PARAQUAT TOLERANCE3 Is an E3 Ligase That Switches off Activated Oxidative Response by Targeting Histone-Modifying PROTEIN METHYLTRANSFERASE4b

PARAQUAT TOLERANCE3 Is an E3 Ligase That Switches off Activated Oxidative Response by Targeting Histone-Modifying PROTEIN METHYLTRANSFERASE4b
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PARAQUAT TOLERANCE3 是一种 E3 连接酶,可通过靶向组蛋白修饰蛋白甲基转移酶 4b 来关闭激活的氧化反应

DOI:
10.1371/journal.pgen.1006332
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发表时间:
2016-09
期刊:
影响因子:
4.5
通讯作者:
Xiang Cheng-Bin
Xiang Cheng-Bin
中科院分区:
生物学2区
文献类型:
--
作者:
Luo Chao;Cai Xiao-Teng;Du Jin;Zhao Tao-Lan;Zhao Ping-Xia;Wang Peng-Fei;Liu Rui;Xie Qi;Cao Xiao-Feng;Xiang Cheng-Bin

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氧化应激是好氧生物不可避免的。当遇到非生物和生物胁迫时,细胞中可能发生氧化损伤。为了避免这种损害,必须及时有效地调节防御机制。虽然植物对氧化应激的反应已被广泛研究,但对氧化应激减少时激活的反应如何关闭知之甚少。通过研究拟南芥突变体百草枯耐受性3,我们确定了遗传位点百草枯耐受性3(PQT 3)作为氧化胁迫耐受性的主要负调节因子。PQT3编码E3泛素连接酶,通过氧化应激快速下调。在泛素化实验中,PQT3具有E3泛素连接酶活性。随后,我们鉴定PRMT4b为PQT 3相互作用蛋白。通过组蛋白甲基化,PRMT4b上调APX1和GPX1的表达,编码两种抗氧化应激的关键酶。另一方面,PRMT4b被PQT 3识别,通过26S蛋白酶体靶向降解。因此,我们已经确定PQT 3作为E3连接酶,其作为氧化应激的活化应答的负调节剂,并发现组蛋白修饰在APX1和GPX1基因座处起重要作用。
Oxidative stress is unavoidable for aerobic organisms. When abiotic and biotic stresses are encountered, oxidative damage could occur in cells. To avoid this damage, defense mechanisms must be timely and efficiently modulated. While the response to oxidative stress has been extensively studied in plants, little is known about how the activated response is switched off when oxidative stress is diminished. By studying Arabidopsis mutant paraquat tolerance3, we identified the genetic locus PARAQUAT TOLERANCE3 (PQT3) as a major negative regulator of oxidative stress tolerance. PQT3, encoding an E3 ubiquitin ligase, is rapidly down-regulated by oxidative stress. PQT3 has E3 ubiquitin ligase activity in ubiquitination assay. Subsequently, we identified PRMT4b as a PQT3-interacting protein. By histone methylation, PRMT4b upregulates the expression of APX1 and GPX1, encoding two key enzymes against oxidative stress. On the other hand, PRMT4b is recognized by PQT3 for targeted degradation via 26S proteasome. Therefore, we have identified PQT3 as an E3 ligase that acts as a negative regulator of activated response to oxidative stress and found that histone modification by PRMT4b at APX1 and GPX1 loci plays an important role in oxidative stress tolerance.
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