Evidence map›Paper›PMID 25673143›Full record

ArticleTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik2015

Pl(17) is a novel gene independent of known downy mildew resistance genes in the cultivated sunflower (Helianthus annuus L.).

L L Qi, Y M Long, C C Jan, G J Ma, T J Gulya

Abstract read
PubMed Publisher
In one paragraph

Article in TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
12.4field-weighted citation impact, top 2% 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

23 citing papers in PubMed, 60 citations in OpenAlex.

  1. Introgression and targeting of the PlTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2023
    Article
  2. Article
  3. Article
  4. Characterization and mapping of a downy mildew resistance gene,Molecular breeding : new strategies in plant improvement · 2022
    Article
  5. Genetic and physiological characterization of sunflower resistance provided by the wild-derived OrTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2022
    Article
  6. Article
  7. Article
  8. High-Density Mapping and Candidate Gene Analysis ofInternational journal of molecular sciences · 2020
    Article
  9. Article
  10. Diversification of the downy mildew resistance gene pool by introgression of a new gene, PlTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. High-throughput genotyping-by-sequencing facilitates molecular tagging of a novel rust resistance gene, RTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2018
    Article
  15. Article
  16. Article
  17. Genotyping-by-sequencing targeting of a novel downy mildew resistance gene PlTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2017
    Article
  18. Article
  19. Review
  20. Discovery and introgression of the wild sunflower-derived novel downy mildew resistance gene PlTAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2017
    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

5 authors at 3 institutions in 2 countries.

L L QiUSDA-Agricultural Research Service, Northern Crop Science Laboratory, 1605 Albrecht Blvd N, Fargo, ND, 58102-2765, USA, lili.qi@ars.usda.gov.
Y M Long
C C Jan
G J Ma
T J Gulya
Institute of Crop Science · JPNorth Dakota State University · USEdward T. Schafer Agricultural Research Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key messagePl 17, a novel downy mildew resistance gene independent of known downy mildew resistance genes in sunflowers, was genetically mapped to linkage group 4 of the sunflower genome. Downy mildew (DM), caused by Plasmopara halstedii (Farl.). Berl. et de Toni, is one of the serious sunflower diseases in the world due to its high virulence and the variability of the pathogen. DM resistance in the USDA inbred line, HA 458, has been shown to be effective against all virulent races of P. halstedii currently identified in the USA. To determine the chromosomal location of this resistance, 186 F 2:3 families derived from a cross of HA 458 with HA 234 were phenotyped for their resistance to race 734 of P. halstedii. The segregation ratio of the population supported that the resistance was controlled by a single dominant gene, Pl 17. Simple sequence repeat (SSR) and single nucleotide polymorphism (SNP) primers were used to identify molecular markers linked to Pl 17. Bulked segregant analysis using 849 SSR markers located Pl 17 to linkage group (LG) 4, which is the first DM gene discovered in this linkage group. An F2 population of 186 individuals was screened with polymorphic SSR and SNP primers from LG4. Two flanking markers, SNP SFW04052 and SSR ORS963, delineated Pl 17 in an interval of 3.0 cM. The markers linked to Pl 17 were validated in a BC3 population. A search for the physical location of flanking markers in sunflower genome sequences revealed that the Pl 17 region had a recombination frequency of 0.59 Mb/cM, which was a fourfold higher recombination rate relative to the genomic average. This region can be considered amenable to molecular manipulation for further map-based cloning of Pl 17.

Indexed as

Chromosome MappingPeronosporaDisease ResistanceGenes, DominantGenes, PlantGenetic LinkageGenetic MarkersGenome, PlantGenotypeHelianthusMicrosatellite RepeatsPhenotypePlant DiseasesPolymorphism, Single NucleotideGenetic Markers

Identifiers

PMID25673143
OpenAlexW1984600300

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.