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拟南芥类成束蛋白阿拉伯半乳聚糖蛋白4基因与脱落酸信号协同作用以控制根的生长。

The Arabidopsis thaliana FASCICLIN LIKE ARABINOGALACTAN PROTEIN 4 gene acts synergistically with abscisic acid signalling to control root growth.

作者信息

Seifert Georg J, Xue Hui, Acet Tuba

机构信息

University of Natural Resources and Life Science, Vienna, Austria; Department of Applied Genetics and Cell Biology, Muthgasse 18, A-1990 Vienna, Austria

University of Natural Resources and Life Science, Vienna, Austria; Department of Applied Genetics and Cell Biology, Muthgasse 18, A-1990 Vienna, Austria.

出版信息

Ann Bot. 2014 Oct;114(6):1125-33. doi: 10.1093/aob/mcu010. Epub 2014 Mar 5.

Abstract

BACKGROUND AND AIMS

The putative FASCICLIN-LIKE ARABINOGALACTAN PROTEIN 4 (At-FLA4) locus of Arabidopsis thaliana has previously been shown to be required for the normal growth of wild-type roots in response to moderately elevated salinity. However, the genetic and physiological pathway that connects At-FLA4 and normal root growth remains to be elucidated.

METHODS

The radial swelling phenotype of At-fla4 was modulated with growth regulators and their inhibitors. The relationship of At-FLA4 to abscisic acid (ABA) signalling was analysed by probing marker gene expression and the observation of the At-fla4 phenotype in combination with ABA signalling mutants.

KEY RESULTS

Application of ABA suppresses the non-redundant role of At-FLA4 in the salt response. At-FLA4 positively regulates the response to low ABA concentration in roots and is required for the normal expression of ABA- and abiotic stress-induced genes. The At-fla4 phenotype is enhanced in the At-abi4 background, while two genetic suppressors of ABA-induced gene expression are required for salt oversensitivity of At-fla4. Salt oversensitivity in At-fla4 is suppressed by the CYP707A inhibitor abscinazole E2B, and salt oversensitivity in At-fla4 roots is phenocopied by chemical inhibition of ABA biosynthesis.

CONCLUSIONS

The predicted lipid-anchored glycoprotein At-FLA4 positively regulates cell wall biosynthesis and root growth by modulating ABA signalling.

摘要

背景与目的

拟南芥假定的类成束蛋白阿拉伯半乳聚糖蛋白4(At-FLA4)位点先前已被证明是野生型根在盐度适度升高时正常生长所必需的。然而,连接At-FLA4与正常根生长的遗传和生理途径仍有待阐明。

方法

用生长调节剂及其抑制剂调节At-fla4的径向肿胀表型。通过探测标记基因表达以及结合ABA信号突变体观察At-fla4表型,分析At-FLA4与脱落酸(ABA)信号的关系。

关键结果

ABA的应用抑制了At-FLA4在盐反应中的非冗余作用。At-FLA4正向调节根对低ABA浓度的反应,并且是ABA和非生物胁迫诱导基因正常表达所必需的。At-fla4表型在At-abi4背景中增强,而At-fla4对盐超敏感需要两个ABA诱导基因表达的遗传抑制子。At-fla4中的盐超敏感性被CYP707A抑制剂脱落唑E2B抑制,并且At-fla4根中的盐超敏感性通过化学抑制ABA生物合成得以模拟。

结论

预测的脂锚定糖蛋白At-FLA4通过调节ABA信号正向调节细胞壁生物合成和根生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c98/4195540/80499bc3cdf1/mcu01001.jpg

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