Tran Lien Hong, Kim Jin-Gil, Jung Sunyo
School of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea.
Front Plant Sci. 2023 Mar 2;14:1098808. doi: 10.3389/fpls.2023.1098808. eCollection 2023.
The most common symptom of iron (Fe) deficiency in plants is leaf chlorosis caused by impairment of chlorophyll biosynthesis. Magnesium (Mg)-chelatase H subunit (CHLH) is a key component in both chlorophyll biosynthesis and plastid signaling, but its role in Fe deficiency is poorly understood. Heterologous expression of the Mg-chelatase H subunit gene () increased Mg-chelatase activity by up to 6-fold and abundance of its product, Mg-protoporphyrin IX (Mg-Proto IX), by 60-75% in transgenic rice () seedlings compared to wild-type (WT) controls. Noticeably, the transgenic seedlings showed alleviation of Fe deficiency symptoms, as evidenced by their less pronounced leaf chlorosis and lower declines in shoot growth, chlorophyll contents, and photosynthetic efficiency, as indicated by / and electron transport rate, compared to those in WT seedlings under Fe deficiency. Porphyrin metabolism was differentially regulated by Fe deficiency between WT and transgenic seedlings, particularly with a higher level of Mg-Proto IX in transgenic lines, showing that overexpression of reprograms porphyrin metabolism in transgenic rice. Leaves of Fe-deficient transgenic seedlings exhibited greater upregulation of deoxymugineic acid biosynthesis-related genes (i.e., , , and ), transporter gene, and Fe-related transcription factor genes and than those of WT, which may also partly contribute to alleviating Fe deficiency. Although CHLH was postulated to act as a receptor for abscisic acid (ABA), exogenous ABA did not alter the phenotypes of Fe-deficient WT or transgenic seedlings. Our study demonstrates that modulation of porphyrin biosynthesis through expression of in transgenic rice alleviates Fe deficiency-induced stress, suggesting a possible role for CHLH in Fe deficiency responses.
植物缺铁最常见的症状是因叶绿素生物合成受损而导致的叶片黄化。镁螯合酶H亚基（CHLH）是叶绿素生物合成和质体信号传导中的关键组分，但其在缺铁中的作用却知之甚少。与野生型（WT）对照相比，镁螯合酶H亚基基因（）在转基因水稻（）幼苗中的异源表达使镁螯合酶活性提高了6倍，其产物镁原卟啉IX（Mg-Proto IX）的丰度提高了60 - 75%。值得注意的是，转基因幼苗缺铁症状得到缓解，缺铁条件下，与野生型幼苗相比，其叶片黄化不那么明显，地上部生长、叶绿素含量和光合效率（通过/和电子传递速率表示）下降幅度更小，这证明了上述结论。野生型和转基因幼苗之间，缺铁对卟啉代谢的调控存在差异，特别是转基因株系中Mg-Proto IX水平较高，表明的过表达改变了转基因水稻中的卟啉代谢。缺铁转基因幼苗的叶片中，脱氧 mugineic 酸生物合成相关基因（即，和）、转运蛋白基因以及铁相关转录因子基因和的上调程度高于野生型，这也可能在一定程度上有助于缓解缺铁状况。尽管推测CHLH可作为脱落酸（ABA）的受体，但外源ABA并未改变缺铁野生型或转基因幼苗的表型。我们的研究表明，通过在转基因水稻中表达来调节卟啉生物合成可缓解缺铁诱导的胁迫，这表明CHLH在缺铁反应中可能发挥作用。
