Evidence map›Paper›PMID 19144166›Full record

ArticleBMC genomics2009

Mapping QTL affecting resistance to Marek's disease in an F6 advanced intercross population of commercial layer chickens.

Eliyahu M Heifetz, Janet E Fulton, Neil P O'Sullivan, James A Arthur, Hans Cheng, Jing Wang, Morris Soller, Jack C M Dekkers

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 60 citations in OpenAlex.

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  16. Fine-mapping QTLs in advanced intercross lines and other outbred populations.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
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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

8 authors at 4 institutions in 2 countries.

Eliyahu M HeifetzDepartment of Animal Science and Center for Integrated Animal Genomics, Iowa State University, Ames, IA 50011, USA. eliyahu100@gmail.com
Janet E Fulton
Neil P O'Sullivan
James A Arthur
Hans Cheng
Jing Wang
Morris Soller
Jack C M Dekkers
Hy-Line (United States) · USIowa State University · USHebrew University of Jerusalem · ILMichigan Department of Agriculture and Rural Development · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMarek's disease (MD) is a T-cell lymphoma of chickens caused by the Marek's disease virus (MDV), an oncogenic avian herpesvirus. MD is a major cause of economic loss to the poultry industry and the most serious and persistent infectious disease concern. A full-sib intercross population, consisting of five independent families was generated by crossing and repeated intercrossing of two partially inbred commercial White Leghorn layer lines known to differ in genetic resistance to MD. At the F6 generation, a total of 1615 chicks were produced (98 to 248 per family) and phenotyped for MD resistance measured as survival time in days after challenge with a very virulent plus (vv+) strain of MDV.

resultsQTL affecting MD resistance were identified by selective DNA pooling using a panel of 15 SNPs and 217 microsatellite markers. Since MHC blood type (BT) is known to affect MD resistance, a total of 18 independent pool pairs were constructed according to family x BT combination, with some combinations represented twice for technical reasons. Twenty-one QTL regions (QTLR) affecting post-challenge survival time were identified, distributed among 11 chromosomes (GGA1, 2, 3, 4, 5, 8, 9, 15, 18, 26 and Z), with about two-thirds of the MD resistance alleles derived from the more MD resistant parental line. Eight of the QTLR associated with MD resistance, were previously identified in a backcross (BC) mapping study with the same parental lines. Of these, 7 originated from the more resistant line, and one from the less resistant line.

conclusionThere was considerable evidence suggesting that MD resistance alleles tend to be recessive. The width of the QTLR for these QTL appeared to be reduced about two-fold in the F6 as compared to that found in the previous BC study. These results provide a firm basis for high-resolution linkage disequilibrium mapping and positional cloning of the resistance genes.

Indexed as

Immunity, InnateQuantitative Trait LociAllelesAnimalsChickensChromosome MappingCrosses, GeneticFemaleGenetic MarkersGenotypeMarek DiseaseMicrosatellite RepeatsPolymorphism, Single NucleotideSequence Analysis, DNAGenetic Markers

Identifiers

PMID19144166
PMCPMC2651900
OpenAlexW2031800443

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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.