水稻抗丙环唑的1-D突变体通过激活DPb转录因子的表达,促进水稻种子产量增加

植物生物学  |   2021-01-06 12:27

来源:植物生物学

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油菜素类固醇(BR)生物合成或信号通路缺陷的突变体通常表现出半矮化,就像促成绿色革命的高产赤霉素突变体一样。然而,BR突变体的营养生长减少并不一定对应于种子产量的增加。

为了更好地理解BR的作用方式,我们在BR生物合成抑制剂丙环唑(Pcz)存在下,通过筛选一个激活标签突变体群体,分离了一个水稻丙环唑抗性1-D(pzr1-D)突变体。在pzr1-D中,与拟南芥二聚化伙伴(DPb)同源的转录因子基因的表达被激活。pzr1-D表现出特征性的表型,如高度降低、种子产量和分蘖数增加。与拟南芥DPb一样,水稻PZR1在所检测的组织中也有不同的表达。

此外,pzr1-D显示出改变的细胞分裂表型,包括产生小的愈伤组织。此外,突变体根和叶的细胞数量和大小与同龄野生型植物不同。

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RNA测序显示,差异表达基因的启动子富含BZR1和EF-DPb转录因子的同源序列,表明PZR1在BR介导的水稻细胞分裂中起作用。因此,我们可以操纵PZR1表达来增加水稻种子的产量。

Mutants defective in brassinosteroid (BR) biosynthesis or signaling pathways often display semi-dwarfism, as do the highly productive gibberellin mutants that enabled the Green Revolution. However, reduced vegetative growth in BR mutants does not necessarily correspond to increased seed yields. To better understand the mode of action of BR, we isolated a rice propiconazole resistant1-D (pzr1-D) mutant by screening an activation-tagging mutant population in the presence of the BR biosynthesis inhibitor propiconazole (Pcz). The expression of a putative transcription factor gene homologous to Arabidopsis Dimerization Partner (DPb) was activated in pzr1-D. pzr1-D exhibited characteristic phenotypes such as reduced height, and increased seed yields and tiller numbers. Like Arabidopsis DPb, rice PZR1 is expressed differentially in the tissues examined. Furthermore, pzr1-D displayed altered cell division phenotypes, including the production of small calli. In addition, the cell number and size in mutant roots and leaves differed from those in wild-type plants of the same age. RNA sequencing revealed that the promoters of differentially expressed genes are enriched with cognate sequences for both BZR1 and EF-DPb transcription factors, suggesting that PZR1 functions in BR-mediated cell division in rice. PZR1 expression may thus be manipulated to increase seed yield in economically important rice varieties.  

来源:PlantBiotech 植物生物学

原文链接:http://mp.weixin.qq.com/s?__biz=MzI5NTk2MTcyOA==&mid=2247494589&idx=6&sn=4850fe5485dcef4e5c9193f2ae0408d2

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