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ERF022通过乙烯相关途径影响拟南芥体细胞胚胎发生的诱导。

ERF022 impacts the induction of somatic embryogenesis in Arabidopsis through the ethylene-related pathway.

作者信息

Nowak Katarzyna, Wójcikowska Barbara, Gaj Małgorzata D

机构信息

Department of Genetics, University of Silesia, Jagiellonska 28, 40-032, Katowice, Poland.

出版信息

Planta. 2015 Apr;241(4):967-85. doi: 10.1007/s00425-014-2225-9. Epub 2014 Dec 23.

DOI:10.1007/s00425-014-2225-9
PMID:25534944
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4361773/
Abstract

The ERF022 gene was found to affect embryogenic transition in somatic cells in Arabidopsis via the ethylene-related pathway. The study provides evidence that ERF022 - LEC2 interaction is involved in the auxin-ethylene crosstalk that operates in somatic embryogenesis induction. The ERF022 gene of the ERF family was previously identified among the transcription factor genes that were differentially expressed in an embryogenic culture of Arabidopsis. A strong inhibition of the gene was found to be associated with the induction of somatic embryogenesis (SE) and an erf022 mutant was indicated to display a substantially impaired capacity for SE. Therefore, the molecular function of ERF022 in the induction of SE was studied in the present work. A phenotype of an erf022 mutant was indicated as being related to an increased content of ethylene. The results further suggest that the ERF022 controls the genes that are involved in both the biosynthesis (ACS7) and signalling (ERF1, ETR1) of ethylene and indicate that the ERF022 is a new regulatory element in ethylene-related responses that negatively control the ethylene content and perception. It is proposed that the negative impact of ethylene on the induction of SE may result from a modulation of the auxin-related genes that control the embryogenic transition in somatic cells. Among them, the LEC2, which is a key regulator of the induction of SE through the stimulation of auxin synthesis, was possibly related to ERF022. The results of the study provide new hormone-related clues to define the genetic network that governs SE. A putative model of the regulatory pathway is proposed that is involved in the induction of SE in which the auxin-ethylene interactions are controlled by ERF022 and LEC2 and their targets.

摘要

研究发现,ERF022基因通过乙烯相关途径影响拟南芥体细胞的胚性转变。该研究提供了证据,表明ERF022与LEC2的相互作用参与了体细胞胚胎发生诱导过程中的生长素 - 乙烯信号转导。ERF家族的ERF022基因先前在拟南芥胚性培养中差异表达的转录因子基因中被鉴定出来。研究发现该基因的强烈抑制与体细胞胚胎发生(SE)的诱导有关,并且表明erf022突变体的SE能力严重受损。因此,本研究对ERF022在SE诱导中的分子功能进行了研究。erf022突变体的表型表明与乙烯含量增加有关。结果进一步表明,ERF022控制参与乙烯生物合成(ACS7)和信号转导(ERF1、ETR1)的基因,并表明ERF022是乙烯相关反应中的一个新的调控元件,对乙烯含量和感知起负调控作用。研究提出,乙烯对SE诱导的负面影响可能是通过调节控制体细胞胚性转变的生长素相关基因实现的。其中,LEC2是通过刺激生长素合成来诱导SE的关键调节因子,可能与ERF022有关。该研究结果为定义控制SE的遗传网络提供了新的激素相关线索。提出了一个参与SE诱导的调控途径的推测模型,其中生长素 - 乙烯相互作用由ERF022和LEC2及其靶标控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/7a20a235a399/425_2014_2225_Fig12_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/acd1a2f6684c/425_2014_2225_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/1533bd364890/425_2014_2225_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/13d898bf1435/425_2014_2225_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/9f804fbfe35a/425_2014_2225_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/75962334c78d/425_2014_2225_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/937aff21c137/425_2014_2225_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/3a649d4fc5e5/425_2014_2225_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/78eec7e1a812/425_2014_2225_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/a9439f65f460/425_2014_2225_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/e5e605d6b87b/425_2014_2225_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/7a20a235a399/425_2014_2225_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/8ab6555422a4/425_2014_2225_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/acd1a2f6684c/425_2014_2225_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/1533bd364890/425_2014_2225_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/13d898bf1435/425_2014_2225_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/9f804fbfe35a/425_2014_2225_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/75962334c78d/425_2014_2225_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/937aff21c137/425_2014_2225_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/3a649d4fc5e5/425_2014_2225_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/78eec7e1a812/425_2014_2225_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/a9439f65f460/425_2014_2225_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/e5e605d6b87b/425_2014_2225_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c93/4361773/7a20a235a399/425_2014_2225_Fig12_HTML.jpg

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