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类成束蛋白阿拉伯半乳聚糖蛋白4以及呼吸爆发氧化酶同源物D和F独立调节脱落酸信号传导。

FASCICLIN LIKE ARABINOGALACTAN PROTEIN 4 and RESPIRATORY BURST OXIDASE HOMOLOG D and F independently modulate abscisic acid signaling.

作者信息

Xue Hui, Seifert Georg J

机构信息

a Department of Applied Genetics and Cell Biology; University of Natural Resources and Life Science ; Vienna , Austria.

出版信息

Plant Signal Behav. 2015;10(2):e989064. doi: 10.4161/15592324.2014.989064.

Abstract

We previously suggested that At-FLA4 and ABA signaling act in synergy. Reactive oxygen species generated from the NADPH oxidases At-RBOHD and At-RBOHF play an important role in cell wall integrity control and ABA signaling and here we investigate their role for the At-FLA4 pathway. We find that in the At-fla4 At-rbohD At-rbohF triple mutant the root phenotype of At-fla4 is enhanced. Moreover, the abnormally high level of reactive oxygen species in At-fla4 mutant does not depend on AtRBOHD and -F. Likewise, suppression of the At-fla4 phenotype by ABA does not depend on the 2 oxidases. Consistent with their lack of effect on ROS level in At-fla4, transcript level of AtRBOHD and -F is reduced in the At-fla4 mutant background. Taken together, our findings suggest that neither At-RBOHD nor At-RBOHF is involved in the synergism between ABA and At-FLA4. Consistently, the oxidases and At-FLA4 act independently of each other in ROS control.

摘要

我们之前曾提出,At-FLA4与脱落酸(ABA)信号传导协同发挥作用。由NADPH氧化酶At-RBOHD和At-RBOHF产生的活性氧在细胞壁完整性控制和ABA信号传导中起重要作用,在此我们研究它们在At-FLA4途径中的作用。我们发现,在At-fla4 At-rbohD At-rbohF三突变体中,At-fla4的根表型增强。此外,At-fla4突变体中异常高水平的活性氧并不依赖于AtRBOHD和AtRBOHF。同样,ABA对At-fla4表型的抑制也不依赖于这两种氧化酶。与它们对At-fla4中活性氧水平缺乏影响一致,在At-fla4突变体背景下,AtRBOHD和AtRBOHF的转录水平降低。综上所述,我们的研究结果表明,At-RBOHD和At-RBOHF均不参与ABA与At-FLA4之间的协同作用。一致地,这些氧化酶和At-FLA4在活性氧控制中相互独立发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cca/4622830/d65ee8a50a5e/kpsb-10-02-989064-g001.jpg

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