation>2025-04-05T12:34:19.221Z</creation></dates><accession>S-EPMC10366173</accession><cross_references><pubmed>37488129</pubmed><doi>10.1038/s41467-023-40176-2</doi></cross_references></HashMap>