Summary of identified suppressors.

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.

为阐明短粗根1（SHORT AND SWOLLEN ROOT1，SSR1）的分子功能，我们针对ssr1-2突变体的抑制子（suppressor，sus）开展筛选，最终获得十余个可不同程度恢复根系生长的候选株系。其中效果最为显著的两个抑制子sus1和sus2，分别源于HSCA2（At5g09590）与ISU1（At4g22220）蛋白中G87D和T55M的单氨基酸替换；HSCA2与ISU1均为线粒体铁硫（Fe-S）簇组装复合体的核心组分。SSR1具备较强的类似共伴侣蛋白的活性，可与HSCA2及ISU1相互作用，促进HSCA2与ISU1的结合。与野生型植株相比，ssr1-2突变体的根尖铁积累量升高，且缺铁响应基因的表达模式发生改变。此外，ssr1-2突变体中多种铁硫蛋白的酶活性及线粒体膜电位均出现下降。值得注意的是，SSR1仅存在于植物谱系中，且可被环境胁迫诱导表达。尽管在适宜培养条件下，HSCA2G87D与ISU1T55M可有效弥补SSR1功能缺失所导致的表型缺陷，但在胁迫条件下其补偿效应会显著减弱。综上，SSR1是线粒体铁硫簇组装（ISC）系统中全新且关键的组分，同时可赋予植物ISC系统响应环境胁迫的适应性优势。