Macrophage migration inhibitory factor MtMIF3 prevents the premature aging of Medicago truncatula nodules
Macrophage migration inhibitory factor MtMIF3 prevents the premature aging of Medicago truncatula nodules
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DOI：
10.1111/pce.14515
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发表时间：
2022-12-21
影响因子：
7.3
通讯作者：
Chou，Minxia
中科院分区：
文献类型：
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作者：
Wang，Li;Yang，Jieyu;Chou，Minxia
巨噬细胞移动抑制因子(MIF)是一种参与动物免疫反应的促炎细胞因子。然而，MIF在像紫花苜蓿这样的植物中的作用，特别是在共生固氮中的作用，仍然不清楚。对FM的调查。元胞菌-融化中华根瘤菌共生研究表明，MtMIF3主要在根瘤的固氮区表达。利用RNA干扰(Ri)技术沉默MtMIF3后，固氮区感染细胞中的结节数量增加，类细菌降解程度增加，表明MtMIF3-Rinodules中诱导了过早衰老。与此一致的是，接种28d后，根瘤中的固氮酶、超氧化物歧化酶和过氧化氢酶的活性低于对照，而半胱氨酸蛋白酶的活性高于对照。相反，MtMIF3的过表达抑制了根瘤的衰老。MtMIF3定位于细胞膜、细胞核和细胞质中，与蛋氨酸亚砜还原酶B(MSRB)相互作用，MSRB也定位于烟草叶绿体中。综上所述，这些结果表明，MtMIF3通过与MtMsrB相互作用，防止根瘤过早衰老，并防止氧化。
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in immune response in animals. However, the role of MIFs in plants such asMedicago truncatula, particularly in symbiotic nitrogen fixation, remains unclear. An investigation ofM. truncatula—Sinorhizobium melilotisymbiosis revealed thatMtMIF3was mainly expressed in the nitrogen‐fixing zone of the nodules. SilencingMtMIF3using RNA interference (Ri) technology resulted in increased nodule numbers but higher levels of bacteroid degradation in the infected cells of the nitrogen‐fixing zone, suggesting that premature aging was induced inMtMIF3‐Rinodules. In agreement with this conclusion, the activities of nitrogenase, superoxide dismutase and catalase were lower than those in controls, but cysteine proteinase activity was increased in nodulated roots at 28 days postinoculation. In contrast, the overexpression ofMtMIF3inhibited nodule senescence. MtMIF3 is localized in the plasma membrane, nucleus, and cytoplasm, where it interacts with methionine sulfoxide reductase B (MsrB), which is also localized in the chloroplasts of tobacco leaf cells. Taken together, these results suggest that MtMIF3 prevents premature nodule aging and protects against oxidation by interacting with MtMsrB.