Arabidopsis Sucrose Transporter AtSuc1 introns act as strong enhancers of expression

Arabidopsis Sucrose Transporter AtSuc1 introns act as strong enhancers of expression
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DOI:
10.1093/pcp/pcaa029
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发表时间:
2020-06-01
影响因子:
4.9
通讯作者:
Ward, John M.
Ward, John M.
中科院分区:
生物学2区
文献类型:
--
作者:
Lasin, Praphapan;Weise, Andreas;Ward, John M.

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AtSUC 1的表达受启动子和基因内序列控制。AtSUC 1在根、花粉和毛状体中表达。然而,AtSUC 1启动子-GUS转基因仅在毛状体和花粉中表达。在这里,我们表明,AtSUC 1的根的表达是由AtSUC 1启动子和两个短内含子之间的相互作用控制。从全基因-GUS构建体中删除任一内含子导致没有根表达,表明两个内含子都是必需的。两个内含子串联,融合到GUS,在整个植物的营养部分产生高组成型表达。当与启动子组合时,由内含子驱动的表达减少并定位于根部。在拟南芥幼苗中,外源施加的蔗糖诱导AtSUC 1在根中的表达,并导致花青素积累。atsuc 1功能缺失突变体在蔗糖诱导的花青素苷积累中有缺陷。我们表明,AtSUC 1全基因GUS构建表达的非功能性AtSUC 1(D152 N)突变体,这是运输失活,是有缺陷的蔗糖诱导的AtSUC 1表达时,在atsuc 1空背景表达。我们还表明,运输缺陷的等位基因不补充损失的蔗糖诱导的花青素积累无效atsuc 1突变体。结果表明,蔗糖诱导的AtSUC 1表达和蔗糖诱导的花青素苷积累所需的蔗糖通过AtSUC 1的吸收和蔗糖检测的网站是细胞内。
The expression of AtSUC1 is controlled by the promoter and intragenic sequences. AtSUC1 is expressed in roots, pollen and trichomes. However, AtSUC1 promoter-GUS transgenics only show expression in trichomes and pollen. Here, we show that the root expression of AtSUC1 is controlled by an interaction between the AtSUC1 promoter and two short introns. The deletion of either intron from whole-gene-GUS constructs results in no root expression, showing that both introns are required. The two introns in tandem, fused to GUS, produce high constitutive expression throughout the vegetative parts of the plant. When combined with the promoter, the expression driven by the introns is reduced and localized to the roots. In Arabidopsis seedlings, exogenously applied sucrose induces the expression of AtSUC1 in roots and causes anthocyanin accumulation. atsuc1 loss-offunction mutants are defective in sucrose-induced anthocyanin accumulation. We show that an AtSUC1 whole-gene-GUS construct expressing a nonfunctional AtSUC1 (D152N) mutant, that is transport inactive, is defective in sucrose-induced AtSUC1 expression when expressed in an atsuc1-null background. We also show that the transport-defective allele does not complement the loss of sucrose-induced anthocyanin accumulation in null atsuc1 mutants. The results indicate that sucrose uptake via AtSUC1 is required for sucrose-induced AtSUC1 expression and sucrose-induced anthocyanin accumulation and that the site for sucrose detection is intracellular.