David Cully, Natalie R Cohen, Peter C Breen, Martin A Newman, Robert H Dowen
{"title":"sgk-1的新型功能增益突变可部分抑制mTORC2缺陷。","authors":"David Cully, Natalie R Cohen, Peter C Breen, Martin A Newman, Robert H Dowen","doi":"10.17912/micropub.biology.001163","DOIUrl":null,"url":null,"abstract":"<p><p>The serine/threonine protein kinase SGK-1 is a downstream target of mTOR complex 2 (mTORC2) and is a conserved regulator of growth and metabolism. In <i>C. elegans</i> , mutations in <i>rict-1</i> , which encodes an essential component of mTORC2, impairs lipid homeostasis and growth; however, these defects are partially suppressed by an activating mutation in SGK-1 , E116K. Here, we describe a stronger gain-of-function mutation in <i>sgk-1</i> , L112F, that was identified in a forward genetic screen for <i>rict-1</i> suppressor mutations <i>.</i> This allele will be useful in further dissecting the mTORC2 pathway and provides new insight into the role of this conserved residue in regulating SGK-1 kinase activity.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2024 ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11474317/pdf/","citationCount":"0","resultStr":"{\"title\":\"A novel gain-of-function mutation in <i>sgk-1</i> partially suppresses mTORC2 defects.\",\"authors\":\"David Cully, Natalie R Cohen, Peter C Breen, Martin A Newman, Robert H Dowen\",\"doi\":\"10.17912/micropub.biology.001163\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The serine/threonine protein kinase SGK-1 is a downstream target of mTOR complex 2 (mTORC2) and is a conserved regulator of growth and metabolism. In <i>C. elegans</i> , mutations in <i>rict-1</i> , which encodes an essential component of mTORC2, impairs lipid homeostasis and growth; however, these defects are partially suppressed by an activating mutation in SGK-1 , E116K. Here, we describe a stronger gain-of-function mutation in <i>sgk-1</i> , L112F, that was identified in a forward genetic screen for <i>rict-1</i> suppressor mutations <i>.</i> This allele will be useful in further dissecting the mTORC2 pathway and provides new insight into the role of this conserved residue in regulating SGK-1 kinase activity.</p>\",\"PeriodicalId\":74192,\"journal\":{\"name\":\"microPublication biology\",\"volume\":\"2024 \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11474317/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"microPublication biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.17912/micropub.biology.001163\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"microPublication biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17912/micropub.biology.001163","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
A novel gain-of-function mutation in sgk-1 partially suppresses mTORC2 defects.
The serine/threonine protein kinase SGK-1 is a downstream target of mTOR complex 2 (mTORC2) and is a conserved regulator of growth and metabolism. In C. elegans , mutations in rict-1 , which encodes an essential component of mTORC2, impairs lipid homeostasis and growth; however, these defects are partially suppressed by an activating mutation in SGK-1 , E116K. Here, we describe a stronger gain-of-function mutation in sgk-1 , L112F, that was identified in a forward genetic screen for rict-1 suppressor mutations . This allele will be useful in further dissecting the mTORC2 pathway and provides new insight into the role of this conserved residue in regulating SGK-1 kinase activity.