Feng Xuanjun, Hu Yue, Xie Tao, Han Huiling, Bonea Diana, Zeng Lijuan, Liu Jie, Ying Wenhan, Mu Bona, Cai Yuanyuan, Zhang Min, Lu Yanli, Zhao Rongmin, Hua Xuejun
State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Wenjiang, Sichuan, China.
Maize Research Institute of Sichuan Agricultural University, Wenjiang, Sichuan, China.
PLoS Genet. 2025 Feb 5;21(2):e1011597. doi: 10.1371/journal.pgen.1011597. eCollection 2025 Feb.
To elucidate the molecular function of SHORT AND SWOLLEN ROOT1 (SSR1), we screened for suppressors of the ssr1-2 (sus) was performed and identified over a dozen candidates with varying degrees of root growth restoration. Among these, the two most effective suppressors, sus1 and sus2, resulted from G87D and T55M single amino acid substitutions in HSCA2 (At5g09590) and ISU1 (At4g22220), both crucial components of the mitochondrial iron-sulfur (Fe-S) cluster assembly machinery. SSR1 displayed a robust cochaperone-like activity and interacted with HSCA2 and ISU1, facilitating the binding of HSCA2 to ISU1. In comparison to the wild-type plants, ssr1-2 mutants displayed increased iron accumulation in root tips and altered expression of genes responsive to iron deficiency. Additionally, the enzymatic activities of several iron-sulfur proteins and the mitochondrial membrane potential were reduced in ssr1-2 mutants. Interestingly, SSR1 appears to be exclusive to plant lineages and is induced by environmental stresses. Although HSCA2G87D and ISU1T55M can effectively compensate for the phenotypes associated with SSR1 deficiency under favorable conditions, their compensatory effects are significantly diminished under stress. Collectively, SSR1 represents a new and significant component of the mitochondrial Fe-S cluster assembly (ISC) machinery. It may also confer adaptive advantages on plant ISC machinery in response to environmental stress.
为了阐明SHORT AND SWOLLEN ROOT1（SSR1）的分子功能，我们对ssr1-2（sus）的抑制子进行了筛选，并鉴定出十几个根生长恢复程度不同的候选基因。其中，两个最有效的抑制子sus1和sus2，是由HSCA2（At5g09590）和ISU1（At4g22220）中的G87D和T55M单氨基酸替换产生的，这两个基因都是线粒体铁硫（Fe-S）簇组装机制的关键组成部分。SSR1表现出强大的伴侣样活性，并与HSCA2和ISU1相互作用，促进HSCA2与ISU1的结合。与野生型植物相比，ssr1-2突变体根尖中铁积累增加，对缺铁响应的基因表达发生改变。此外，ssr1-2突变体中几种铁硫蛋白的酶活性和线粒体膜电位降低。有趣的是，SSR1似乎是植物谱系所特有的，并受环境胁迫诱导。虽然HSCA2G87D和ISU1T55M在有利条件下可以有效补偿与SSR1缺陷相关的表型，但在胁迫条件下它们的补偿作用会显著减弱。总的来说，SSR1是线粒体Fe-S簇组装（ISC）机制中一个新的重要组成部分。它也可能赋予植物ISC机制在应对环境胁迫时的适应性优势。
