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角质层沟突变体中代谢和溶酶体相关基因的表达增加。

Increased expression of metabolism and lysosome-associated genes in a cuticle furrow mutant.

作者信息

Fong Aiden, Rodriguez Michael, Choe Keith Patrick

机构信息

Biology, University of Florida, Gainesville, Florida, United States.

Department of Biology and Genetics Institute, University of Florida, Gainesville, FL USA.

出版信息

MicroPubl Biol. 2024 Jul 31;2024. doi: 10.17912/micropub.biology.001241. eCollection 2024.

DOI:10.17912/micropub.biology.001241
PMID:39144098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11322832/
Abstract

The collagen-based epidermal 'cuticle' of 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 ( , , , , and ) 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 mutants, but none were reduced by suggesting parallel or distinct regulatory mechanisms.

摘要

基于胶原蛋白的表皮“角质层”作为一种细胞外损伤传感器,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,SKN-1是哺乳动物Nrf转录因子的直系同源物,可激活角质层损伤下游的核心解毒基因。先前的RNA测序数据表明,在角质层胶原蛋白突变体中,五个在氧化还原平衡、ATP稳态和溶酶体功能方面起作用的基因( 、 、 、 和 )的表达增加;本研究采用RT-qPCR来验证这一观察结果,并测试SKN-1的作用。在 突变体中验证了所有五个基因的激活,但没有一个基因因 而减少,这表明存在平行或不同的调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4df5/11322832/2f7693368195/25789430-2024-micropub.biology.001241.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4df5/11322832/2f7693368195/25789430-2024-micropub.biology.001241.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4df5/11322832/2f7693368195/25789430-2024-micropub.biology.001241.jpg

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