Evidence map›Paper›PMID 30406469›Full record

ArticlePlant molecular biology2018

Trithorax-group protein ATX5 mediates the glucose response via impacting the HY1-ABI4 signaling module.

Yutong Liu, Jie Wang, Hao Yin, Ai Zhang, Shuangzhan Huang, Tian-Jing Wang, Qingxiang Meng, Nan Nan, Yifan Wu, Peng Guo and 3 more

Abstract read
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In one paragraph

Article in Plant molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. PARP1 Hinders Histone H2B Occupancy at the NFATc1 Promoter to Restrain Osteoclast Differentiation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
    Article
  7. Review
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Yutong LiuKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Jie WangKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Hao YinKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Ai ZhangKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Shuangzhan HuangKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Tian-Jing WangKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Qingxiang MengKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Nan NanKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Yifan WuKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Peng GuoKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Rafiq AhmadKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China.
Bao LiuKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China. baoliu@nenu.edu.cn.
Zheng-Yi XuKey Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, Changchun, 130024, People's Republic of China. xuzy100@nenu.edu.cn.

Funding

Fundamental Research Funds for the Central Universities #2412018BJ002National Key Research and Development Program of China 2016YFD0102003National Natural Science Foundation of China 31601311National Natural Science Foundation of China 31771352Natural Science Foundation of Jilin Province of China 20180101233JC
6 · The paper itself

Abstract

key messageTrithorax-group Protein ARABIDOPSIS TRITHORAX5 modulates the glucose response. Glucose is an evolutionarily conserved modulator from unicellular microorganisms to multicellular animals and plants. Extensive studies have shown that the Trithorax-group proteins (TrxGs) play essential roles in different biological processes by affecting histone modifications and chromatin structures. However, whether TrxGs function in the glucose response and how they achieve the control of target genes in response to glucose signaling in plants remain unknown. Here, we show that the Trithorax-group Protein ARABIDOPSIS TRITHORAX5 (ATX5) affects the glucose response and signaling. atx5 loss-of-function mutants display glucose-oversensitive phenotypes compared to the wild-type (WT). Genome-wide RNA-sequencing analyses have revealed that ATX5 impacts the expression of a subset of glucose signaling responsive genes. Intriguingly, we have established that ATX5 directly controls the expression of HY1 by trimethylating H3 lysine 4 of the Arabidopsis Heme Oxygenase1 (HY1) locus. Glucose signaling causes the suppression of ATX5 activity and subsequently reduces the H3K4me3 levels at the HY1 locus, thereby leading to the increased expression of ABSCISIC ACID-INSENSITIVE4 (ABI4). This result suggests that an important ATX5-HY1-ABI4 regulatory module governs the glucose response. This idea is further supported by genetic evidence showing that an atx5 hy1-100 abi4 triple mutant showed a similar glucose-insensitive phenotype as compared to that of the abi4 single mutant. Our findings show that a novel ATX5-HY1-ABI4 module controls the glucose response in Arabidopsis thaliana.

Indexed as

Signal TransductionAbscisic AcidArabidopsisArabidopsis ProteinsGene Expression Regulation, PlantGlucoseHeme Oxygenase (Decyclizing)Histone-Lysine N-MethyltransferaseMutationPhenotypePlant Growth RegulatorsTranscription FactorsABI4 protein, ArabidopsisAbscisic AcidArabidopsis ProteinsATX5 protein, ArabidopsisGlucoseHeme Oxygenase (Decyclizing)Histone-Lysine N-MethyltransferaseHY1 protein, ArabidopsisPlant Growth RegulatorsTranscription FactorsArabidopsis thalianaChromatin immunoprecipitationGlucose signalingHistone methyltransferaseRNA-sequencingTranscriptional regulation

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.