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Through analyses of yeast mutants with various deletion combinations of complex\u2010sphingolipid\u2010metabolising enzyme genes (\n                    <jats:italic>CSG1<\/jats:italic>\n                    ,\n                    <jats:italic>CSH1<\/jats:italic>\n                    ,\n                    <jats:italic>IPT1<\/jats:italic>\n                    ,\n                    <jats:italic>SUR2<\/jats:italic>\n                    and\n                    <jats:italic>SCS7<\/jats:italic>\n                    ), it was previously shown that less structural diversity of complex sphingolipids leads to increased sensitivity to multiple environmental stresses, with impaired plasma\u2010membrane and cell\u2010wall integrity. In this study, we screened for suppressor mutations that can alleviate the stress hypersensitivities of\n                    <jats:italic>csg1<\/jats:italic>\n                    \u0394\n                    <jats:italic>csh1<\/jats:italic>\n                    \u0394\n                    <jats:italic>sur2<\/jats:italic>\n                    \u0394\n                    <jats:italic>scs7<\/jats:italic>\n                    \u0394 (\n                    <jats:italic>ccss<\/jats:italic>\n                    \u0394) cells. Mutations of trafficking protein particle complex III\u2010specific subunit 85 (\n                    <jats:italic>TRS85<\/jats:italic>\n                    ; encodes a component of the TRAPPIII complex, involved in membrane trafficking) and phospholipid\u2010transporting ATPase Dnf2 (\n                    <jats:italic>DNF2<\/jats:italic>\n                    ; encodes the plasma\u2010membrane glycerophospholipid flippase) were identified as suppressor mutations. Loss of Trs85 or phospholipid\u2010transporting ATPase accessory subunit Lem3 (\n                    <jats:italic>LEM3<\/jats:italic>\n                    ; encodes a regulatory subunit of Dnf2) differed in the type of stress being conferred resistance to\n                    <jats:italic>ccss\u2206<\/jats:italic>\n                    cells. Furthermore, it was also found that impaired plasma\u2010membrane and cell\u2010wall integrities in\n                    <jats:italic>ccss\u0394<\/jats:italic>\n                    cells were suppressed by\n                    <jats:italic>trs85\u2206<\/jats:italic>\n                    but not\n                    <jats:italic>lem3\u2206<\/jats:italic>\n                    . Moreover,\n                    <jats:italic>ccss<\/jats:italic>\n                    \u2206 cells exhibited abnormal localisation of yeGFP\u2010Snc1 in endosomes, which is suppressed by\n                    <jats:italic>trs85\u2206<\/jats:italic>\n                    but not\n                    <jats:italic>lem3\u2206<\/jats:italic>\n                    . Overexpression of GTP\u2010binding protein Ypt1, which is regulated by TRAPPIII and involved in vesicular trafficking, exacerbated plasma\u2010membrane integrity abnormalities and stress sensitivities in\n                    <jats:italic>ccss\u2206<\/jats:italic>\n                    cells. Thus, it was suggested that\n                    <jats:italic>TRS85<\/jats:italic>\n                    and\n                    <jats:italic>LEM3<\/jats:italic>\n                    deletion confer stress tolerances to\n                    <jats:italic>ccss<\/jats:italic>\n                    \u0394 cells through distinct mechanisms. These findings will provide insights into the physiological significance of the structural diversity of complex sphingolipids.\n                  <\/jats:p>","DOI":"10.1111\/febs.70094","type":"journal-article","created":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T12:31:09Z","timestamp":1745411469000},"page":"4694-4719","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["<scp>\n                      <i>TRS85<\/i>\n                    <\/scp>\n                    and\n                    <scp>\n                      <i>LEM3<\/i>\n                    <\/scp>\n                    suppressor mutations rescue stress hypersensitivities caused by lack of structural diversity of complex sphingolipids in budding yeast"],"prefix":"10.1111","volume":"292","author":[{"given":"Momoko","family":"Matsuzaki","sequence":"first","affiliation":[{"name":"Department of Chemistry, Faculty of Sciences Kyushu University  Fukuoka 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