SINAT E3 ligases regulate the stability of the ESCRT component FREE1 in response to iron deficiency in plants.
SINAT E3 ligases regulate the stability of the ESCRT component FREE1 in response to iron deficiency in plants.
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SINAT E3 连接酶可调节 ESCRT 成分 FREE1 的稳定性，以响应植物缺铁的情况。
DOI：
10.1111/jipb.13005
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发表时间：
2020-08
影响因子：
11.4
通讯作者：
Shen Wenjin
中科院分区：
文献类型：
--
作者：
Xiao Zhidan;Yang Chao;Liu Chuanliang;Yang Lianming;Yang Shuhong;Zhou Jun;Li Faqiang;Jiang Liwen;Xiao Shi;Gao Caiji;Shen Wenjin
内体转运所需的分选复合物（ESCRT）是一种古老的、进化上保守的膜重塑复合物，对真核生物中的多泡体（MVB）生物发生至关重要。内体分选所需的FYVE结构域蛋白1（FREE 1），其先前被鉴定为植物特异性ESCRT组分，调节MVB介导的内体分选和自噬降解。虽然FREE 1作为ESCRT组分的基本细胞功能已经被描述，但控制FREE 1周转的调节剂仍然未知。在这里，我们分析了如何FREE 1稳态介导的环指E3泛素连接酶，拟南芥（SINATs），在响应铁缺乏。在缺铁生长条件下，SINAT 1 -4被诱导并泛素化FREE 1，从而促进FREE 1的降解，缓解FREE 1对铁吸收的抑制作用。相比之下，SINAT 5，另一个由于缺少RING结构域而缺乏泛素连接酶活性的SINAT成员，作为稳定FREE 1的保护蛋白发挥作用。总的来说，我们的研究结果揭示了一个迄今为止未知的FREE 1的稳态调节机制，并证明了一个独特的调节SINAT-FREE 1模块，巧妙地调节植物对缺铁胁迫的反应。本文受版权保护。All rights reserved.
The endosomal sorting complex required for transport (ESCRT) machinery is an ancient, evolutionarily conserved membrane remodeling complex that is essential for multivesicular body (MVB) biogenesis in eukaryotes. FYVE DOMAIN PROTEIN REQUIRED FOR ENDOSOMAL SORTING 1 (FREE1), which was previously identified as a plant-specific ESCRT component, modulates MVB-mediated endosomal sorting and autophagic degradation. Although the basic cellular functions of FREE1 as an ESCRT component have been described, the regulators that control FREE1 turnover remain unknown. Here, we analyzed how FREE1 homeostasis is mediated by the RING-finger E3 ubiquitin ligases, SINA of Arabidopsis thaliana (SINATs), in response to iron deficiency. Under iron-deficient growth conditions, SINAT1-4 were induced and ubiquitinated FREE1, thereby promoting its degradation and relieving the repressive effect of FREE1 on iron absorption. By contrast, SINAT5, another SINAT member that lacks ubiquitin ligase activity due to the absence of the RING domain, functions as a protector protein that stabilizes FREE1. Collectively, our findings uncover a hitherto unknown mechanism of homeostatic regulation of FREE1, and demonstrate a unique regulatory SINAT-FREE1 module that subtly regulates plant response to iron deficiency stress. This article is protected by copyright. All rights reserved.
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