Genetic analysis of a divergent selection for resistance to Rous sarcomas in chickens†. This article is dedicated to the memory of Pierrick Thoraval (1960–2000).

Genetics Selection Evolution (Impact Factor: 3.82). 01/2004; 36(1):1-17. DOI: 10.1186/1297-9686-36-1-65


Selection for disease resistance related traits is a tool of choice for evidencing and exploring genetic variability and studying
underlying resistance mechanisms. In this framework, chickens originating from a base population, homozygote for the B
19 major histocompatibility complex (MHC) were divergently selected for either progression or regression of tumors induced at
4 weeks of age by a SR-D strain of Rous sarcoma virus (RSV). The first generation of selection was based on a progeny test
and subsequent selections were performed on full-sibs. Data of 18 generations including a total of 2010 birds measured were
analyzed for the tumor profile index (TPI), a synthetic criterion of resistance derived from recording the volume of the tumors
and mortality. Response to selection and heritability of TPI were estimated using a restricted maximum likelihood method with
an animal model. Significant progress was shown in both directions: the lines differing significantly for TPI and mortality
becoming null in the "regressor" line. Heritability of TPI was estimated as 0.49 ± 0.05 and 0.53 ± 0.06 within the progressor
and regressor lines respectively, and 0.46 ± 0.03 when estimated over lines. Preliminary results showed within the progressor
line a possible association between one Rfp-Y type and the growth of tumors.

chicken-selection-resistance-Rous sarcoma-
Rfp - Y

Download full-text


Available from: Marie-Hélène Pinard-van der Laan,
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Transcriptionally active, MHC class I (MHCI) loci are located in two separate polymorphic genomic regions in the chicken called B and Y. The YMHCI gene sequences encode molecules with uncommon substitutions in the antigen-binding region indicating that YMHCI molecules are likely unique and may bind a specialized form of antigen distinct from that of other antigen-binding MHCI molecules. To learn whether YMHCI gene expression results in the production of alloantigens at the cell surface, we immunized 15I(5) x 7(2) : chickens using syngeneic RP9 cells expressing transduced YF1w*7.1, a potentially alloimmunogenic YMHCI allele from the Y7 haplotype present in line C. The resulting antisera show that YF1w*7.1 MHCI molecules are immunogenic and expressed on the surfaces of cells in blood and spleen of line C chickens. Virtually all CD3+, CD4+, and CD8+ cells circulating in line C blood are positive, as are BU1+ cells. The YF1w*7.1 MHCI allele is dynamically expressed at levels comparable to but transcriptionally independent of classical BMHCI on erythrocytes, lymphocytes, granulocytes, monocytes, and thrombocytes within the spleen pre- and post-hatching. The antisera react with cells from two among four haplotypes segregating in closed populations of lines N and P. YMHCI shares features associated with both classical and non-classical MHCI. It is becoming increasingly likely that YMHCI has a fundamental role in avian immunity and thereby needs to be included in the growing spectrum of functionally active, diverse MHCI molecules no longer adequately described by the classical/non-classical dichotomy.
    Immunogenetics 06/2006; 58(4):297-307. DOI:10.1007/s00251-005-0074-1 · 2.23 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: YF1*7.1 is an allele of a polymorphic major histocompatibility complex (MHC) class I-like locus within the chicken Y gene complex. With the aim of understanding the possible role of the YF1*7.1 molecule in antigen presentation, the complex of YF1*7.1 heavy chain and beta(2)-microglobulin was reconstituted and purified without a peptide. Crystals diffracted synchrotron radiation to 1.32 A resolution and belonged to the monoclinic space group P2(1). The phase problem was solved by molecular replacement. A detailed examination of the structure may provide insight into the type of ligand that could be bound by the YF1*7.1 molecule.
    Acta Crystallographica Section F Structural Biology and Crystallization Communications 05/2009; 65(Pt 4):422-5. DOI:10.1107/S1744309109009026 · 0.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Photosensitive reflex epilepsy is caused by the combination of an individual's enhanced sensitivity with relevant light stimuli, such as stroboscopic lights or video games. This is the most common reflex epilepsy in humans; it is characterized by the photoparoxysmal response, which is an abnormal electroencephalographic reaction, and seizures triggered by intermittent light stimulation. Here, by using genetic mapping, sequencing and functional analyses, we report that a mutation in the acceptor site of the second intron of SV2A (the gene encoding synaptic vesicle glycoprotein 2A) is causing photosensitive reflex epilepsy in a unique vertebrate model, the Fepi chicken strain, a spontaneous model where the neurological disorder is inherited as an autosomal recessive mutation. This mutation causes an aberrant splicing event and significantly reduces the level of SV2A mRNA in homozygous carriers. Levetiracetam, a second generation antiepileptic drug, is known to bind SV2A, and SV2A knock-out mice develop seizures soon after birth and usually die within three weeks. The Fepi chicken survives to adulthood and responds to levetiracetam, suggesting that the low-level expression of SV2A in these animals is sufficient to allow survival, but does not protect against seizures. Thus, the Fepi chicken model shows that the role of the SV2A pathway in the brain is conserved between birds and mammals, in spite of a large phylogenetic distance. The Fepi model appears particularly useful for further studies of physiopathology of reflex epilepsy, in comparison with induced models of epilepsy in rodents. Consequently, SV2A is a very attractive candidate gene for analysis in the context of both mono- and polygenic generalized epilepsies in humans.
    PLoS ONE 10/2011; 6(10):e26932. DOI:10.1371/journal.pone.0026932 · 3.23 Impact Factor