Evidence map›Paper›PMID 33036282›Full record

ArticleInternational journal of molecular sciences2020

Effects of Host-Adaptive Mutations on Hop Stunt Viroid Pathogenicity and Small RNA Biogenesis.

Zhixiang Zhang, Changjian Xia, Takahiro Matsuda, Akito Taneda, Fumiko Murosaki, Wanying Hou, Robert A Owens, Shifang Li, Teruo Sano

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2020. 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
–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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Progress in 50 years of viroid research-Molecular structure, pathogenicity, and host adaptation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021
    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

9 authors.

Zhixiang ZhangState Key Laboratory of Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Changjian XiaState Key Laboratory of Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Takahiro MatsudaPlant Pathology Laboratory, Faculty of Agriculture and Life Science, Hirosaki University, Bunkyo-cho 3, Hirosaki 036-8561, Japan.
Akito TanedaGraduate School of Science and Technology, Hirosaki University, Bunkyo-cho 3, Hirosaki 036-8561, Japan.
Fumiko MurosakiPlant Pathology Laboratory, Faculty of Agriculture and Life Science, Hirosaki University, Bunkyo-cho 3, Hirosaki 036-8561, Japan.
Wanying HouState Key Laboratory of Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Robert A OwensMolecular Plant Pathology Laboratory, USDA/ARS, Beltsville, MD 20705, USA.
Shifang LiState Key Laboratory of Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Teruo SanoPlant Pathology Laboratory, Faculty of Agriculture and Life Science, Hirosaki University, Bunkyo-cho 3, Hirosaki 036-8561, Japan.

Funding

Japan Society for the Promotion of Science (JSPS) KAKENHI 15H04455 and 18H0221the National Natural Science Foundation of China 31401714 and 31670149
6 · The paper itself

Abstract

Accidental transmission of hop stunt viroid (HSVd) from grapevine to hop has led to several epidemics of hop stunt disease with convergent evolution of HSVd-g(rape) into HSVd-h(op) containing five mutations. However, the biological function of these five mutations remains unknown. In this study, we compare the biological property of HSVd-g and HSVd-h by bioassay and analyze HSVd-specific small RNA (HSVd-sRNA) using high-throughput sequencing. The bioassay indicated an association of these five mutations with differences in infectivity, replication capacity, and pathogenicity between HSVd-g and HSVd-h, e.g., HSVd-g induced more severe symptoms than HSVd-h in cucumber. Site-directed mutagenesis of HSVd-g showed that the mutation at position 54 increased pathogenicity. HSVd-sRNA analysis of cucumber and hop plants infected with different HSVd variants showed that several sRNA species containing adaptive nucleotides were specifically down-regulated in plants infected with HSVd-h. Several HSVd-sRNAs containing adaptive mutations were predicted to target cucumber genes, but changes in the levels of these genes were not directly correlated with changes in symptom expression. Furthermore, expression levels of two other cucumber genes targeted by HSVd-RNAs, encoding ethylene-responsive transcription factor ERF011, and trihelix transcription factor GTL2, were altered by HSVd infection. The possible relationship between these two genes to HSVd pathogenicity is discussed.

Indexed as

MutationRNA, CircularCucumis sativusHigh-Throughput Nucleotide SequencingHumulusPlant DiseasesPlant VirusesSequence Analysis, RNARNA, Circularcircular RNAhopnon-coding RNARNA silencingsmall RNAviroid

Identifiers

PMID33036282
PMCPMC7582576

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.