Evidence map›Paper›PMID 32277429›Full record

ArticlePlant molecular biology2020

SUPPRESSOR OF GAMMA RESPONSE 1 acts as a regulator coordinating crosstalk between DNA damage response and immune response in Arabidopsis thaliana.

Kaoru Okamoto Yoshiyama, Naoki Aoshima, Naoki Takahashi, Tomoaki Sakamoto, Kei Hiruma, Yusuke Saijo, Jun Hidema, Masaaki Umeda, Seisuke Kimura

Abstract read
PubMed Publisher
In one paragraph

Article in Plant molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Molecular Mechanisms ofInternational journal of molecular sciences · 2026
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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

9 authors at 3 institutions in 1 country.

Kaoru Okamoto YoshiyamaGraduate School of Life Sciences, Tohoku University, 2-1-1 Katahira, Aoba-ku, Sendai, 980-8577, Japan.ORCID http://orcid.org/0000-0002-8115-4778
Naoki AoshimaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.
Naoki TakahashiGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.
Tomoaki SakamotoLife Sciences, Kyoto Sangyo University, Kamigamo Motoyama Kitaku, Kyoto, 603-8555, Japan.
Kei HirumaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.
Yusuke SaijoGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.
Jun HidemaGraduate School of Life Sciences, Tohoku University, 2-1-1 Katahira, Aoba-ku, Sendai, 980-8577, Japan.
Masaaki UmedaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara, 630-0192, Japan.
Seisuke KimuraLife Sciences, Kyoto Sangyo University, Kamigamo Motoyama Kitaku, Kyoto, 603-8555, Japan. seisuke@cc.kyoto-su.ac.jp.ORCID http://orcid.org/0000-0002-6796-3675
Nara Institute of Science and Technology · JPKyoto Sangyo University · JPTohoku University · JP

Funding

Japan science and technology agency JPMJPR16Q7Japan Society for the Promotion of Science 15H05945Japan Society for the Promotion of Science 16H01472Japan Society for the Promotion of Science 16K07408Japan Society for the Promotion of Science 16KT0031Japan Society for the Promotion of Science 17H01872Japan Society for the Promotion of Science 17H03965Japan Society for the Promotion of Science 17H06470Japan Society for the Promotion of Science 17H06477Japan Society for the Promotion of Science 17K07455Japan Society for the Promotion of Science 18H02467Japan Society for the Promotion of Science 18H04787Japan Society for the Promotion of Science 18H04822Japan Society for the Promotion of Science 18H04844Japan Society for the Promotion of Science 19K06708MEXT S1511023Sumitomo Foundation 181147
6 · The paper itself

Abstract

Plants live in constantly changing and often unfavorable or stressful environments. Environmental changes induce biotic and abiotic stress, which, in turn, may cause genomic DNA damage. Hence, plants simultaneously suffer abiotic/biotic stress and DNA damage. However, little information is available on the signaling crosstalk that occurs between DNA damage and abiotic/biotic stresses. Arabidopsis thaliana SUPPRESSOR OF GAMMA RESPONSE1 (SOG1) is a pivotal transcription factor that regulates thousands of genes in response to DNA double-strand break (DSB), and we recently reported that SOG1 has a role in immune responses. In the present study, the effects of SOG1 overexpression on the DNA damage and immune responses were examined. Results found that SOG1 overexpression enhances the regulation of numerous downstream genes. Relative to the wild type plants, then, DNA damage responses were observed to be strongly induced. SOG1 overexpression also upregulates chitin (a major components of fungal cell walls) responsive genes in the presence of DSBs, implying that pathogen defense response is activated by DNA damage via SOG1. Further, SOG1 overexpression enhances fungal resistance. These results suggest that SOG1 regulates crosstalk between DNA damage response and the immune response and that plants have evolved a sophisticated defense network to contend with environmental stress.

Indexed as

ApoptosisArabidopsisArabidopsis ProteinsBase SequenceDNA DamageDNA, PlantGene Expression Regulation, PlantPlant LeavesProtein BindingStress, PhysiologicalTranscription FactorsArabidopsis ProteinsDNA, PlantSOG1 protein, ArabidopsisTranscription FactorsChitinDNA damage responseDNA double-strand breakDNA repairImmune responseSOG1

Identifiers

PMID32277429
OpenAlexW3015855475

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.