{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["77(6)"],"submitter":["Vallieres C"],"pubmed_abstract":["The mutation G143A in the inhibitor binding site of cytochrome b confers a high level of resistance to fungicides targeting the bc(1) complex. The mutation, reported in many plant-pathogenic fungi, has not evolved in fungi that harbor an intron immediately after the codon for G143 in the cytochrome b gene, intron bi2. Using Saccharomyces cerevisiae as a model organism, we show here that a codon change from GGT to GCT, which replaces glycine 143 with alanine, hinders the splicing of bi2 by altering the exon/intron structure needed for efficient intron excision. This lowers the levels of cytochrome b and respiratory growth. We then investigated possible bypass mechanisms that would restore the respiratory fitness of a resistant mutant. Secondary mutations in the mitochondrial genome were fou"],"journal":["Applied and environmental microbiology"],"pagination":["2088-93"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3067308"],"repository":["biostudies-literature"],"pubmed_title":["Deleterious effect of the Qo inhibitor compound resistance-conferring mutation G143A in the intron-containing cytochrome b gene and mechanisms for bypassing it."],"pmcid":["PMC3067308"],"pubmed_authors":["Meunier B","Dujardin G","Vallieres C","Trouillard M"],"additional_accession":[]},"is_claimable":false,"name":"Deleterious effect of the Qo inhibitor compound resistance-conferring mutation G143A in the intron-containing cytochrome b gene and mechanisms for bypassing it.","description":"The mutation G143A in the inhibitor binding site of cytochrome b confers a high level of resistance to fungicides targeting the bc(1) complex. The mutation, reported in many plant-pathogenic fungi, has not evolved in fungi that harbor an intron immediately after the codon for G143 in the cytochrome b gene, intron bi2. Using Saccharomyces cerevisiae as a model organism, we show here that a codon change from GGT to GCT, which replaces glycine 143 with alanine, hinders the splicing of bi2 by altering the exon/intron structure needed for efficient intron excision. This lowers the levels of cytochrome b and respiratory growth. We then investigated possible bypass mechanisms that would restore the respiratory fitness of a resistant mutant. Secondary mutations in the mitochondrial genome were fou","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Mar","modification":"2026-05-02T23:02:59.136Z","creation":"2019-03-27T00:40:12Z"},"accession":"S-EPMC3067308","cross_references":{"pubmed":["21278281"],"doi":["10.1128/aem.02548-10","10.1128/AEM.02548-10"]}}