genome-screen experiment to detect quantitative trait loci affecting resistance to facial eczema disease in sheep
Facial eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this cent...
Saved in:
Published in: | Animal genetics Vol. 40; no. 1; pp. 73 - 79 |
---|---|
Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Oxford, UK
Oxford, UK : Blackwell Publishing Ltd
01-02-2009
Blackwell Publishing Ltd |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Facial eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F₁ sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79-91%) were tested for linkage to the FE traits. Data were analysed using Haley-Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis. |
---|---|
Bibliography: | http://dx.doi.org/10.1111/j.1365-2052.2008.01803.x ArticleID:AGE1803 istex:44A142D5E484B0829ADF29C8B57D3A2C866F85E9 ark:/67375/WNG-C8J08GMJ-D ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0268-9146 1365-2052 |
DOI: | 10.1111/j.1365-2052.2008.01803.x |