Wang Haihai, Tang Renjie, Wang Cuiting, Qi Qi, Gai Ying, Jiang Xiangning, Zhang Hongxia
National Key Laboratory of Plant Molecular Genetics, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, 300 Fenglin Road, Shanghai 200032, China.
National Key Laboratory of Plant Molecular Genetics, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, 300 Fenglin Road, Shanghai 200032, China Present address: Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720, USA.
Tree Physiol. 2015 Jan;35(1):95-105. doi: 10.1093/treephys/tpu100. Epub 2014 Dec 15.
Using chimeric repressor silencing technology, we previously reported that functional repression of PtSND2 severely arrested wood formation in transgenic poplar (Populus). Here, we provide further evidence that auxin biosynthesis, transport and signaling were disturbed in these transgenic plants, leading to pleiotropic defects in their growth patterns, including inhibited leaf enlargement and vascular tissue development in the leaf central vein, suppressed cambial growth and fiber elongation in the stem, and arrested growth in the root system. Two transgenic lines, which displayed the most remarkable phenotypic deviation from the wild-type, were selected for detailed studies. In both transgenic lines, expression of genes for auxin biosynthesis, transport and signaling was down-regulated, and indole-3-acetic acid distribution was severely disturbed in the apical buds, leaves, stems and roots of field-grown transgenic plants. Transient transcription dual-luciferase assays of ProPtTYDC2::LUC, ProPttLAX2::LUC and ProPoptrIAA20.2::LUC in poplar protoplasts revealed that expression of auxin-related genes might be regulated by PtSND2 at the transcriptional level. All these results indicate that functional repression of PtSND2 altered auxin biosynthesis, transport and signaling, and thereby disturbed the normal growth and development of transgenic plants.
利用嵌合阻遏物沉默技术,我们之前报道过,在转基因杨树(Populus)中,PtSND2的功能抑制严重阻碍了木材形成。在此,我们提供进一步的证据表明,这些转基因植物中的生长素生物合成、运输和信号传导受到干扰,导致其生长模式出现多效性缺陷,包括叶片增大受抑制、叶片中央叶脉的维管组织发育受阻、茎中形成层生长和纤维伸长受抑制以及根系生长停滞。选择了两个与野生型表现出最显著表型差异的转基因株系进行详细研究。在这两个转基因株系中,生长素生物合成、运输和信号传导相关基因的表达均下调,并且在田间种植的转基因植物的顶芽、叶片、茎和根中,吲哚 - 3 - 乙酸分布严重紊乱。在杨树原生质体中对ProPtTYDC2::LUC、ProPttLAX2::LUC和ProPoptrIAA20.2::LUC进行瞬时转录双荧光素酶测定,结果表明生长素相关基因的表达可能在转录水平上受PtSND2调控。所有这些结果表明,PtSND2的功能抑制改变了生长素的生物合成、运输和信号传导,从而扰乱了转基因植物的正常生长和发育。