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在拟南芥中,APETALA2在调控花干细胞过程中拮抗AGAMOUS的转录活性。

APETALA2 antagonizes the transcriptional activity of AGAMOUS in regulating floral stem cells in Arabidopsis thaliana.

作者信息

Huang Zhigang, Shi Ting, Zheng Binglian, Yumul Rae Eden, Liu Xigang, You Chenjiang, Gao Zhihong, Xiao Langtao, Chen Xuemei

机构信息

Hunan Provincial Key Laboratory of Phytohormones and Growth Development, Hunan Provincial Key Laboratory for Crop Germplasm Innovation and Utilization, Hunan Agricultural University, Changsha, 410128, China.

Department of Botany and Plant Sciences, Institute of Integrative Genome Biology, University of California, Riverside, CA, 92521, USA.

出版信息

New Phytol. 2017 Aug;215(3):1197-1209. doi: 10.1111/nph.14151. Epub 2016 Sep 8.

Abstract

APETALA2 (AP2) is best known for its function in the outer two floral whorls, where it specifies the identities of sepals and petals by restricting the expression of AGAMOUS (AG) to the inner two whorls in Arabidopsis thaliana. Here, we describe a role of AP2 in promoting the maintenance of floral stem cell fate, not by repressing AG transcription, but by antagonizing AG activity in the center of the flower. We performed a genetic screen with ag-10 plants, which exhibit a weak floral determinacy defect, and isolated a mutant with a strong floral determinacy defect. This mutant was found to harbor another mutation in AG and was named ag-11. We performed a genetic screen in the ag-11 background to isolate mutations that suppress the floral determinacy defect. Two suppressor mutants were found to harbor mutations in AP2. While AG is known to shut down the expression of the stem cell maintenance gene WUSCHEL (WUS) to terminate floral stem cell fate, AP2 promotes the expression of WUS. AP2 does not repress the transcription of AG in the inner two whorls, but instead counteracts AG activity.

摘要

APETALA2(AP2)因其在花的外两轮中的功能而最为人所知,在拟南芥中,它通过将AGAMOUS(AG)的表达限制在内两轮来决定萼片和花瓣的身份。在此,我们描述了AP2在促进花干细胞命运维持中的作用,不是通过抑制AG转录,而是通过在花的中心拮抗AG活性来实现。我们用表现出较弱花确定性缺陷的ag-10植株进行了遗传筛选,并分离出一个具有较强花确定性缺陷的突变体。发现该突变体在AG中存在另一个突变,被命名为ag-11。我们在ag-11背景下进行了遗传筛选,以分离出抑制花确定性缺陷的突变。发现两个抑制突变体在AP2中存在突变。虽然已知AG会关闭干细胞维持基因WUSCHEL(WUS)的表达以终止花干细胞命运,但AP2会促进WUS的表达。AP2不会抑制内两轮中AG的转录,而是相反地对抗AG活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3cbf/5516154/68e1577674cd/NPH-215-1197-g001.jpg

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