<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Del Chiaro A</submitter><funding>Austrian Science Fund FWF</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>European Research Council</funding><funding>Austrian Academy of Sciences</funding><funding>Vienna Science and Technology Fund</funding><funding>HORIZON EUROPE Marie Sklodowska-Curie Actions</funding><pagination>jcs263803</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12450472</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>138(17)</volume><pubmed_abstract>Autophagy sustains cellular health by recycling damaged or excess components through autophagosomes. Autophagy is mediated by conserved ATG proteins, among which the ubiquitin-like ATG8 proteins play a central role by linking cargo to the growing autophagosomes. Unlike most ATG proteins, the ATG8 gene family is significantly expanded in vascular plants, but its functional specialization remains poorly understood. Using transcriptional and translational reporters in Arabidopsis thaliana, we revealed that ATG8 isoforms are differentially expressed across tissues and form distinct autophagosomes. To explore ATG8 specialization, we generated the nonuple Δatg8 mutant, lacking all nine ATG8 isoforms. The mutant displayed hypersensitivity to carbon and nitrogen starvation, coupled with defects in</pubmed_abstract><journal>Journal of cell science</journal><pubmed_title>An A. thaliana mutant lacking all nine ATG8 isoforms provides genetic evidence for functional specialization of ATG8 in plants.</pubmed_title><pmcid>PMC12450472</pmcid><funding_grant_id>P34944</funding_grant_id><funding_grant_id>LS21-09</funding_grant_id><funding_grant_id>LS21-009</funding_grant_id><funding_grant_id>847548</funding_grant_id><funding_grant_id>Heisenberg Professorship</funding_grant_id><funding_grant_id>LS17-47</funding_grant_id><funding_grant_id>LS17-047</funding_grant_id><funding_grant_id>SFB F79</funding_grant_id><funding_grant_id>P32355</funding_grant_id><funding_grant_id>101043370</funding_grant_id><funding_grant_id>DOC 111</funding_grant_id><pubmed_authors>Kang BH</pubmed_authors><pubmed_authors>Papareddy RK</pubmed_authors><pubmed_authors>Berger F</pubmed_authors><pubmed_authors>Grujic N</pubmed_authors><pubmed_authors>Gao P</pubmed_authors><pubmed_authors>Lofke C</pubmed_authors><pubmed_authors>Gruetzner R</pubmed_authors><pubmed_authors>Del Chiaro A</pubmed_authors><pubmed_authors>Bhattacharya A</pubmed_authors><pubmed_authors>Marillonnet S</pubmed_authors><pubmed_authors>Bourguet P</pubmed_authors><pubmed_authors>Ma J</pubmed_authors><pubmed_authors>Dagdas Y</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>An A. thaliana mutant lacking all nine ATG8 isoforms provides genetic evidence for functional specialization of ATG8 in plants.</name><description>Autophagy sustains cellular health by recycling damaged or excess components through autophagosomes. Autophagy is mediated by conserved ATG proteins, among which the ubiquitin-like ATG8 proteins play a central role by linking cargo to the growing autophagosomes. Unlike most ATG proteins, the ATG8 gene family is significantly expanded in vascular plants, but its functional specialization remains poorly understood. Using transcriptional and translational reporters in Arabidopsis thaliana, we revealed that ATG8 isoforms are differentially expressed across tissues and form distinct autophagosomes. To explore ATG8 specialization, we generated the nonuple Δatg8 mutant, lacking all nine ATG8 isoforms. The mutant displayed hypersensitivity to carbon and nitrogen starvation, coupled with defects in</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-06-03T17:30:35.274Z</modification><creation>2026-04-30T03:07:22.026Z</creation></dates><accession>S-EPMC12450472</accession><cross_references><pubmed>40814261</pubmed><doi>10.1242/jcs.263803</doi></cross_references></HashMap>