硫元素是植物生長發(fā)育必不可少的大量元素之一,。植物主要通過根從土壤中以硫酸根的形式獲取硫元素，并將其轉運到植物的不同組織,，然后被組織細胞同化利用,，參與植物新陳代謝。植物所吸收獲得的硫酸根經(jīng)過硫同化途徑被還原為低價硫,，然后參與含硫化合物（如半胱氨酸,，甲硫氨酸等）的形成，而多余的硫酸根則被運輸?shù)狡渌M織和（或）在細胞的葉泡內儲存,。
中國科學院西雙版納植物園植物基因功能研究組余迪求研究員領銜的研究小組在microRNA調控擬南芥發(fā)育調節(jié)研究方面取得新進展,，相關成果文章公布在The Plant Journal上。
研究組系統(tǒng)解釋了microRNA395如何參與調控硫酸根在擬南芥體內的吸收,、轉運和同化的生物學過程及其分子機制,。
在成熟葉衰老過程中，硫元素一般被認為是不能向幼葉轉移的,。但是該研究發(fā)現(xiàn),，在硫充足的情況下，擬南芥的硫轉蛋白SULTR2;1可以將游離態(tài)形的硫酸根從老葉轉運到正在發(fā)育的幼葉,。當植物處于硫缺乏條件時,，植物的幼葉往往首先表現(xiàn)出缺硫癥狀（如黃化）,，這似乎說明硫酸根是不可以轉移的。但進一步的研究表明,，在缺硫情況下,，植物體內MicroRNA395的表達水平被顯著地誘導提高。受到誘導的microRNA395迅速而有效地抑制了其靶基因SULTR2;1的表達,，從而限制了硫酸根從老葉向新葉的轉運,。
microRNA395不僅參與硫酸根的轉運，而且還在硫酸根的同化途徑中起作用,。micorRNA395所調控的另外一組靶基因是APS酶,，它們在硫同化途徑中負責活化硫酸根。在缺硫條件下microRNA395通過抑制APS1和APS4,，部分限制了硫酸根進入同化途徑。通過高表達microRNA395基因,，研究發(fā)現(xiàn)轉基因植物過量積累了硫酸根,，這說明microRNA395參與了硫酸根的積累。
通過生物信息學預測發(fā)現(xiàn),，microRNA395在單子葉和雙子葉植物中非常保守,，并且其所調控的靶基因也是非常保守的。這表明microRNA395參與硫代謝調控的分子機制也適用于其他植物物種,。
該研究詳盡的闡述了microRNA395如何調控硫酸根在擬南芥葉片中的積累和轉運,，解釋了植物應對缺硫情況的機制，為現(xiàn)代農(nóng)業(yè)耕作提供了一定的理論依據(jù),。(生物谷Bioon.com)
生物谷推薦原文出處：
The Plant Journal doi: 10.1111/j.1365-313X.2010.04216.x
MicroRNA395 mediates regulation of sulfate accumulation and allocation in Arabidopsis thaliana
Gang Liang a,b , Fengxi Yang a and Di-Qiu Yu a,*
a Key Laboratory of Tropical Forest Ecology, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences, Kunming, Yunnan 650223, PR China
b Graduate University of Chinese Academy of Sciences, Beijing 100049, PR China
Sulfur is a macronutrient necessary for plant growth and development. Sulfate, a major source of sulfur, is taken up by plant roots and transported into different tissues for assimilation. During sulfate limitation, expression of miR395 is significantly up-regulated. miR395 targets two families of genes, ATP Sulfurylases (APS) and Sulfate Transporter2;1 (SULTR2;1, also called AST68), both of which are involved in the sulfate metabolism pathway. Their transcripts are suppressed strongly in miR395-overexpressing transgenic Arabidopsis, which over-accumulates sulfate in the shoot, but not in the root. APS1 knock-down mutants accumulate two-fold more sulfate compared with the wild-type. By constructing APS4-RNAi transgenic plants, we found that silencing the APS4 gene also results in over-accumulation of sulfate. Even though miR395-overexpressing transgenic plants over-accumulate sulfate in the shoot, they display sulfur deficiency symptoms. Additionally, the distribution of sulfate from old to younger leaves is impaired in miR395-overexpressing plants, which is similar to a SULTR2;1 loss-of-function mutant. The aps1-1sultr2;1APS4RNAi triple repressed mutants phenocopied miR395-overexpressing plants. Our research revealed that miR395 is involved in the regulation of sulfate accumulation and allocation by targeting APSs and SULTR2;1, respectively.
