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NGATHA 活性改变对拟南芥雌蕊中生长素信号通路的影响。

The effect of NGATHA altered activity on auxin signaling pathways within the Arabidopsis gynoecium.

机构信息

Consejo Superior de Investigaciones Científicas - Instituto de Biología Molecular y Celular de Plantas (CSIC-UPV) Valencia, Spain.

Consejo Superior de Investigaciones Científicas - Instituto de Biología Molecular y Celular de Plantas (CSIC-UPV) Valencia, Spain ; Department of Plant Sciences, Faculdade de Agronomia Eliseu Maciel, Plant Genomics and Breeding Center, Universidade Federal de Pelotas Pelotas, Brasil.

出版信息

Front Plant Sci. 2014 May 21;5:210. doi: 10.3389/fpls.2014.00210. eCollection 2014.

DOI:10.3389/fpls.2014.00210
PMID:24904608
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4033193/
Abstract

The four NGATHA genes (NGA) form a small subfamily within the large family of B3-domain transcription factors of Arabidopsis thaliana. NGA genes act redundantly to direct the development of the apical tissues of the gynoecium, the style, and the stigma. Previous studies indicate that NGA genes could exert this function at least partially by directing the synthesis of auxin at the distal end of the developing gynoecium through the upregulation of two different YUCCA genes, which encode flavin monooxygenases involved in auxin biosynthesis. We have compared three developing pistil transcriptome data sets from wildtype, nga quadruple mutants, and a 35S::NGA3 line. The differentially expressed genes showed a significant enrichment for auxin-related genes, supporting the idea of NGA genes as major regulators of auxin accumulation and distribution within the developing gynoecium. We have introduced reporter lines for several of these differentially expressed genes involved in synthesis, transport and response to auxin in NGA gain- and loss-of-function backgrounds. We present here a detailed map of the response of these reporters to NGA misregulation that could help to clarify the role of NGA in auxin-mediated gynoecium morphogenesis. Our data point to a very reduced auxin synthesis in the developing apical gynoecium of nga mutants, likely responsible for the lack of DR5rev::GFP reporter activity observed in these mutants. In addition, NGA altered activity affects the expression of protein kinases that regulate the cellular localization of auxin efflux regulators, and thus likely impact auxin transport. Finally, protein accumulation in pistils of several ARFs was differentially affected by nga mutations or NGA overexpression, suggesting that these accumulation patterns depend not only on auxin distribution but could be also regulated by transcriptional networks involving NGA factors.

摘要

四个 NGATHA 基因(NGA)在拟南芥 B3 结构域转录因子大家族中形成一个小亚家族。NGA 基因通过上调两个不同的编码参与生长素生物合成的黄素单加氧酶的 YUCCA 基因,在雌蕊发育的远端指导生长素的合成,从而冗余地指导雌蕊的顶端组织、花柱和柱头的发育。先前的研究表明,NGA 基因至少可以通过这种方式发挥作用,通过上调两个不同的编码参与生长素生物合成的黄素单加氧酶的 YUCCA 基因,在雌蕊发育的远端指导生长素的合成。我们比较了来自野生型、nga 四重突变体和 35S::NGA3 系的三个发育中的雌蕊转录组数据集。差异表达的基因显著富集了与生长素相关的基因,支持了 NGA 基因作为生长素在发育中的雌蕊中积累和分布的主要调节剂的观点。我们已经在 NGA 功能获得和功能丧失背景下引入了几个参与生长素合成、运输和响应的差异表达基因的报告基因系。我们在这里介绍了这些报告基因对 NGA 失调反应的详细图谱,这有助于阐明 NGA 在生长素介导的雌蕊形态发生中的作用。我们的数据表明,nga 突变体中发育中的顶端雌蕊生长素合成减少,这可能是这些突变体中观察到的 DR5rev::GFP 报告基因活性缺乏的原因。此外,NGA 改变的活性影响调节生长素外排调节剂细胞定位的蛋白激酶的表达,因此可能影响生长素运输。最后,几个 ARFs 的蛋白积累在 nga 突变或 NGA 过表达时受到不同影响,这表明这些积累模式不仅依赖于生长素的分布,还可能受到涉及 NGA 因子的转录网络的调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/8cb8c6c41cf7/fpls-05-00210-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/528b5e2de547/fpls-05-00210-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/29599e0fd394/fpls-05-00210-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/d97cc8464875/fpls-05-00210-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/a9b052771b9d/fpls-05-00210-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/3a7b7ee38523/fpls-05-00210-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/8cb8c6c41cf7/fpls-05-00210-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/528b5e2de547/fpls-05-00210-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/29599e0fd394/fpls-05-00210-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/d97cc8464875/fpls-05-00210-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/a9b052771b9d/fpls-05-00210-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/3a7b7ee38523/fpls-05-00210-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/701c/4033193/8cb8c6c41cf7/fpls-05-00210-g0006.jpg

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