Pang Yongqi, Li Jintong, Qi Bishu, Tian Mi, Sun Lirong, Wang Xuechen, Hao Fushun
State Key Laboratory of Cotton Biology, Henan Key Laboratory of Plant Stress Biology, College of Life Sciences, Henan University, Kaifeng 475004, P.R. China.
North China Key Laboratory for Crop Germplasm Resources of Education Ministry, Agricultural University of Hebei, Baoding 071000, P.R. China.
Funct Plant Biol. 2018 Feb;45(3):305-314. doi: 10.1071/FP16444.
Aquaporins play essential roles in growth and development including stem elongation in plants. Tonoplast aquaporin AtTIP5;1 has been proposed to positively regulate hypocotyl elongation under high concentrations of boron (high-B) in Arabidopsis thaliana (L.) Heynh. However, the mechanism underlying this process remains unanswered. Here, we show that paclobatrazol, an inhibitor of GA biosynthesis, significantly suppressed the hypocotyl cell elongation of wild-type (WT) seedlings, and more strongly suppressed that of AtTIP5;1 overexpressors under high-B stress. Two AtTIP5;1 null mutants displayed arrested elongation of cells in the upper part of hypocotyls compared with the WT in the presence of high-B or GA3. Moreover, paclobatrazol treatment completely inhibited the increases in AtTIP5;1 transcripts induced by high-B, whereas GA3 application upregulated AtTIP5;1 expression in the WT. In addition, treatment with high-B remarkably elevated the expression levels of GA3ox1, GA20ox1 and GA20ox2 - key biosynthesis genes of GAs - in WT seedlings. The GA3 and GA4 content also increased in WT seedlings grown in MS medium containing high-B. Additionally, application of high-B failed to enhance AtTIP5;1 expression in the double mutant rga-24-gai-t6 of DELLA genes. Together, these results suggest that AtTIP5;1 is an essential downstream target of GAs. High-B induces the accumulation of GAs, which activates AtTIP5;1 through modulation of the DELLA proteins Repressor of ga1-3 and GA-insensitive, further promoting hypocotyl elongation in A. thaliana.
水通道蛋白在植物的生长和发育过程中发挥着重要作用，包括茎的伸长。液泡膜水通道蛋白AtTIP5;1被认为在拟南芥中高硼浓度（高硼）条件下正向调节下胚轴伸长。然而，这一过程背后的机制仍未得到解答。在这里，我们表明，多效唑（一种赤霉素生物合成抑制剂）显著抑制了野生型（WT）幼苗的下胚轴细胞伸长，并且在高硼胁迫下更强烈地抑制了AtTIP5;1过表达植株的下胚轴细胞伸长。与野生型相比，在高硼或赤霉素GA3存在的情况下，两个AtTIP5;1基因敲除突变体的下胚轴上部细胞伸长受阻。此外，多效唑处理完全抑制了高硼诱导的AtTIP5;1转录本增加，而GA3处理上调了野生型中AtTIP5;1的表达。此外，高硼处理显著提高了野生型幼苗中GA3ox1、GA20ox1和GA20ox2（赤霉素关键生物合成基因）的表达水平。在含有高硼的MS培养基中生长的野生型幼苗中，GA3和GA4含量也增加。此外，在DELLA基因的双突变体rga - 24 - gai - t6中，高硼处理未能增强AtTIP5;1的表达。总之，这些结果表明AtTIP5;1是赤霉素的一个重要下游靶点。高硼诱导赤霉素积累，通过调节DELLA蛋白ga1 - 3的阻遏物和对赤霉素不敏感的蛋白来激活AtTIP5;1，进一步促进拟南芥下胚轴伸长。
