The Multivesicular Bodies (MVBs)-Localized AAA ATPase LRD6-6 Inhibits Immunity and Cell Death Likely through Regulating MVBs-Mediated Vesicular Trafficking in Rice.
The Multivesicular Bodies (MVBs)-Localized AAA ATPase LRD6-6 Inhibits Immunity and Cell Death Likely through Regulating MVBs-Mediated Vesicular Trafficking in Rice.
复制标题
水稻中多囊泡体 (MVB) 定位的 AAA ATP 酶 LRD6-6 可能通过调节 MVB 介导的囊泡运输来抑制免疫和细胞死亡
DOI：
10.1371/journal.pgen.1006311
复制
发表时间：
2016-09
期刊：
影响因子：
4.5
通讯作者：
Chen X
中科院分区：
文献类型：
--
作者：
Zhu X;Yin J;Liang S;Liang R;Zhou X;Chen Z;Zhao W;Wang J;Li W;He M;Yuan C;Miyamoto K;Ma B;Wang J;Qin P;Chen W;Wang Y;Wang W;Wu X;Yamane H;Zhu L;Li S;Chen X
以往的研究表明，多泡体（MVB）/内体介导的囊泡运输可能在植物免疫和细胞死亡中发挥关键作用。然而，在水稻中的分子调控知之甚少。在这里，我们报告的MVBs定位AAA ATP酶LRD 6 -6在水稻中的鉴定和表征。LRD 6 -6的破坏导致水稻免疫力增强和细胞死亡。LRD 6 -6的ATP酶活性和同源二聚化对于其调节植物免疫和细胞死亡是必需的。ATP酶失活突变（LRD 6 - 6 E315 Q）导致植物中的显性负抑制。LRD 6 -6蛋白与MVB标记蛋白RabF 1/ARA 6共定位，并与ESCRT-III组分OsSNF 7和OsVPS 2相互作用。进一步的分析表明，LRD 6 -6是MVB介导的囊泡运输所必需的，并抑制抗微生物化合物的生物合成。总的来说，我们的研究表明，AAA ATP酶LRD 6 -6抑制植物免疫和细胞死亡最有可能通过调节MVB介导的囊泡运输水稻。植物在抵抗细菌、真菌和卵菌等病原微生物的过程中，进化出了一套复杂的免疫系统。在感知病原体时，免疫系统激活快速细胞死亡，其特征在于通常在感染部位中和周围的过敏反应形式，以限制病原体入侵并防止疾病发展。最近的研究表明，MVB介导的囊泡运输可能在植物免疫和细胞死亡中起关键作用。然而，分子调控知之甚少。通过使用病变类似疾病（lrd）突变体，lrd 6 -6，它表现出自身免疫和自发性细胞死亡，我们的特点是LRD 6 -6作为一个MVB定位AAA ATP酶。我们发现ATP酶LRD 6 -6是MVB介导的囊泡运输所需的，并抑制水稻免疫反应中抗菌化合物的生物合成。ATP酶活性和同源二聚体化是LRD 6 -6抑制免疫和细胞死亡的必要条件。无催化活性的ATP酶LRD 6 - 6 E315 Q对植物免疫抑制起显性-负性作用。此外，LRD 6 -6蛋白与MVB传播标记蛋白RabF 1/ARA 6共定位，并且还与ESCRT-III组分OsSNF 7和OsVPS 2相互作用。总之，我们的研究表明，AAA ATP酶LRD 6 -6抑制植物免疫和细胞死亡最有可能通过调节水稻中MVB介导的囊泡运输。
Previous studies have shown that multivesicular bodies (MVBs)/endosomes-mediated vesicular trafficking may play key roles in plant immunity and cell death. However, the molecular regulation is poorly understood in rice. Here we report the identification and characterization of a MVBs-localized AAA ATPase LRD6-6 in rice. Disruption of LRD6-6 leads to enhanced immunity and cell death in rice. The ATPase activity and homo-dimerization of LRD6-6 is essential for its regulation on plant immunity and cell death. An ATPase inactive mutation (LRD6-6E315Q) leads to dominant-negative inhibition in plants. The LRD6-6 protein co-localizes with the MVBs marker protein RabF1/ARA6 and interacts with ESCRT-III components OsSNF7 and OsVPS2. Further analysis reveals that LRD6-6 is required for MVBs-mediated vesicular trafficking and inhibits the biosynthesis of antimicrobial compounds. Collectively, our study shows that the AAA ATPase LRD6-6 inhibits plant immunity and cell death most likely through modulating MVBs-mediated vesicular trafficking in rice. Plants have evolved sophistical immunity system in fighting against pathogenic micro-organisms including bacteria, fungi and oomycetes. Upon perception of pathogens, the immune system activates rapid cell death, characterized as a form of hypersensitive response typically in and around the infection sites to restrict pathogen invasion and prevent disease development. Recent studies have suggested that MVBs-mediated vesicular trafficking might play key roles in plant immunity and cell death. However, the molecular regulation is poorly known. By using the lesion resembling disease (lrd) mutant, lrd6-6, which exhibits autoimmunity and spontaneous cell death, we characterized LRD6-6 as a MVBs-localized AAA ATPase. We found that the ATPase LRD6-6 was required for MVBs-mediated vesicular trafficking and inhibited the biosynthesis of antimicrobial compounds for immune response in rice. Both the ATPase activity and homo-dimerization of LRD6-6 were essential for its inhibition on immunity and cell death. The catalytically inactive ATPase, LRD6-6E315Q, played dominant-negative effect on inhibition of immunity in plants. In addition, the LRD6-6 protein co-localized with the MVBs-spread marker protein RabF1/ARA6 and also interacted with ESCRT-III components OsSNF7 and OsVPS2. In summary, our study has shown that the AAA ATPase LRD6-6 inhibits plant immunity and cell death most likely through modulating MVBs-mediated vesicular trafficking in rice.
登录
查看更多内容
影响因子：
6.4
作者：
Cai, Kunzheng;Gao, Dan;Zhu, Xiaoyuan
通讯作者：
Zhu, Xiaoyuan
影响因子：
14.9
作者：
Harris, MA;Clark, J;White, R
通讯作者：
White, R
影响因子：
4.3
作者：
CAMPBELL, MM;ELLIS, BE
通讯作者：
ELLIS, BE
影响因子：
4
作者：
Fujita, H;Yamanaka, M;Himeno, M
通讯作者：
Himeno, M
影响因子：
7.5
作者：
Dell'Angelica, Esteban C.
通讯作者：
Dell'Angelica, Esteban C.