优雅小鼠 dpy-7 角质层沟突变体中代谢和溶酶体相关基因的表达增加。

microPublication biology Pub Date : 2024-07-31 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001241
Aiden Fong, Michael Rodriguez, Keith Patrick Choe
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引用次数: 0

摘要

草履虫基于胶原蛋白的表皮 "角质层 "具有细胞外损伤传感器的功能,可调节促进渗透平衡、先天免疫和解毒的基因。先前的研究表明,哺乳动物 Nrf 转录因子的同源物 SKN-1 能激活角质层损伤下游的核心解毒基因。之前的 RNAseq 数据表明,在角质层胶原蛋白突变体中,具有氧化还原平衡、ATP 稳态和溶酶体功能的五个基因(gst-15、gst-24、cyts-1、argk-1 和 mfsd-8.4)的表达量增加;本研究采用 RT-qPCR 验证了这一观察结果,并检验了 SKN-1 的作用。在 dpy-7 突变体中,所有五个基因的激活都得到了验证,但 skn-1 (RNAi) 均未降低这五个基因的激活,这表明存在平行或不同的调控机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Increased expression of metabolism and lysosome-associated genes in a C. elegans dpy-7 cuticle furrow mutant.

The collagen-based epidermal 'cuticle' of Caenorhabditis elegans functions as an extracellular sensor for damage that regulates genes promoting osmotic balance, innate immunity, and detoxification. Prior studies demonstrate that SKN-1 , an ortholog of the mammalian Nrf transcription factors, activates core detoxification genes downstream from cuticle damage. Prior RNAseq data suggested that expression of five genes with functions in redox balance, ATP homeostasis, and lysosome function ( gst-15 , gst-24 , cyts-1 , argk-1 , and mfsd-8.4 ) were increased in a cuticle collagen mutant; this study employed RT-qPCR to verify this observation and to test the role of SKN-1 . Activation of all five genes was verified in dpy-7 mutants, but none were reduced by skn-1 (RNAi) suggesting parallel or distinct regulatory mechanisms.

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