ATG7 is dispensable for LC3-PE conjugation in thioglycolate-elicited mouse peritoneal macrophages

被引：21

作者：

Vujic, Nemanja ^{[1
,2
]}

Bradic, Ivan ^{[1
,2
]}

Goeritzer, Madeleine ^{[1
,2
]}

Kuentzel, Katharina B. ^{[1
]}

Rainer, Silvia ^{[1
]}

Kratky, Dagmar ^{[1
,2
]}

Radovic, Branislav ^{[1
,2
]}

机构：

[1] Med Univ Graz, Gottfried Schatz Res Ctr, Graz, Austria

[2] BioTechMed Graz, Graz, Austria

来源：

AUTOPHAGY | 2021年 / 17卷 / 11期

基金：

奥地利科学基金会;

关键词：

ATG3; ATG5; ATG7; LC3; lipidation; LC3-II; macrophages;

D O I：

10.1080/15548627.2021.1874132

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Thioglycolate-elicited macrophages exhibit abundant conjugation of LC3 with PE (LC3-II). Among other autophagy-related (ATG) proteins, it is proposed that, like in yeast, both ATG5 and ATG7 are essential for LC3 conjugation. Using atg5-deficient ((-/-)) and atg7(-/-) macrophages, we provide evidence that loss of ATG5 but not of ATG7 resulted in LC3-II depletion. Accumulation of LC3-II in elicited atg7(-/-) macrophages in response to bafilomycin A(1) validated these data. Furthermore, complete loss of ATG3 in atg7(-/-) macrophages demonstrated that ATG7 and ATG3 are dispensable for LC3-PE conjugation. In contrast to thioglycolate-elicited macrophages, naive peritoneal and bone marrow-derived atg7(-/-) macrophages exhibited no LC3-II, even under inflammatory stimuli in vitro. Hence, the macrophage metabolic status dictates the level of LC3-PE conjugation with a supportive but nonessential role of ATG7, disclosing the eukaryotic exception from the LC3 lipidation model based on yeast data.

引用

页码：3402 / 3407

页数：6

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