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Ascites syndrome is a metabolic disorder found in modern broilers that have insufficient pulmonary vascular capacity. Commercial breeding programs have heavily focused on high growth rate, which led to fast-growing chickens, but as a negative consequence, the incidence of ascites syndrome increased. However, not all birds with a high growth rate will suffer from ascites syndrome, which might indicate a genetic susceptibility to ascites. Information on blood gas parameters measured early in life and their relation to ascites susceptibility is expected to contribute to identification on the cause of ascites syndrome. In this study, several physiological parameters, such as blood gas parameters [pH, partial pressure of CO2 in venous blood (pvCO2), and partial pressure of O2 in venous blood], hematocrit, electrolytes (Na+, Ca2+, and K+), metabolites (lactate and glucose), were measured at d 11 to 12 of age from 100 female and 100 male broilers. From d 14 onward, the birds were challenged to provoke the development of ascites syndrome. Our results showed that high pvCO2 values together with low pH values (males) or high pH values (females) in the venous blood of juvenile broilers coincided with ascites. Therefore, blood pvCO2 and pH in both juvenile male and female broilers seem to be critical factors in ascites pathophysiology and can be used as phenotypic traits to predict ascites susceptibility in juvenile broilers at d 11 to 12. A prediction model was built on a subpopulation of the broilers without any loss in sensitivity (0.52) and specificity (0.78) when applied to the validation population. The parameter sex was included in the prediction model because levels of pvCO2 and pH that associated with ascites susceptibility are different between males and females. Commercial breeders can include these phenotypic traits in their genetic selection programs to reduce the incidence of ascites syndrome. [ABSTRACT FROM AUTHOR]

A correction to the article "Detection of Different Quantitative Trait Loci for Antibody Responses to Keyhole Limpet Hemocyanin and Mycobacterium butyricum in Two Unrelated Populations of Laying Hens" that was published in the 2003 issue is presented.

A correction to the article "Mapping Quantitative Trait Loci Affecting Feather Pecking Behavior and Stress Response in Laying Hens" that was published in the 2003 issue is presented.

A correction to the article "Quantitative Trait Loci for Body Weight in Layers Differ From Quantitative Trait Loci Specific for Antibody Responses to Sheep Red Blood Cells" that was published in the 2004 issue is presented.

Quantitative trait loci for BW at 4, 6, 8, 12, and 18 wk of age were detected in an experimental F2 cross of layers divergently selected for primary antibody response to SRBC. A negative phenotypic correlation between levels of antibody titers and BW, was reported earlier within founder lines. The entire experimental population was genotyped with 174 microsatellite markers equally distributed over the genome. Two genetic models were applied in the QTL analysis: a half-sib model and a line-cross model, both using the regression interval method. In the half-sib model, 3 QTL for BW at 4 wk of age on chromosomes GGA2, GGA3, and GGA9 were detected. For BW at 6 wk of age, 3 QTL were detected on GGA2, GGA3, and GGA6. For BW at 8 wk of age, a QTL was detected on GGA7, and for BW at 12 and 18 wk of age, a QTL was detected on GGAZ. With the line-cross analysis model, one QTL on GGA7 for BW at 4 wk of age was detected. Two QTL were detected on GGA3 and GGA7 for BW at 6 wk of age, and one on GGA3 was detected for BW for 8 and 12 wk of age. For BW at 18 wk of age, there were no QTL under the line-cross analysis model. The present data suggest that 1) a different set of genes affects the early and the late growth, and 2) genes selected to humoral immune responsiveness are different from genes underlying growth.

A cross between 2 genetically different outcross broiler dam lines, originating from the White Plymouth Rock breed, was used to produce a large 3-generation broiler population. This population was used to detect and localize QTL affecting fatness in chicken. Twenty full-sib birds in generation 1 and 456 full-sib birds in generation 2 were typed for microsatellite markers, and phenotypic observations were collected for 3 groups of generation 3 birds (approximately 1,800 birds per group). Body weight, abdominal fat weight, and percentage abdominal fat was recorded at the age of 7, 9, and 10 wk. To study the presence of QTL, an across-family weighted regression interval mapping approach was used in a full-sib QTL analysis. Genotypes from 410 markers mapped on 25 chromosomes were available. For the 3 traits, 26 QTL were found for 18 regions on 12 chromosomes. Two genomewise significant QTL (P < 0.05) were detected, one for percentage abdominal fat at the age of 10 wk on chicken chromosome 1 at 241 cM (MCW0058 to MCW0101) with a test statistic of 2.75 and the other for BW at the age of 10 wk on chicken chromosome 13 at 9 cM (MCW0322 to MCW0110) with a test statistic of 2.77. Significance levels were obtained using the permutation test. Multiple suggestive QTL were found on chromosomes 1, 2, 4, 13, 15, and 18, whereas chromosomes 3, 7, 10, 11, 14, and 27 had a single suggestive QTL.

Quantitative trait loci involved in the primary antibody response to keyhole lympet hemocyanin (KLH) and Mycobacterium butyricum were detected in two independent populations of laying hens. The first population was an F2 cross (H/L) of lines divergently selected for either high or low primary antibody responses to SRBC, and the second population was an F2 cross between 2 commercial layer lines displaying differences in feather pecking behavior (FP). Both populations were typed with microsatellite markers widely distributed over the genome with similar intervals between markers. Titers of antibodies binding KLH and M. butyricum were measured for all individuals by ELISA. Two genetic models were applied to detect QTL involved in the humoral immune response: a half-sib model and a line-cross model, both using the regression interval method. In the half-sib analysis, 2 QTL (on GGA14 and GGA27) were detected for the antibody response to KLH for the H/L population, and 2 QTL (on GGA14 and GGA18) were detected for the FP population. Only 1 QTL was detected for M. butyricum on GGA14 in the FP population using the half-sib analysis model. Two QTL were detected for the FP population on GGA2 and GGA3 using the line-cross analysis model. A QTL for the primary antibody response to KLH detected on GGA14 was validated in both populations under the half-sib analysis model. The present data suggest differences in the genetic regulation of antibody responses to two different T-cell dependent antigens.

Feather pecking (FP) is a major problem in cage and free-range housing systems. In free-range systems, FP is more difficult to control. It is not known why a victim is being pecked. It could be that a bird is genetically predisposed to be pecked. To study the genetics of FP behavior, a large F2 population of 630 hens was generated from a cross between two commercial laying lines differing in their propensity to feather peck. The traits measured at 6 and 30 wk of age were receiving gentle FP, receiving severe FP, and receiving aggressive pecking. In addition, receiving toe pecking (TP) was also measured at 30 wk of age. For receiving gentle FP at 6 wk of age, a significant QTL on GGA1 and three different suggestive QTL were identified on GGA2, GGA6, and GGA7, respectively. For receiving gentle FP at 30 wk of age, a suggestive QTL on GGA5 was detected. For receiving aggressive pecking, a suggestive QTL was detected on GGA3. For receiving TP, three suggestive QTL were detected on GGA1, GGA5, and GGA23, respectively. The different QTL detected for receiving gentle FP at different ages indicate that this trait is regulated by different genes in young and adult hens.

In the European Union, legislation concerning animal housing is becoming stricter because of animal welfare concerns. Feather pecking (FP) in large group housing systems is a major problem. It has been suggested that corticosterone (CORT) response to manual restraint as a measure for stress is associated with FP behavior. The aim of the current study was to identify QTL involved in FP behavior and stress response in laying hens. An F2 population of 630 hens was established from a cross between two commercial lines of laying hens differing in their propensity to feather peck. The behavioral traits, measured at 6 and 30 wk of age, were gentle FP, severe FP, and aggressive pecking. Toe pecking was measured at 30 wk of age and CORT response to manual restraint was measured at 32 wk. All animals were genotyped for 180 microsatellite markers. A QTL analysis was performed using a regression interval mapping method. At 6 wk of age, a suggestive QTL on GGA10 was detected for gentle FP. At 30 wk of age, suggestive QTL were detected on GGA1 and GGA2 for gentle FP. A significant QTL was detected on GGA2 for severe FP. At 32 wk of age, a suggestive QTL was detected on GGA18 for CORT response to manual restraint. In addition, a suggestive QTL was detected on GGA5 with possible maternal parent-of-origin effect for CORT response.

For 17 microsatellite markers, allele frequencies were determined in nine highly selected commercial broiler and six highly selected commercial layer lines using pooled blood samples from 60 animals. The average number of marker alleles was 5.8 over all lines, 5.2 over broiler lines, and 3.0 over layer lines. The average number of marker alleles within a line was 2.9, 3.6, and 2.0 for all, broiler, and layer lines, respectively. Over all 15 lines, the average percentage of heterozygosity was 42, whereas the heterozygosity in the broiler lines was 53% and in the layer lines only 27%. In broiler lines, 50% of the marker-line combinations showed a heterozygosity above 60%, whereas this was only 5% in layer lines. Estimation of allele frequencies with microsatellite markers was first assessed in pooled and individual samples before usage in the commercial lines. Allele frequencies for 19 microsatellite markers were estimated in chicken pooled blood samples and compared with allele frequencies from individual typed animals. Similar results were obtained when pooled blood samples (heterozygosity of 35.3%) or individual typed animals (heterozygosity of 34.2%) were used. The method to determine allele frequencies using pooled blood samples is faster, cheaper, and as reliable and repeatable as determining allele frequencies using individual typings.

Microsatellite polymorphisms are finding increasing use in genetics. The objectives of this study were 1) to enlarge the number of markers to contribute to a well-defined linkage map of the chicken genome; and 2) to create a preliminary linkage map only based on microsatellite markers. The need for microsatellite markers is high for performing a whole genome scan for the identification of quantitative trait loci. Seventy-seven newly developed microsatellite markers that were polymorphic on either one or both of the reference populations were mapped and in combination with all previously described markers, used to construct a preliminary linkage map of the chicken genome. The 128 microsatellite markers mapped thus far cover 23 of the 38 linkage groups of the East Lansing reference population. In the case of the Compton reference population, 20 linkage groups out of 40 are covered with microsatellite markers. No linkage was found in the East Lansing population with five markers, and in the case of the Compton population four markers were unlinked. About 42 and 32% of the East Lansing and Compton maps, respectively, were covered by the 128 microsatellite markers. The microsatellite markers are well dispersed among the various linkage groups and there was no evidence for clustering of the markers within the map. With the 38 markers that were mapped on both reference populations, 10 of the East Lansing linkage groups could be associated with 13 of the Compton linkage groups.