作者: T.G. Turi , P. Webster , J.K. Rose
DOI: 10.1016/S0021-9258(19)51072-9
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摘要: The fungal metabolite brefeldin A (BFA) causes the inhibition of protein secretion and disruption structure function Golgi complex in mammalian cells. Here we show that BFA has identical effects fission yeast Schizosaccharomyces pombe which normally contains a stacked cisternae similar to complexes animal After treatment with BFA, was inhibited, disappeared, there an accumulation endoplasmic reticulum. These results indicate fungi are very those cells provide direct evidence for effect on morphology fungi. Five spontaneous BFA-resistant mutants were isolated. Genetic analysis showed mutations conferring resistance dominant two separate linkage groups. One found be allelic crm1, gene affecting chromatin structure. All overexpressed 20-kDa protein, corresponding obr1 isolated sequenced. However, overexpression not sufficient confer resistance. Plasmids capable wild type from libraries constructed mutants. plasmids contain six different genes when present high copy. these encoded transcription factor pap1, homolog AP1 protein. pap1 probably confers indirectly by inducing expression one or more other proteins. isolation several suggests mechanisms involved.