Evidence map›Paper›PMID 30382816›Full record

ArticleBMC plant biology2018

Functional inactivation of OsGCNT induces enhanced disease resistance to Xanthomonas oryzae pv. oryzae in rice.

Xia Xu, Zheng Chen, Yong-Feng Shi, Hui-Mei Wang, Yan He, Lei Shi, Ting Chen, Jian-Li Wu, Xiao-Bo Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC plant biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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  5. International journal of molecular sciences · 2019
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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 1 institution in 1 country.

Xia XuState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Zheng ChenState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Yong-Feng ShiState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Hui-Mei WangState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Yan HeState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Lei ShiState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Ting ChenState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China.
Jian-Li WuState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China. beishangd@163.com.
Xiao-Bo ZhangState Key Laboratory of Rice Biology, Chinese National Center for Rice Improvement, China National Rice Research Institute, Hangzhou, 310006, China. 13989818328@163.com.ORCID http://orcid.org/0000-0002-1518-2287
China National Rice Research Institute · CN

Funding

Ministry of Science and Technology of the People's Republic of China 2016YFD0101104National Natural Science Foundation of China 31471572
6 · The paper itself

Abstract

backgroundSpotted-leaf mutants are important to reveal programmed cell death and defense-related pathways in rice. We previously characterized the phenotype performance of a rice spotted-leaf mutant spl21 and narrowed down the causal gene locus spl21(t) to an 87-kb region in chromosome 12 by map-based cloning.

resultWe showed that a single base substitution from A to G at position 836 in the coding sequence of Oryza sativa beta-1,6-N-acetylglucosaminyl transferase (OsGCNT), effectively mutating Tyr to Cys at position 279 in the translated protein sequence, was responsible for the spotted-leaf phenotype as it could be rescued by functional complementation. Compared to the wild type IR64, the spotted-leaf mutant spl21 exhibited loss of chlorophyll, breakdown of chloroplasts, down-regulation of photosynthesis-related genes, and up-regulation of senescence associated genes, which indicated that OsGCNT regulates premature leaf senescence. Moreover, the enhanced resistance to the bacterial leaf blight pathogen Xanthomonas oryzae pv. oryzae, up-regulation of pathogenesis-related genes and increased level of jasmonate which suggested that OsGCNT is a negative regulator of defense response in rice. OsGCNT was expressed constitutively in the leaves, sheaths, stems, roots, and panicles, and OsGCNT-GFP was localized to the Golgi apparatus. High throughput RNA sequencing analysis provided further evidence for the biological effects of loss of OsGCNT function on cell death, premature leaf senescence and enhanced disease resistance in rice. Thus, we demonstrated that the novel OsGCNT regulated rice innate immunity and immunity-associated leaf senescence probably by changing the jasmonate metabolic pathway.

conclusionsThese results reveal that a novel gene Oryza sativa beta-1,6-N-acetylglucosaminyl transferase (OsGCNT) is responsible for the spotted-leaf mutant spl21, and OsGCNT acts as a negative-regulator mediating defense response and immunity-associated premature leaf senescence probably by activating jasmonate signaling pathway.

Indexed as

Cell DeathCloning, MolecularCyclopentanesDisease ResistanceGene Expression Regulation, PlantHigh-Throughput Nucleotide SequencingHost-Pathogen InteractionsMutationOryzaOxylipinsPhylogenyPlant DiseasesPlant ImmunityPlant LeavesPlant ProteinsPlants, Genetically ModifiedCyclopentanesjasmonic acidOxylipinsPlant ProteinsDefense responseOryza sativa L.OsGCNTPremature leaf senescenceSpotted-leaf

Identifiers

PMID30382816
PMCPMC6211509
OpenAlexW2899235348

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.