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GENETICS |
* Faculty of Agricultural, Food and Environmental Quality Sciences, Hebrew University, Rehovot 76100, Israel; and Be’er Tuvia Regional Poultry Disease Laboratory, Be’er Tuvia 83103, Israel
1 Corresponding author: cahaner{at}agri.huji.ac.il
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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Key Words: ascites • broiler • heritability • divergent selection • progeny testing
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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Recent reports (Cisar et al., 2003; Hadad et al., 2006; Druyan et al., 2007) indicate that about 50% of the broilers in commercial stocks develop AS under experimental protocols of high-challenge ascites-inducing conditions (AIC). The term "high challenge" is used for AIC that apparently induce AS in all AS-susceptible (AS-S) individuals, whereas "low challenge" AIC induce lower rates of AS, probably only in the AS-S individuals with higher demand for O2 due to higher growth rate. The rates of AS reported in recent years are similar to those found under high-challenge AIC in the 1990s (Lubritz et al., 1995; Wideman and French, 2000). In recent years, however, actual AS mortality in commercial flocks has been significantly reduced, or even completely avoided, by management practices that reduce feed intake and growth rate and, consequently, reduce the physiological demand for O2 (Julian, 2000; Balog, 2003). The problem with this approach is that it compromises the efficiency of broiler production: Although the breeding companies successfully improve the genetic potential for rapid growth, its full expression is not allowed at the farm level, to avoid morbidity and mortality of AS-S birds. A better solution would be to select against AS susceptibility; once all the broilers are resistant to AS, a managed reduction in growth rate would no longer be needed. However, breeding is feasible only if there is an inherent susceptibility to AS and if effective selection against it can be performed.
The tendency of broilers to develop AS has been found to be under genetic control in several studies, with estimates of heritability ranging from 0.1 to 0.7 (Lubritz et al., 1995; de Greef et al., 2001a,b; Moghadam et al., 2001; Druyan et al., 2007). Significant heritability of 0.5 to 0.6 has also been found for the weight ratio of right ventricle to total ventricle, a postmortem indicator for AS development and severity (de Greef et al., 2001a,b; Pakdel et al., 2002; Druyan et al., 2007). These data indicate the feasibility of selecting against susceptibility to AS, but only if all the genetically susceptible birds are identified at the phenotypic level. Mortality or morbidity due to AS provides the ultimate identification of AS-S individuals. However, actual development of AS in susceptible birds depends on environmental conditions that lead to hypo-xemia, either by reducing O2 supply or increasing the demand for O2 (Julian, 2000). Anthony and Balog (2003) found that a hypobaric chamber with a reduced partial pressure of O2, as at 2,900 m above sea level, successfully induced 66% AS in a commercial sire line, suggesting full exposure of genetic variation in AS susceptibility. Surgical inactivation of 1 lung induces AS in all or most of the susceptible individuals (Wideman and Kirby, 1995a,b; Wideman et al., 1997; Wideman and French, 1999, 2000). Recently, a novel AIC protocol was reported by Druyan et al. (2007). Housed in individual cages, the broilers tested under this protocol cannot avoid the environmental conditions, consisting of cool movement of air caused by a fan. Combined with high-energy pelleted feed and 23 h of light per day, this protocol induced about 50% AS among commercial broilers (Hadad et al., 2006; Druyan et al., 2007), suggesting that all (or at least most) of the susceptible broilers developed AS.
The successful induction of AS, using any of these approaches, suggests that breeding for AS resistance can be conducted by keeping all selection candidates under high-challenge AIC and awaiting mortality of all susceptible individuals. However, this direct-selection approach has not been used by the breeding companies, because it would force them to compromise the selection for more important traits, such as growth rate and meat yield, which are not fully expressed under AIC. Therefore, specific indicators of AS susceptibility (or AS resistance) are needed to integrate indirect selection against AS susceptibility into a multitrait breeding program of commercial broilers. To serve as a useful indicator for such indirect selection, a trait measured under standard rearing conditions must differ significantly between all AS-S vs. all AS-resistant (AS-R) individuals. In an effort to identify such indicators, Druyan et al. (2007) measured AS-related traits in a family-structured population of commercial broilers that were held under standard brooding conditions and later moved to high-challenge AIC, to distinguish between the AS-S and AS-R individuals. The O2 saturation of hemoglobin in the arterial blood (SaO2) on d 7 or 10 was slightly lower in the susceptible birds, and there was a consistent significant negative genetic correlation between SaO2 and the %AS. Indeed, in recent years, breeding companies have selected against broilers with low SaO2, measured in flocks of selection candidates when they reach about 5 wk of age. However, due to low heritability and dominance of high SaO2 (Navarro et al., 2006), the usefulness of low SaO2 as an effective indicator for further selection against AS susceptibility is expected to be limited.
To effectively select against AS susceptibility without interfering with the normal expression of other selected traits, one has to identify the genes responsible for the primary cause of AS or measure their phenotypic expression. There is evidence that the primary cause of AS is manifested in the prenatal or very early postnatal phases, when the cardiovascular system is being developed and starting to function (Dewil et al., 1996; De Smit et al., 2005; Tona et al., 2005). Measurements of such a manifestation, especially at the embryonic stage, require terminating the lives of the investigated individuals, and hence it is not possible to later determine, under AIC, if these individuals were susceptible or resistant to AS. Therefore, to conduct advanced physiological and genomic research on AS, one needs a pair of selected lines in which all the individuals are either AS-S or AS-R. Comparisons of tissues or functions of individuals from the divergent lines can help to identify the primary cause of AS and an effective indicator for selection against susceptibility. Resource populations derived from crosses between such divergent lines may facilitate genomic research aimed at detecting the genes involved in susceptibility or resistance to AS. Studies with a pair of AS-S and AS-R lines have revealed that they differ in several growth-related parameters that may have relevancy to anti-AS breeding or management (Anthony and Balog, 2003; Pavlidis et al., 2005). However, a second, independent pair of divergently selected lines is needed to confirm and generalize the findings from the lines developed by Anthony and coworkers (Anthony et al., 2001; Anthony and Balog, 2003) and to widen the spectrum of advanced AS-related research. The objective of the present study was, therefore, to develop a pair of genetically divergent lines, AS-S and AS-R, from a commercial stock of broilers by using a full-pedigree progeny-testing scheme with %AS as the selection criterion.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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Management.
Chicks from all families were reared together in a single commercial broiler house on a wood-shavings litter. To ensure the development of AS in the majority of the susceptible broilers, the trial was conducted in the cool season, in an open-sided house with curtains, located 500 m above sea level. As planned, ambient temperatures dropped occasionally below 30°C during the first 2 wk and fluctuated from 20 to 24°C during most of the third week. The temperatures continued to fall, fluctuating from 18 to 22°C in the fourth week and from 15 to 20°C thereafter. To increase the metabolic challenge, growth of a broiler was enhanced by a feeding program consisting of prestarter (d 0 to 10), starter (d 11 to 21), grower (d 22 to 33), and high-energy pelleted finisher (d 34 onward) diets, with respective contents of CP (%) and energy (kcal/kg of ME) as follows: 22 and 3,100, 20.5 and 3,125, 19.5 and 3,150, and 18.3 and 3,225, respectively. Feed and water were provided ad libitum, with 23 h of light during the entire trial. The standard vaccination regimen used for broilers in Israel was applied. Newcastle disease virus (NDV) and infectious bronchitis virus vaccines were sprayed at day of hatch; NDV and infectious bursa disease virus vaccines were injected s.c. on d 12, and NDV vaccine was administered by fogging on d 20.
Diagnosis of AS.
Mortality during the first 2 wk reflected random variation in chick quality; hence, those that died up to 14 d of age were excluded from the data. All the chicks that died during the third to seventh weeks were necropsied at the Be’er Tuvia Regional Poultry Disease Laboratory to visually determine the cause of death, and the sex of each necropsied bird was recorded. Chicks that accumulated ascitic fluid in the abdominal cavity or around the heart (hydropericardium) were diagnosed as having died due to AS, and their phenotype was recorded as susceptible (SUS). After excluding mortality due to other causes, the total population consisted of 5,765 individuals, with 44 to 99 chicks per family and an average of 68 chicks. In this population, the phenotype of all the birds that survived to the end of the trial was recorded as resistant (RES).
BW.
The 935 sexed and color-marked chicks, 11 per sire family, were individually weighed at 10 d of age. The same chicks, except those that died, were individually weighed 3 more times during the trial, on d 17, 28, and 48 (the last day of the trial).
Generation S1 — Repeated Progeny Testing of Selected Families Under Experimental AIC
Experimental Populations.
Based on results from the field trial, sires of 7 families with very high %ASF were mated again with the same dams to produce more SUS full-pedigree progeny. Similarly, the sires and dams of 7 families with very low %ASF in the field trial were mated again to produce more RES full-pedigree progeny. Male and female progeny from these 14 families were reared to sexual maturity and used as S1 sires and dams. Additional male progeny from these 14 families were tested in 2 consecutive trials under experimental high-challenge AIC protocol. Trial 1 consisted of 106 and 112 male chicks from SUS and RES families, respectively. Trial 2 consisted of 122 and 90 male chicks from the SUS and RES families, respectively, and 28 male chicks from a commercial broiler stock, included as an industry reference.
Experimental High-Challenge AIC Protocol.
All of the chicks were brooded under standard brooding conditions on a concrete floor covered with wood shavings. At 19 d of age, the chicks were placed in individual cages with cool air (18 to 20°C) blown on them by fans at about 3 m/s. Growth rate of these chicks was enhanced by using an accelerated feeding program consisting of providing a prestarter from d 0 to 4 (instead of d 0 to 10), starter from d 5 to 14 (instead of d 11 to 21), grower from d 15 to 24 (instead of d 22 to 33), and a high-energy pelleted finisher feed from d 25 to 44. The contents of CP (%) and energy (kcal/kg of ME) in these 4 diets were as follows: 22 and 3,100, 20.5 and 3,125, 19.5 and 3,150, and 18.3 and 3,225, respectively. Feed and water were provided ad libitum. Growth rate was further enhanced by exposure to 23 h/d of light from hatch to the end of the trials, on d 44.
Diagnosis of AS.
Throughout the phase of AIC (d 19 to 44), all dead chicks were necropsied and examined to determine the cause of death. Chicks with ascitic fluid or hydropericardium were diagnosed as having died due to AS, and their phenotype was recorded as SUS. The few birds that died from other causes were excluded from the data. On d 44, all surviving birds were killed by cervical dislocation, necropsied, and visually examined. Birds showing ascitic fluid or hydropericardium were diagnosed as exhibiting AS, and their phenotype was also recorded as SUS; all other birds not showing these manifestations were recorded as being RES.
Generation S2 — Further Divergent Selection in the AS-R and AS-S Lines
Due to the differences in magnitude and ranking of %ASF values of the 14 selected sire families between the 2 rounds of S1 progeny testing (field trial and AIC), no further selection was applied among the S0 sire families. Thus, S1 males and females were kept for breeding from all 14 S0 families (7 in each of the 2 selected lines). Avoiding sib mating, 10 S1 sires were mated to 42 S1 dams in the AS-S line, and 9 S1 sires were mated to 36 S1 dams in the AS-R line. They produced full-pedigree progeny in 4 consecutive hatches. Male progeny from each hatch were tested under the same high-challenge AIC to determine susceptibility or resistance to AS. In total, 363 SUS and 245 RES male chicks were tested under AIC in generation S2. Whereas all sire families were included in the first-hatch trial, some families were not represented in later hatches, because the sires died or became infertile. Based on %ASF under AIC, and availability of additional S2 progeny, males and females from 6 AS-S families and 5 AS-R families were reared to sexual maturity and used as S2 sires and dams.
Generation S3 — Establishing the AS-R and AS-S Divergent Lines
Avoiding sib mating, 7 S2 sires were mated with 45 S2 dams in the AS-S line, and 8 S2 sires were mated with 46 S2 dams in the AS-R line, producing full-pedigree progeny in 3 consecutive hatches. As in previous generations, all male progeny were tested under AIC to determine susceptibility or resistance to AS, totaling 191 in AS-S and 164 in AS-R. Some sire families were not represented in later hatches due to sire infertility. Based on %ASF under AIC, and availability of more S3 progeny, males and females from all 7 AS-S families and from 5 AS-S families were reared to sexual maturity and used as S3 sires and dams. They were mated within line, sib mating avoided, to establish the AS-S and AS-R lines.
Statistical Analysis
At the end of the field trial and each AIC trial, the birds were divided into 2 phenotypes: those with AS manifestations were identified as SUS, and the healthy ones were designated RES. The birds that died from causes not related to AS were excluded from the data. The data of each AIC trial were analyzed by 
2 test, comparing the incidence of SUS vs. RES birds between AS-S- and AS-R-selected lines. Field trial data (BW and weight gain) were subjected to ANOVA according to a mixed model with the parental flock (1 or 2), sex (male or female), and AS phenotype (SUS or RES) as fixed main effects, sire (nested within flock) as a random effect, and all interactions among the 3 fixed-effect factors. These statistical analyses were conducted with JMP software (SAS Institute, 2005).
Being a categorical trait (RES or SUS), the heritability of the AS phenotype in the field trial (base population, generation S0) was estimated by GFCAT, a software dedicated to the estimation of genetic parameters for categorical traits, named after the authors (Gianola and Foulley, 1983) of the theoretical framework (V. Ducrocq, Institut National de la Recherche Agronomique, Jouyen-Josas Cedex, France, personal communication). The model included the random sire effect and the fixed effect of parental flock.
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RESULTS AND DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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The %ASF was calculated for each sire family, and the distribution of these 85 values is presented graphically in Figure 1
, panel A. The %ASF values ranged from 2 families with no mortality (0.00) to the most susceptible family with a rate of 0.491, namely 49.1% of the birds in this family died from AS. The software GFCAT calculated a value of 0.166 for the sire variance component of AS, with the value 1 assigned to the remaining phenotypic variation. Thus, the heritability of %ASF was estimated as follows: (4 x 0.166)/(1 + 0.166) = 0.57, very similar to the estimate of 0.52 obtained in another trial with half-sib families derived earlier from the same commercial population and tested under high-challenge AIC (Druyan et al., 2007). Similar heritabilities (0.41 and 0.44) were estimated in 2 independent studies (Lubritz et al., 1995; Moghadam et al., 2001).
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, panel A) was compared with a distribution based on the hypothesis that differences among families in the rate of AS were of a random nature. The function of random binomial distribution was applied, using the proportion of AS in the entire population (0.172) to randomly designate each of the 5,765 chicks in the data file as AS-dead or AS-healthy. The rate of this randomly assigned AS mortality was calculated per family. Figure 1, panel B, is based on these values and hence presents the expected distribution with no genetic variation among families. The distribution of the observed AS mortality per family was much wider than that of the expected random mortality, demonstrating the substantial genetic variation in AS mortality among families in the broiler dam line used as the base population.
BW.
At the end of the trial (d 48), BW of the healthy broilers (designated RES) averaged 2,384 g (Table 1), with the heaviest individuals reaching over 3,000 g. These figures indicate that, despite the suboptimal conditions in the broiler house, e.g., lower-than-recommended ambient temperatures, growth rate in the field trial was only slightly lower than that of contemporary broilers under standard conditions in the year 2000. The broilers that later died from AS exhibited a lower mean BW than the healthy ones only on d 28, because many of them started to develop AS during the fourth week. Similar BW means were exhibited on d 10 and 17 by the broilers that later developed AS (SUS) and those that remained healthy (RES; Table 1). Similar results were obtained in a study with commercial broilers reared under AIC similar to those in the present study (cold environment after d 17 and pelleted feed provided 23 h/d); the individuals that later developed AS and those that remained healthy exhibited similar BW on d 17 or 21 (Wideman and French, 2000). In contrast to some publications stating that AS is developed in individuals with more rapid early growth (Julian, 2000), the findings of the present study and the cited one suggest that variation in susceptibility to AS is not associated with the variation in growth rate within broiler stocks.
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). The possibility that the higher BW of the families with the highest %ASF reflected a genuine genetic association between rapid growth and AS susceptibility contradicts the lack of equivalent differences in mean BW between the SUS and RES individuals in the entire population. Alternatively, it is suggested that the difference in mean BW between the 2 groups of families with extreme levels of %ASF could be related to the moderate AIC in the field trial. The overall AS mortality in this trial was only 17.2%, substantially less than the 30% AS mortality (44% mortality + morbidity) in a previous study in which birds from the same line were tested under high-challenge AIC (Druyan et al., 2007). This difference indicates that the relatively moderate degree of cold (AIC) in the field trial did not induce AS in all AS-S broilers. It is suggested that under low-challenge AIC, as in the field trial of the current study, SUS birds with genetically lower growth rates escape the AS phenotype due to lower demand for O2. Thus, the values of %ASF are biased downward in the slow-growing families and upward in the fast-growing families. Therefore, if families with low %ASF are selected as AS-R, and families with high %ASF are selected as AS-S, such divergent selection may cause divergence in growth rate. However, this apparent correlated response to selection may not reflect a true symmetrical association between rapid growth and AS. Alternatively, it may result from an asymmetrical association between growth rate and AS. Genetically AS-S birds need a threshold level of rapid growth to manifest the AS phenotype, with the threshold being higher, because the AIC are less challenging. The same levels of growth rate, and also higher ones, do not cause AS in genetically RES individuals, even under high-challenge AIC. This interpretation agrees with several reports suggesting that AS develops in broilers in which growth rate exceeds their pulmonary vascular capacity, but they do not necessarily have to be the fastest growing birds in a flock (Wideman, 1998; Wideman and French, 1999, 2000; Decuypere and Buyse, 2005; Druyan et al., 2007).
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). Table 3 presents the %ASF among the S1 progeny of these 14 families. Among the 7 families selected to establish the AS-S line, 1 family had the highest %ASF (49.1%), and another family had a similar rate (47.1%). The other 5 families had %ASF ranging from 28.2 to 41.4%. Among the 7 families selected to establish the AS-R line, 1 family had no AS mortalities at all (%ASF = 0), and in the other families, %ASF ranged from 1.5 to 8.9%.
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). In the AS-S line, %ASF ranged from 94.1 to 25%. In the AS-R line, %ASF ranged from 11.1 to 68.4%. In 13 of the 14 families, %ASF was lower in the field trial than under the experimental high-challenge AIC protocol, clearly indicating the superiority of the latter, mainly due to the novel use of individual cages. The second trial also included 28 broilers from a commercial stock, and 9 of them (32%) developed AS, indicating that the efficacy of this AIC protocol does not apply for only the base population used in the divergent selection.
Generation S2 — Progeny Testing and Divergent Selection in the AS-R and AS-S Lines
The S2 progeny of 10 AS-S sire families and 9 AS-R sire families were tested in replicated trials under the high-challenge AIC. Mortality and morbidity due to AS were recorded and summarized by family (Table 4). In the AS-S line, %ASF in 7 families was above 63%, with a maximum of 92.8%. Within these 7 sire families, progeny of dams with %ASF = 100 were selected; in total, 7 males and 45 females were kept to sexual maturity, to reproduce the AS-S line. Sires number 40 and 7 died before they could produce additional progeny for reproduction, and only 2 females were kept from S1 sire number 31. Two families (sires number 1 and 11) were culled due to intermediate %ASF, and, from sire number 24, which was found to be fairly resistant (%ASF = 14.3%), 11 S1 females were kept as reinforcement of the AS-R breeders.
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). Four AS-R families were culled due to intermediate %ASF and, from sire number 13, found to be more than moderately susceptible (%ASF = 77.8), 7 S1 females were kept as potential replacements of nonsuccessful AS-S breeders. All the sexually mature S2 males and females were mated within line, sib mating avoided, to produce S3 progeny for testing under AIC.
Generations S3 — Progeny Testing and Divergent Selection in the AS-R and AS-S Lines
The S3 progeny of 7 AS-S sire families and 8 AS-R sire families were tested in replicated trials under the high-challenge AIC. Mortality and morbidity due to AS were recorded and summarized by family (Table 5). In the AS-S line, %ASF in 6 families was above 86%, with a maximum of 96%. The S3 male and female breeders were kept from all 6 of these AS-S sire families but only from dams with 100% AS among their AIC-tested progeny. Female breeders were also kept from the family of sire number 8, from dams with 100% AS.
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). To increase the number of AS-R breeders and help avoid sib mating in the following generation, 5 female progeny were also kept as breeders from 2 dams (mated to sire number 45), none of whose AIC-tested male progeny developed AS.
The selected S3 breeders in the AS-S line were progeny of 4 out of the 7 S0 sires that were originally selected based on the field trial data. On the resistant side, there was also good agreement between AS mortality in the field trial and later generations. There was no AS mortality among the field-tested progeny of S0 sire number 140, and among the progeny of S0 sires number 71 and 94, %ASF was only 1.2 and 3.9% in the field trial (Table 3).
Summary of %AS Under AIC in Generations S1, S2, and S3
The 3 cycles of family selection, in generations S0, S2 and S3, resulting in the 2 divergent lines, AS-R and AS-S, are presented graphically in Figure 2. The overall %AS in the AS-S and AS-R lines in each generation is presented in Table 6. The 2 lines differ significantly in all 3 generations. In generation S1, %AS was 69.2 vs. 31.7% in AS-S and AS-R, respectively, a divergence of 37.5%. In generation S2, %AS was 69.4 vs. 26.1% in AS-S and AS-R, respectively. The divergence, 43.3%, was only slightly larger than in S1; this was expected because no selection was applied between S1 and S2. Family selection was applied in S2, in which breeders were not kept from families with intermediate %ASF. This family selection is reflected in the overall incidence of susceptible individuals in the AS-S- and AS-R-selected families; with %AS of 79.5 vs. 11.7% in AS-S and AS-R, respectively, the divergence increased to 67.8%. In generation S3, %AS was 88.5 vs. 15.8% in AS-S and AS-R, respectively. The divergence, 72.7%, was, as expected, similar to that between the selected S2 families of AS-S and AS-R. At this stage, before establishing the selected lines, additional family selection was applied, mainly in the AS-R line. Consequently, %AS in the selected S3 families, weighted by the number of selected breeders, was 91.3 vs. 4.5% in AS-S and AS-R, respectively, with a divergence of 86.6% between AS-S and AS-R individuals that were reared together under the same high-challenge AIC protocol.
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Divergent selection on AS, similar to that reported in the present study, was also conducted by Anthony and coworkers (Anthony et al., 2001; Anthony and Balog, 2003). A hypobaric chamber, simulating the altitude of 2,900 m above sea level, was used to induce AS, and divergent sire family selection was applied for 10 generations. Under the hypobaric chamber conditions, %AS was 66% in the base population used in that study, an elite commercial sire line. Additionally, %AS was higher than the 45% found in the dam line base population of the present study, when exposed to the cage-based AIC protocol (Druyan et al., 2007). The different %AS in the dam line used in the present study, compared with the sire line used by Anthony et al. (2001), may reflect AS-challenge differences between the 2 AIC protocols or true genetic difference between the 2 lines, due to different breeding history. The divergent selection under hypobaric conditions elevated %AS to about 90% in the AS-S line and reduced it to about 20% in the AS-R line, reaching a divergence of about 70% (Anthony and Balog, 2003). In the present study, larger divergence (86.6%) was achieved after only 3 selection cycles. The more rapid divergence in the present study may have resulted from the full-sib selection procedure that also accounted for dam effects, as compared with the sire family half-sib selection applied by Anthony and coworkers (Anthony et al., 2001; Anthony and Balog, 2003). Yet it is remarkable that divergent selection for AS-R and AS-S was similarly successful in 2 unrelated broiler breeding lines.
The successful establishment of the AS-R line with less than 5% AS under the same high-challenge AIC that induced almost 100% AS in the AS-S line indicated that direct selection for AS resistance is feasible, if it is conducted under efficacious AIC. These results are in general agreement with those of Wideman and French (2000) and those from the AS-R line of Anthony (Anthony and Balog, 2003; Balog et al., 2003). The very rapid genetic divergence between the selected lines, along with pedigree analysis of %ASF within the selected lines, imply that a single or few major genes are responsible for the difference in %AS between the AS-S and AS-R lines in the current study. The suggestion of a single or few major genes for AS susceptibility or resistance is supported by 2 independent studies. Wideman and French (2000), based on the rapid genetic response to 2 cycles of selection of birds that survived surgical AS challenge in a fully pedigreed elite commercial broiler breeder line, concluded that there is a gene or more than 1 gene involved in ascites susceptibility. The single gene notion was also suggested by Navarro et al. (2006). The latter authors performed a complex segregation analysis of data on SaO2, a trait closely associated with AS (Julian and Mirsalimi, 1992; Wideman and Kirby, 1995a,b; Druyan et al., 2007). Data on SaO2 from 12,000 males in fully pedigreed populations of commercial broiler breeding lines were available for that study, and the results suggested that a single di allelic locus was responsible for 87% of the genetic variation in SaO2. In a later trial in the same study (Navarro et al., 2006), the same conclusion was reached except that much lower heritability was estimated for SaO2.
Having AS-S and AS-R lines with almost complete genetic divergence facilitates sensitive and reliable research on genetic, physiological, and management aspects of AS. Divergent AS-S and AS-R lines can be used to search for differences in the sequence or expression of candidate genes. One such study has been reported (Cisar et al., 2001, 2003), although no difference was found in the examined candidate gene between AS-S and AS-R broilers. An alternative genetic approach might be based on a genome-wide scan for DNA markers that exhibit significant differences in allelic frequency between individuals with AS and healthy ones. This approach has been used in several studies, but the findings of Rabie et al. (2005) were limited to a few QTL with very small effects, instead of the expected single or few major genes with a large effect. But the resource population in that study was derived from a cross between 2 commercial broiler lines that did not differ in %AS. A genome-wide scan is expected to be more efficient if the resource population is derived from a cross between lines that are as divergent as the AS-S and AS-R lines developed in the present study. The F2 and backcross families also allow classical segregation analysis, aimed at determining the number of major genes and their mode of action. Such information may help in the molecular detection of the AS gene(s). Once such a gene is identified at the DNA sequence level, it can be used to genotype individuals in breeding populations and identify those that carry the allele(s) for AS susceptibility. Such genotyping may lead to a total elimination of AS susceptibility from commercial breeding stocks within a few generations. Once this is done, it will no longer be necessary to restrict by management the growth rate of modern broilers flocks, as is currently done to avoid AS. That will improve the efficiency and profitability of broiler production, especially in cold climates and at high altitudes.
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ACKNOWLEDGMENTS |
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Received for publication May 15, 2006. Accepted for publication December 6, 2006.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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Cisar, C. R., J. M. Balog, N. B. Anthony, and A. M. Donoghue. 2001. Genetic selection of broiler lines that differ in their ascites susceptibility. 2. Progress on identification of differentially expressed genes in ascitic and non-ascitic birds. Pages 331–332 in Proc. 13th Eur. Poult. Nutr. Symp., Blankenberge, Belgium. World’s Poult. Sci. Assoc., Geel, Belgium.
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