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Iizumi, R.

Publications and source records attributed to Iizumi, R..

2 recordsLinked to original sources

An extremophilic Nocardiopsis strain from Great Salt Lake expands the taxonomic range of mycolic acid biosynthesis

Mycolic acids, long-chain fatty acids that form the characteristic and relatively impermeable mycomembrane, have long been considered a defining chemotaxonomic feature of the order Mycobacteriales. Here, we report that Nocardiopsis bonnevillensis, a new type strain isolated from the hypersaline environment of Great Salt Lake, is the first organism outside of this order known to produce mycolic acids. Lipid profiling, acid-fast staining, isoniazid sensitivity, and genome mining confirmed hallmark features of mycolic acid biosynthesis. Evaluation of the strains metabolic capabilities led to the isolation of bonnevanoside, a thiophenyl nonulopyranoside reported here for the first time from a natural source. Moreover, additional Great Salt Lake-derived Nocardiopsis isolates exhibited acid-fast staining, suggesting that this trait may be more widespread than previously recognized. Altogether, these findings expand the taxonomic distribution of mycolic acid biosynthesis, challenge long-standing chemotaxonomic boundaries, and highlight the potential ecological significance of mycolate-containing envelopes in supporting bacterial survival in extreme environments.

microbiology↗

Formation of giant ER sheets by pentadecanoic acid causes lipotoxicity in fission yeast

Excess amounts of saturated fatty acids are toxic to organisms, a condition termed lipotoxicity, which is often accompanied by pleiotropic cellular and tissue dysfunction. Here we show that pentadecanoic acid (C15:0) exerts toxicity on the fission yeast Schizosaccharomyces pombe by generating an aberrantly planar endoplasmic reticulum (ER) structure, which we named a "giant ER sheet." Untargeted lipidomics revealed that C15:0 is incorporated into complex lipids depending on an acyl-CoA ligase Lcf1 and an acyl-CoA transferase Slc1, thereby increasing the saturation level of the acyl chains. The toxicity and giant ER sheet formation were abolished by deleting Lcf1 or Slc1, indicating that the incorporation of C15:0 into glycerophospholipids causes giant ER sheet formation. The giant ER sheets disrupted the correct migration of Mid1, a protein determining the cell division site, and physically blocked septum formation, hindering correct cell separation. Our results suggest that the ER is the primary site targeted by saturated fatty acids, leading to lipotoxicity.

cell biology↗