sgk-1的新型功能增益突变可部分抑制mTORC2缺陷。

microPublication biology Pub Date : 2024-09-30 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001163
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}
引用次数: 0

摘要

丝氨酸/苏氨酸蛋白激酶 SGK-1 是 mTOR 复合物 2(mTORC2)的下游靶标,是生长和新陈代谢的保守调节因子。在秀丽隐杆线虫中,编码 mTORC2 重要成分的 rict-1 基因突变会损害脂质稳态和生长;然而,SGK-1 的激活突变 E116K 能部分抑制这些缺陷。在这里,我们描述了一种更强的 sgk-1 功能增益突变 L112F,它是在对 rict-1 抑制突变的正向遗传筛选中发现的。这一等位基因将有助于进一步剖析 mTORC2 通路,并为了解这一保守残基在调节 SGK-1 激酶活性中的作用提供了新的视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
审稿时长
3 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信