Soybean Fe–S cluster biosynthesis regulated by external iron or phosphate fluctuation
Soybean Fe–S cluster biosynthesis regulated by external iron or phosphate fluctuation
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DOI：
10.1007/s00299-014-1718-0
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发表时间：
2015-03
影响因子：
6.2
通讯作者：
L. Qin;Meihuan Wang;Liyu Chen;Xuejiao Liang;Zhigeng Wu;Zhihao Lin;J. Zuo;Xiangyang Feng;Jing Zhao-;H. Liao;H. Ye
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文献类型：
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作者：
L. Qin;Meihuan Wang;Liyu Chen;Xuejiao Liang;Zhigeng Wu;Zhihao Lin;J. Zuo;Xiangyang Feng;Jing Zhao-;H. Liao;H. Ye
铁和磷是大豆结瘤所必需的。我们的研究结果表明，缺铁或缺磷通过不同的机制影响功能铁硫团簇的组装，从而损害了结瘤。摘要铁（Fe）和磷(P)是大豆重要的矿质营养素，是大豆结瘤不可缺少的营养物质。然而，铁的代谢途径如何响应外部铁或磷的波动仍然是未知的。铁是高等植物铁硫（Fe - s）簇组装所必需的。本文以结瘤大豆为研究对象，研究了Fe-S簇生物合成基因在结瘤大豆中的表达模式。大豆基因组编码42个推测的Fe-S簇生物合成基因，这些基因在茎和根中的表达不同，表明它们具有生理相关性。根瘤菌接种后大豆根部形成根瘤。铁浓度在根瘤中比在茎中高3倍。铁- s簇生物合成基因在根瘤中被激活，多个铁- s蛋白活性增加，表明铁- s簇生物合成更有效伴随着结瘤。缺铁使铁- s簇生物合成基因被大量抑制，部分铁- s蛋白活性降低，导致结节微小。值得注意的是，缺磷在根瘤中引起了类似的缺铁反应，即一定程度的铁s酶活性丧失和微小的根瘤。然而，与缺铁结核不同，缺磷结核积累了较高的铁浓度，Fe-S簇生物合成基因没有受到抑制。综上所述，缺铁和缺磷都影响铁-硫簇的形成，但它们影响铁-硫簇组装的机制可能不同。铁- s簇生物合成可能与大豆根和根瘤细胞的铁代谢和磷代谢有关。
Key messageIron and phosphorus are essential for soybean nodulation. Our results suggested that the deficiency of Fe or P impairs nodulation by affecting the assembly of functional iron–sulfur cluster via different mechanisms.AbstractIron (Fe) and phosphorus (P) are important mineral nutrients for soybean and are indispensable for nodulation. However, it remains elusive how the pathways of Fe metabolism respond to the fluctuation of external Fe or P. Iron is required for the iron–sulfur (Fe–S) cluster assembly in higher plant. Here, we investigated the expression pattern of Fe–S cluster biosynthesis genes in the nodulated soybean. Soybean genome encodes 42 putative Fe–S cluster biosynthesis genes, which were expressed differently in shoots and roots, suggesting of physiological relevance. Nodules initiated from roots of soybean after rhizobia inoculation. In comparison with that in shoots, iron concentration was three times higher in nodules. The Fe–S cluster biosynthesis genes were activated and several Fe–S protein activities were increased in nodules, indicating that a more effective Fe–S cluster biosynthesis is accompanied by nodulation. Fe–S cluster biosynthesis genes were massively repressed and some Fe–S protein activities were decreased in nodules by Fe deficiency, leading to tiny nodules. Notably, P deficiency induced a similar Fe-deficiency response in nodules, i.e, certain Fe–S enzyme activity loss and tiny nodules. However, distinct from Fe-deficient nodules, higher iron concentration was accumulated and the Fe–S cluster biosynthesis genes were not suppressed in the P-deficiency-treated nodules. Taken together, our results showed that both Fe deficiency and P deficiency impair nodulation, but they affect the assembly of Fe–S cluster maybe via different mechanisms. The data also suggested that Fe–S cluster biosynthesis likely links Fe metabolism and P metabolism in root and nodule cells of soybean.