Mutation analysis of the aggrecan gene in chickens with tibial dyschondroplasia.

Expression studies suggest that the incidence and severity of tibial dyschondroplasia (TD) in chickens, Gallus gallus, may be affected by the aggrecan gene, AGC 1. Here, results are described of a scan for single nucleotide polymorphisms (SNP) in AGC1 in genetic lines divergently selected for TD incidence in chickens. A total of 3,048 bp of DNA sequence obtained from amplicons produced by 4 primer-pairs designed from the GenBank AGC1 cDNA sequence were scanned for SNP. Among the 18 SNP detected and validated, only 2 were nonsynonymous. Allelic frequency differences between TD-affected and nonaffected birds were not statistically significant for all the SNP. The current results do not support an association of Gallus gallus AGC1 variation at the DNA level with the incidence of TD in chickens. The genomic resources described, however, including the SNP, could be useful in further evaluating AGC1 in other populations for association with TD or other skeletal abnormalities.

Immunolocalization analysis of transforming growth factor-beta1 in the growth plates of broiler chickens with high and low incidences of tibial dyschondroplasia.

Immunolocalization of transforming growth factor-beta1 (TGF-beta1) was determined in growth plates of two lines of broiler chickens with low and high incidences of tibial dyschondroplasia (TD). Ultrathin sections of growth plates from each line were treated with a polyclonal antibody specific for TGF-beta1, followed by colloidal gold-labeled protein A. Immunolocalization for TGF-beta1 was observed in chondrocytes of all zones of growth plates of low and high TD incidence lines. However, immunolocalization in extracellular matrix was restricted to the hypertrophic zones of both lines. In the hypertrophic zone of low TD incidence line, immunolocalization of TGF-beta1 in the extracellular matrix adjacent to collapsed cartilage canals (matrix streaks) was significantly greater than immunolocalization between patent cartilage canals. A similar increase was not observed in the high TD incidence line. Results indicate that chondrocytes of all zones of the growth plate contain TGF-beta1 but do not release it into extracellular matrix until hypertrophy has occurred. Greater concentrations of TGF-beta1 adjacent to collapsed cartilage canals may play a role in controlling angiogenesis and directing invasion of mineralized hypertrophic cartilage by metaphyseal blood vessels. A low concentration of TGF-beta1 in the extracellular matrix adjacent to collapsed cartilage canals of the high TD incidence line may be a factor in limiting vascular invasion of dyschondroplastic cartilage of TD lesions.

Effects of divergent selection for incidence of tibial dyschondroplasia (TD) on purebred and crossbred performance. 1. TD incidence and calcium and phosphorus plasma concentrations.

1. The effect of divergent selection for high (H) or low (L) incidence of tibial dyschondroplasia (TD) for 7 generations on blood calcium (Ca) and phosphorus (P) concentrations was studied. 2. The chicks used in this experiment were obtained from diallel crosses between H and L lines to obtain HH, HL, LH, and LL lines. A random-bred control (CC) line was also used. 3. The chicks were reared under standard management conditions. Body weight and plasma Ca and P concentrations were measured at 2, 4, and 7 weeks of age. Incidence of TD was recorded at 4 and 7 weeks. 4. Although HH birds had lower body weights than the other lines, there was no significant effect attributable to line selection for body weight at 2, 4, and 7 weeks of age. 5. The LL line birds had no incidence of TD at 4 weeks of age; however, the incidence of TD in LL line birds was 5.3% at 7 weeks of age. The incidence of TD was higher in HH line birds than the other line at 4 and 7 weeks of age. 6. Plasma Ca and P concentrations and Ca:P ratios increased with age. These results showed that HH line birds had higher plasma Ca, lower plasma P and higher Ca:P ratios than birds of the LL line.

Effects of divergent selection for incidence of tibial dyschondroplasia (TD) on purebred and crossbred performance. 2. Processing yield.

1. An experiment was conducted to determine the effect of selection for high (H) or low (L) incidence of tibial dyschondroplasia for 7 generations on processing performance of broilers. 2. Birds were obtained from diallel matings of the H and L lines (HH, HL, LH, and LL) and a randombred control (CC) line. Birds were reared to 7 weeks of age under standard management conditions. All birds were processed at 7 weeks of age. Body weight at 7 weeks, carcase weight, and carcase part weights were recorded on each bird. 3. An interaction between sire line and dam line was caused by lighter body and carcase weight at 7 weeks of age in HH birds than from the birds of the other crosses. 4. Birds by L line dams had heavier drumstick weights. The influences of sire line and dam line on weight of total breast muscle were not significant. Thigh weights and Pectoralis minor weights were lighter in HH line birds than those other matings. 5. Heterosis for body weight and for weights of carcases, drumstick and thigh was negative. Total breast muscle weight and P. major weight did not show significant heterosis. 6. It was concluded that selecting against TD does not reduce processing yield of broilers.

Effect of Natuphos Phytase supplementation to feed on performance and ileal digestibility of protein and amino acids of broilers.

Nutrient equivalency of Natuphos Phytase for minerals, amino acids, and energy has been estimated elsewhere for broiler chickens. The current study was to evaluate equivalent values of 600 FTU/kg Natuphos Phytase for amino acids and energy in 3,150 broiler chicks from hatch to 7 wk of age. Treatments consisted of a 3 x 3 factorial arrangement of three levels of dietary amino acids (AA; 100, 92.5, and 85% of Illinois Ideal Protein for Broiler Chickens) and three phytase inclusion approaches (positive control: 0 FTU/kg with no reduction of Lys, TSAA, and ME; negative control: 0 FTU/kg with reduction of 2% Lys, 1% TSAA, and 0.5% ME; and reformulation with phytase: 600 FTU/kg with reduction of 2% Lys, 1% TSAA, and 0.5% ME). The effect of AA was linear on BW gain and feed conversion (FC); a greater AA level improved performance. No interaction of AA and phytase inclusion approach was significant in terms of BW gain, feed intake (FI), and FC of growing and finishing broilers. Birds fed the positive control diet had greater BW gain than those fed the negative control diet. Body weight gain of birds fed the diet reformulated with phytase did not differ from those of birds fed the positive control. Feed conversion was not affected by phytase inclusion approaches. Effects of phytase supplement on apparent ileal digestibilities (AID) of CP and AA were not significant. Restoring BW gain lost in the negative control by reformulated feed with 600 FTU/kg phytase indicates that equivalent values estimated elsewhere might be adequate.

Body weight and semen production of broiler breeder males as influenced by crude protein levels and feeding regimens during rearing.

An appropriate dietary CP level and feeding regimen during rearing is considered important for controlling BW and improving semen production in broiler breeder males. A total of 640 day-old broiler breeder male chicks of two commercial strains (A and B) received treatments of a factorial arrangement of two CP levels (12 and 16%) of corn-soybean grower diets and two feeding regimens [changing feed to a grower diet from the standard broiler starter at 0.45 and 0.68 kg BW and then skip-a-day feeding]. Four- to 28-wk BW differed between CP levels during rearing, with heavier BW on the 16% CP diet than on the 12% CP diet in spite of isocaloric feed intake. Strains did not show a significant difference in BW prior to 40 wk of age. Feed restriction initiated at 0.45 or 0.68 kg BW had no effect in controlling BW after 4 wk of age. Uniformity of BW did not differ between CP levels. Semen volume was greater on the 12% than on the 16% CP diet from 28 to 36 wk of age. Semen concentration was not affected by CP levels, feeding regimens, or strains. Spermatozoa per ejaculate from 28 to 52 wk of age was correlated negatively with 8- to 20-wk BW. This negative relationship was attenuated with age, until at Week 46 or later spermatozoa per ejaculate was associated positively with BW after sexual maturity. No difference in percentage of males in semen production was noted between strains, CP levels, or feeding regimens. In brief, diet changes at 0.45 or 0.68 kg BW were not important in improving semen production, whereas the low CP diet (12%) had advantages in semen production over the high CP diet (16%). A negative relationship existed between semen production and BW during rearing; however, continued BW gain after sexual maturity was necessary to optimize semen production, especially during the late breeding period.

Response to ten generations of divergent selection for tibial dyschondroplasia in broiler chickens: growth, egg production, and hatchability.

Continued genetic selection for improved BW gain has met an obstacle of skeletal disorders in broiler chickens. Two broiler chicken lines (HTD and LTD) were developed by 10 generations of divergent selection for tibial dyschondroplasia (TD) incidence originating from commercial primary breeders. The reference population was a randombred control line maintained along with the selected lines. Relationships of TD incidence with BW, egg production (EP), and hatchability were assessed using these lines. The response of TD to selection was asymmetric, favoring an increased TD incidence. Mean TD incidence increased 7.6 percentage points per generation during Generation 1 through 10 in males and 9.1 percentage points in females of the HTD line but did not change significantly in the LTD line at 4 wk of age. Responses of the HTD line in early (1 to 4) generations were greater than in later (6 to 10) generations, in contrast to nonsignificant responses for both durations in the LTD line. The 4-wk BW of the HTD line was slightly heavier than or similar to that of the LTD line within generations. The HTD line birds tended to decrease 7-wk BW with advancing generations. The trend of changes in BW was not as clear in the LTD lines as in the HTD line. The variability of 7-wk BW had an increased trend with advancing generations in the HTD line, accompanied by a decreased additive genetic variability of TD due to continued selection. The average EP in the LTD hens was 7.6 percentage points higher than in the HTD from Generations 1 through 10. Mean hatchability in the LTD line did not differ from that in the HTD line within generation. Responses of EP and hatchability, components associated with fitness, appeared slower towards increased fitness than towards decreased fitness.

Genetic variation of phytate phosphorus utilization from hatch to three weeks of age in broiler chicken lines selected for incidence of tibial dyschondroplasia.

Ability to utilize dietary phytate P was evaluated in 1,387 broiler chicks of 45 sire and 180 dam families, by feeding a corn-soybean base diet supplemented with no inorganic P and a low level of Ca. These chicks were the progeny of high and low incidence of tibial dyschondroplasia (TD) selected divergently for 11 generations and a nonselected control line. Chicks from the control line utilized phytate P better than those from the high or low lines in terms of livability, mortality, and growth performance. Chicks did not differ in mortality and body weight between the high and low lines. Variation in livability and mortality was greater among lines than among families, whereas families accounted for a greater part of variation than lines in body weight. Dams accounted for a slightly larger proportion of variation than sires in traits studied. Genetic selection for improved utilization of dietary phytate P could be effective.

Comparison of several enzymes between normal physeal and tibial dyschondroplastic cartilage of broiler chickens.

Normal physeal and dyschondroplastic cartilage of broiler chickens was examined for six enzymes by isoelectric focusing in thin-layer polyacrylamide slab gels. Acid phosphatase (ACP), esterase (EST), malate dehydrogenase (MDH), and peroxidase (PRX) were present in the normal physeal cartilage but not in the dyschondroplastic cartilage. Staining intensity of glucose-6-phosphate isomerase (GPI) and triose-phosphate isomerase (TPI) was reduced in the dyschondroplastic cartilage compared with that of the physeal cartilage. Differences in the presence of these enzymes possibly demonstrated their roles in processes of bone formation, cartilage resorption, and calcification. ACP could be involved in calcification. Lack of EST and PRX may be related to the failure of vascular invasion in dyschondroplastic cartilage of afflicted birds. A deficiency of MDH and reduced GPI and TPI in dyschondroplastic cartilage may reflect a reduction in the activity of energetic metabolism, causing the dissipation of energy and necrotic cells.

Dietary 1,25-dihydroxycholecalciferol has variable effects on the incidences of leg abnormalities, plasma vitamin D metabolites, and vitamin D receptors in chickens divergently selected for tibial dyschondroplasia.

Three experiments were conducted to examine the efficacy of dietary 1,25-dihydroxycholecalciferol [(1,25-(OH)2D3)] on the development of tibial dyschondroplasia (TD) in chickens divergently selected for high (HTD) and low (LTD) incidences of TD. In Experiment 1, chickens from the two lines were fed two calcium levels (0.75 and 1.0%), with and without 5 micrograms/ kg dietary 1,25-(OH)2D3. In Experiment 2, both lines were fed diets containing 1.0% calcium and 0, 5, 10, or 15 micrograms/kg 1,25-(OH)2D3. The addition of 1,25-(OH)2D3 did not reduce the overall incidence of TD in Experiment 1, but did reduce the incidence of severe TD from 69 to 48% in the chickens receiving the 0.75% calcium diet. In this experiment, LTD chickens had higher plasma phosphorus and bone ash. No line differences were noted between plasma vitamin D metabolites or intestinal vitamin D receptors. In Experiment 2, 5 micrograms/kg of 1,25-(OH)2D3 decreased the incidence of TD from 94 to 76% and number three scores from 69 to 44% (P < or = 0.001). Higher amounts of 1,25-(OH)2D3 further decreased TD, but there was a reduction in body weight above 5 micrograms/kg. Plasma 25-hydroxycholecalciferol [25-(OH)D3] and 1,25-(OH)2D3 were higher and intestinal vitamin D receptors were lower in HTD chickens than in LTD chickens. Plasma 1,25-(OH)2D3 was not affected by dietary treatment, but 25-(OH)D3 was reduced by dietary 1,25-(OH)2D3. Experiment 3 was conducted to examine effects of line and dietary 1,25-(OH)2D3 on plasma vitamin D metabolites and intestinal and growth plate receptors. No effect of genetic line or dietary 1,25-(OH)2D3 was observed for vitamin D receptors concentration or plasma 1,25-(OH)2D3 levels. Plasma 25-(OH)D3 was reduced when 1,25-(OH)2D3 was fed. These results indicate that HTD chickens are somewhat responsive to dietary 1,25-(OH)2D3, but this treatment failed to prevent the lesion in a large portion of the population.

The effects of ultraviolet light and cholecalciferol and its metabolites on the development of leg abnormalities in chickens genetically selected for a high and low incidence of tibial dyschondroplasia.

Four experiments were conducted to investigate the effects of ultraviolet (UV) light exposure and several cholecalciferol metabolites on the development of tibial dyschondroplasia (TD) and other parameters associated with vitamin D metabolism in chickens selected for high (HTD) and low (LTD) incidence of TD. In Experiment 1, exposure of chickens to UV light reduced the incidence and severity of TD more in LTD chickens than in HTD chickens, as evident by the significant interactions (P < 0.10 and 0.04). In Experiment 2, the addition of cholecalciferol to diets that were deficient in cholecalciferol linearly decreased the incidence of vitamin D rickets and increased bone ash, but increased the incidence of severe TD. The LTD chickens had a higher maximal bone ash of 40.0 +/- 0.7% than did the HTD chickens, which had a maximal bone ash of 37.0 +/- 0.7%. In Experiment 3, the addition of 5 micrograms/kg of 25-hydroxycholecalciferol [25-(OH)D3], 1-alpha-hydroxycholecalciferol, or 1,25- dihydroxycholecalciferol decreased the incidence and severity of TD in the LTD chickens and had no effect on TD in HTD chickens. In Experiment 4, increasing dietary 25-(OH)D3 increased plasma 25-(OH)D3 levels in both lines, but HTD chickens had higher plasma 25-(OH)D3 levels at 20 and 40 micrograms/kg of dietary 25-(OH)D3. The incidence and severity of TD were reduced in the LTD chickens by dietary 25-(OH)D3, but little effect was noted in HTD chickens. The LTD chickens reached a maximal bone ash at 9.7 +/- 1.9 micrograms/kg and HTD chickens reached the same bone ash at 33.0 +/- 7.0 micrograms/kg. These results indicate that UV light and vitamin D metabolites are not effective in preventing TD in HTD chickens, but that altered vitamin D metabolism does exist between HTD and LTD chickens.

Estimates of heritabilities and genetic correlations between tibial dyschondroplasia expression and body weight at two ages in broilers.

Genetic variances and covariances were estimated by multiple-trait, derivative-free restricted maximum likelihood (DFREML) using an animal model for tibial dyschondroplasia (TD) expression and body weight at 4 and 7 wk of age. Data were collected from 7,483 broiler progeny obtained from 421 sires and 977 dams as part of a seven-generation selection experiment for high, and low TD expression, along with a randomly selected control line. Heritability estimates for TD expression and body weight at 7 wk were 0.42 and 0.50, respectively, larger than the corresponding estimates of 0.37 and 0.42 at 4 wk of age. Genetic correlations of TD expression or body weight at 4 wk with the same trait at 7 wk were greater than 0.80. Corresponding phenotypic correlations were 0.54 and 0.75 for TD incidence and body weight, respectively. Genetic correlations, however, of TD expression at either age with body weight at either age ranged from -0.01 to 0.10. Phenotypic correlations between the TD and body weight traits were of similar magnitude. TD expression and body weight at 4 and 7 wk of age, based on these data, are genetically and phenotypically independent traits.

Promoter and transcription of type X collagen gene in broiler chickens with tibial dyschondroplasia.

Type X collagen is produced exclusively in hypertrophic chondrocytes of the growth plate of the proximal tibiotarsus and is believed to play an important role during normal development from chondrogenesis to osteogenesis. Chondrocytes of chickens with tibial dyschondroplasia (TD) fail to attain full hypertrophy and the amount of type X collagen, being a marker of hypertrophy, is likely to be reduced. It is not clear whether transcriptional regulation is functional for expression of the type X collagen gene in TD birds. Nucleotide sequence of the type X collagen gene promoter was determined by sequencing PCR-based DNA clones. Nucleotide identity of this fragment between the normal and TD carriers was 97.6%. Both normal and TD birds were similar in a putative transcription start site, the site of TATAA box, and neither had a CCAAT box. However, there were two gaps in TD carriers, four gaps in normals, and five nucleotide substitution sites. By rapid amplification of cDNA ends by PCR (RACE-PCR), transcription of the gene was assessed using total RNA and mRNA from both normal chondrocytes and TD lesions at 3 and 4 wk of age. The RACE-PCR product for type X collagen mRNA was detectable in both normal and TD birds at two stages. No difference was found between them. This result does not support the hypothesis that transcriptional regulation of type X collagen gene is important in TD development of chickens. Variations in the promoter region did not affect transcription of type X collagen gene in TD carrier chickens.

Immunohistochemical study of a chondroitin-6-sulfate in growth plates of broiler chickens with high and low genetic predispositions to tibial dyschondroplasia.

The distribution of a chondroitin-6-sulfate (C6S) epitope, which is a biochemical marker of chondrocyte hypertrophy, was studied in the growth plates of two lines of 3-week-old broiler chickens with low and high genetic predispositions to tibial dyschondroplasia (TD). Ultrathin sections of growth plates from both groups were subjected to immunolocalization with monoclonal antibody 3-B-3(-), the epitope of which is increased on proteoglycans made by hypertrophic chondrocytes. Bound antibody was localized with colloidal gold-labeled protein A for observation with an electron microscope. The 3-B-3(-) epitope was localized in pericellular and interterritorial matrix of growth plates of both lines. In the low-TD-incidence birds, the concentration of 3-B-3(-) bound to C6S progressively increased from the proliferative zone to the hypertrophic zone. However, in the high-TD-incidence line, the epitope expression remained at a low level in all zones. The increase of the 3-B-3(-) epitope produced by maturing growth-plate chondrocytes is indicative of changes in the glycosaminoglycan chains of proteoglycans that may be important in the process of matrical calcification. Thus, failure of chondrocytes of the high-TD-incidence line to produce this change in post-translational modification of their proteoglycans could be important in the pathological process.

Effect of selection for high or low incidence of tibial dyschondroplasia for seven generations on live performance.

An experiment was conducted to determine the effect of divergent selection for tibial dyschondroplasia (TD) on live performance of broilers. Broilers used in the experiment were produced from the parental lines selected for high (H) and low (L) incidence of TD and a randombred control (C) line. Diallel crosses were made between H and L lines. The offspring produced were HH, HL, LH, LL, and CC, where the first letter refers to sire line and the second letter refers to dam line. Body weights, average daily body weight gains, and exponential growth rates were determined at weekly intervals. The incidence of TD was recorded at 4 and 7 wk of age. There was no difference among body weights of lines up to 5 wk of age. Sire lines influenced body weights of birds from 5 to 7 wk of age. A significant interaction between sire and dam lines for body weight was the result of decreased body weights of birds in the HH line from 5 to 6 wk of age. There was a similar interaction for body weight gain, which resulted in a slower growth rate of birds in the HH line from 3 to 5 wk of age. Tibial dyschondroplasia incidence was 84.1 and 92.0% in the HH line, 5.6 and 5.4% in the LL line, and 7.0 and 13.2% in the CC line at 4 and 7 wk of age, respectively. It was suggested that genetic predisposition for TD was independent of body weight.

Random amplified polymorphic DNA comparisons among broiler lines selected for incidence of tibial dyschondroplasia.

Lines selected for high (H) and low (L) incidence of tibial dyschondroplasia (TD) for eight generations and a randombred control (C) line of broiler chickens were fingerprinted by random amplification of genomic DNA mixed from 20 individuals of each line with 20 oligonucleotide primers. Among these 20 primers, 15 could distinguish the H from the L line, 14 the H from the C line, and 13 the L from the C line. Band sharing (BS), on the average over 20 primers, was .7 for the H vs L comparison and .8 for both H vs C and L vs C comparisons. The levels of BS calculated from individuals was .6 between the H and L line, .7 between the H and C line, and .7 between the L and C line. The ranking of BS values obtained from individual DNA samples was consistent with that obtained from the mixed DNA samples. Genomic distance between divergently selected lines (H vs L) was larger than that between the divergently selected lines and randombred line (H vs C and L vs C). Individual variation within lines was detected in spite of eight generations of selection. Results showed that eight generations of divergent selection for TD incidence in broiler chickens had resulted in genetic variation among lines. The procedure of random amplified polymorphic DNA assay using mixed DNA samples could be used to evaluate genetic distance among lines of chickens.

Genetic correlations of tibial dyschondroplasia incidence with carcass traits in broilers.

Relationships among the incidence of tibial dyschondroplasia (TD) with 7-wk live BW, carcass component weights (CCW), and abdominal fat weight (AFW) were assessed using high and low incidence of TD lines developed by a seven-generation divergent selection experiment, along with a randombred control line. The incidence of TD exhibited negative genetic correlations with both BW (-.65 and -.46 estimated from sire's and dam's components of variance and covariance, respectively) and with CCW (< -.28). The incidence of TD and AFW was not correlated based on sire's components of variance and covariance. The correlation of TD incidence with AFW was not as high as with the other traits under consideration based on dam's components of variance and covariance. Correlations of AFW with CCW were negative based on sire's components of variance and covariance, but positive based on dam's components of variance and covariance. Heritabilities of TD, BW, AFW, and CCW estimated by sire's variance components were lower than those estimated by dam's variance component. Dams might have a greater influence on TD incidence than sires. Selection for decreasing TD incidence should be feasible while simultaneously increasing BW and CCW in broilers.

Ultrastructural changes of chondrocytes of growth plates of young broiler chickens predisposed to tibial dyschondroplasia.

Growth plates from the proximal tibiotarsal bones of growing broiler chickens from lines exhibiting high and low incidences of tibial dyschondroplasia (TD) were compared for ultrastructural differences. Samples of growth plates were collected from five chickens of each line at 2, 7, 14, and 21 d of age. Each sample was prepared for ultrastructural evaluation after initial fixation in 2.5% glutaraldehyde and secondary fixation in 1% osmium tetroxide, each containing .7% ruthenium hexamine trichloride. No gross TD lesions were observed. The ultrastructure of growth plates of birds at 2, 7, and 14 d of age was similar between the groups. However, at 21 d of age, chondrocytes in the prehypertrophic zone of the high incidence group contained large lipid inclusions and vesiculated and disarranged stacks of rough endoplasmic reticulum with greatly dilated cisternae. Apoptotic and necrotic chondrocytes were present in the hypertrophic zone. Nuclei of apoptotic chondrocytes contained crescentic caps of condensed chromatin. The cytoplasm contained short segments of dilated granular endoplasmic reticulum, lipid droplets, and vacuoles. Necrotic chondrocytes appeared as amorphous masses with pyknotic and karyorrhectic nuclei. These changes were not observed in chondrocytes of the low TD incidence group and have not been previously reported in nonthickened growth plate cartilage.

A correlation method for detecting and estimating linkage between a marker locus and a quantitative trait locus using inbred lines.

The advent of molecular genetic markers has stimulated interest in detecting linkage between a marker locus and a quantitative trait locus (QTL) because the marker locus, even without direct effect on the quantitative trait, could be useful in increasing the response to selection. A correlation method for detecting and estimating linkage between a marker locus and a QTL is described using selfing and sib-mating populations. Computer simulations were performed to estimate the power of the method, the sample size (N) needed to detect linkage, and the recombination value (r). The power of this method was a function of the expected recombination value E(r), the standardized difference (d) between the QTL genotypic means, and N. The power was highest at complete linkage, decreased with an increase in E(r), and then increased at E(r)=0.5. A larger d and N led to a higher power. The sample size needed to detect linkage was dependent upon E(r) and d. The sample size had a minimum value at E(r)=0, increased with an increase in E(r) and a decrease in d. In general, the r was overestimated. With an increase in d, the r was closer to its expectation. Detection of linkage by the proposed method under incomplete linkage was more efficient than estimation of recombination values. The correlation method and the method of comparison of marker-genotype means have a similar power when there is linkage, but the former has a slightly higher power than the latter when there is no linkage.

Effects of increased rearing period body weights and early photostimulation on broiler breeder egg production.

Broiler breeder pullets were subjected to photostimulation (PS) at either 14, 17, or 20 wk of age after attaining greater than recommended BW during rearing in order to determine effects on age at onset of lay, egg weight, and egg production. During rearing, feed was consumed ad libitum (AL) or provided in allotments resulting in growth to projected BW of 2.8 (heavy, HV) or 2.3 kg (light, LT) at 20 wk. Rearing period feeding and age at PS treatments made up a 3 x 3 factorial arrangement. A single restricted feeding program was provided during lay. Although age at first egg in the AL treatment was earlier than in HV and LT treatments, total production by HV and LT birds was greater because peak and postpeak production by AL birds were depressed. Relative to PS at 20 wk, PS at 14 and 17 wk advanced age at first egg and increased cumulative production to 30 wk. However, early PS decreased peak production and, therefore, did not affect total production. Mean egg weight and settable egg production (egg weight > 50 g) were increased in HV and LT treatments. Egg weight and settable egg production were not affected by age at PS. These results indicate that the onset of lay by broiler breeders can be advanced by early PS and that increased BW facilitates this. However, allowing greater BW during rearing does not compensate for reduced early egg weights and results in decreased total production and mean egg weights when feed is provided at recommended levels during lay.