Major histocompatibility (B) complex effects on acquired immunity to cecal coccidiosis

The influence of the major histocompatibility (B) complex on acquired immunity to the avian coccidium Eimeria tenella was studied in 217 F₄ segregants (B ² B ², B ² B ⁵, B ⁵ B ⁵) of a cross between inbred lines 6₁ (B ² B ²) and 15₁ (B ⁵ B ⁵) and segregating haplotype combinations of UNH105 (B ²³ B ²³ B ²³ B ²⁴, B ²⁴ B ²⁴), a noninbred line of New Hampshire chickens. Chickens were immunized at 6 weeks of age with 500 oocysts daily for 5 days, then challenged 14 days later with 10000 oocysts. Responses to infection were evaluated by cecal lesion scores, body weight gain, delayed wattle reaction (DWR), and spleen weight. The F₄ segregants of genotypes B ² B ⁵ and B ⁵ B ⁵ exhibited greater immunity to challenge than B ² B ² chickens. B ⁵ B ⁵ chickens showed a significantly greater DWR following immunization and larger spleens 6 days after the challenge than either of the other genotypes. However, both BIBS and B ⁵ B ⁵ chickens demonstrated significantly lower lesion scores than B ² B ² chickens. There were no significant differences in weight gain among these genotypes. Among 139 line UNH105 segregants, B ²³ B ²³ hosts had significantly lower lesion scores than B ²⁴ B ²⁴ chickens. No other differences in immune response among line UNH105 genotypes were detected.     

Influence of different B-complex recombinants on the outcome of Rous sarcomas in chickens

Seven major histocompatibility (B) complex recombinants were evaluated for anti-Rous sarcoma response. In experiment 1, the B^R5(F21-G19) recombinant haplotype both homozygous and in heterozygous combinations with B¹⁹ and B²¹ haplotypes were compared to B¹⁹/B¹⁹ and B²¹/B²¹ chickens to determine the relative influence of the B^F versus B^G chromosomal segments on regression of Rous sarcoma virus-induced tumours. In experiment 2, six recombinant haplotypes B^R1(F24-G23), B^R2(F2-G23), B^R3(F2-G23), B^R4(F2-G23), B^R6(F21-G23) and B^R8(F2-G2a,23) present in chickens heterozygous for normal haplotypes B¹⁹, B²³ or B²⁶ were compared for anti-sarcoma response. A total of 1328 chickens were blood typed for B alloanti-gens at 17 days of age, inoculated in the wingweb with Rous sarcoma virus at 6 weeks and monitored for anti-tumour immune response over a 10-week period. Genotypes which shared the same B^F haplotype, but differed in their B^G regions, had similar anti-tumour responses, implicating the B^F but not the B^G region in tumour regression. Chickens carrying B^F2 or B^F21 had a strong anti-tumour response, while B^F24 conferred a weaker response, regardless of the accompanying normal haplotype.     

Tests of association of immunoglobulin allotype genes and viral oncogenesis in chickens

Chickens from Regional Poultry Research Laboratory (RPRL) inbred line 6₃ are resistant to virally-induced Marek's disease (MD) and lymphoid leukosis (LL) and are relatively strong regressors of virally-induced Rous sarcomas. In contrast, RPRL line 100 chickens are highly susceptible to MD and LL and are weaker regressors of Rous sarcomas than line 6₃. RPRL lines 100 and 6₃ differ for alleles at the IgG-1 (G-1) allotype locus, but have identical IgM-1 (M-1) allotype alleles. To test the possible association of the G-1 locus with variations in resistance to virally-induced tumors, homozygous and heterozygous genotypes among F₃ crosses were infected. F₃ chickens with different G-1 types were comparable in their resistance to MD tumors following inoculation with the JM strain of the MD virus, and for their ability to regress Rous sarcoma tumors induced by the Rous sarcoma virus (RSV) RAV-1. However, following RAV-1 virus infection a smaller proportion of G-1 ^a /G-1 ^a F₃ or F₄ birds developed LL tumors than G-1 ^a /G-1 ^e and G-1 ^e /G-1 ^e birds. Genes determining immunoglobulin heavy chains were therefore associated with a recessive resistance to B-cell lymphomagenesis in chickens.Deceased     

TheB locus (MHC) in the chicken: Association with the fate of RSV-induced tumors

The fate of tumors induced by Rous sarcoma virus (RSV) was determined in anF ₂ population segregating at three alloantigen loci. TheF ₁ resulted from crossing tumor-resistant RPRL line 6₁ (B ² B ² D ³ D ³ I ² I ²) with tumor-susceptible RPRL line 15₁ (B ⁵ B ⁵ D ⁴ D ⁴ I ⁸ I ⁸). Among theF ₂ segregantsB ² B ²,B ² B ⁵, andB ⁵ B ⁵, the percentage of chicks dying of terminal tumors (by 70 days post-inoculation) was 5, 26, and 93, respectively (P0.01). NeitherD orI genotypes nor sex significantly affected tumor growth. In chickens with terminal tumors, the incidence of metastatic lesions was also significantly associated withB genotypes. Thus, the MHC chromosomal region in the chicken appears to exert a crucial role in determining the outcome of RSV-induced tumors.     

Cross-reactivity between RSV-induced tumor antigen and B5 MHC alloantigen in the chicken

Lymphocytes from chickens homozygous (B ² B ²) at the major histocompatibility complex (MHC) were tested for cytotoxic activity against five types of target chicken embryo fibroblasts (CEF). Lymphocytes from B²B² chickens bearing RSV-induced tumors lysed in vitro targets of B ² B ² and B ⁵ B ⁵ RSV-infected CEF and B ⁵ B ⁵ normal CEF, but did not lyse B ² B ² and B ²⁴ B ²⁴ normal CEF. Lymphocytes from normal B ² B ² chickens did not lyse any of the five types of CEF targets. Alloantisera absorption studies showed that both RSV-infected and uninfected CEF shared alloantigens, in particular B-F alloantigens, with syngeneic erythrocytes. Absorption with B ² B ² RSV-infected CEF significantly lowered the titer of B ² B ² anti-B ⁵ B ⁵ alloantisera. Cross-reactivity between B ₅ antigen(s) and tumor-associated antigen was suggested and the nature of the cross-reactivity was discussed. It is hypothesized that this cross-reactivity prevents B ⁵ B ⁵ chickens from recognizing RSV-induced tumors as foreign, enhances tumor growth and leads to death of the host.     

Genetic control of avian scleroderma

The inheritance of avian scleroderma, a fibrotic autoimmune disease of chickens resembling human scleroderma, was investigated. Comb inflammations and lesions were used to determine the state of disease of 4-week-old chickens. All line 200 males and 60% of female line 200 chicks showed abnormalities. Crosses (F₄) between line 200 and eight partially inbred lines of chickens maintained at the University of California at Davis were all normal. Backcrosses of F, cocks to line 200 hens showed a higher incidence of scleroderma in males than in females for all lines. The incidence of affected birds varied between backcrosses from a low of 42% for backcross line 217 males derived from a New Hampshire line, to 88% for males of backcross line 213 derived from a partially inbred Leghorn line, demonstrating the presence of genes modifying the penetrance of presumed major genes causing the disease. Backcross genotypes segregating for haplotypes of the major histocompatibility complex (MHC) derived from inbred lines showed consistently lower penetrance of scleroderma than homozygotes carrying the line 200 haplotype. Thus B³ B^S (lines 211 and 215), B¹⁴Bu^s (line 217), and B¹⁵B^S (lines 212, 213, 216, and 218) all had fewer affected individuals than B^SB^S homozygotes from the same families.     

Cosegregation of the polymorphic C4 with the MHC in the frog,Xenopus laevis

Employing isoeletric focusing combined with enzyme-linked immunoelectrotransfer blot analysis, the fourth component of complement (C4) was analyzed in the two highly histocompatible, major histocompatibility complex homozygous groups (J and K) of Xenopus laevis. Each group had a characteristic C4 isoelectric focusing pattern, i. e., an isoelectric point range of 8.0–8.5 for J (C4 ^j C4 ^j ) and 7.6–8.1 for K (C4 ^k C4 ^k ). In (J x K)F₁ frogs, C4 proteins were expressed in a codominant fashion (C4 ^j C4 ^k ). In the backcrossed progeny B₁ [J × (J × K)F₁], those with C4 ^j C4 ^j rejected (J × K)F₁ skins hyperacutely (< 17 days), were high responders against (J × K)F₁ cells, and nonstimulators to J cells in mixed lymphocyte reaction (MLR), but they did not suffer from the graft-versus-host reaction (GVHR), even after the injection of (J x K)F₁ cell-stimulated J splenocytes. On the other hand, the B₁ frogs with C4 ^j C4 ^k acutely or chronically (> 17 days) rejected (J × K)F₁ skins, were low or nonresponders against (J × K)F₁ cells and high stimulators to J cells in MLR, and they suffered from GVHR after the injection of prestimulated J splenocytes. These results argue for the notion that the genes equivalent to mammalian class III map to the MHC at the phylogenetic level of the anuran amphibian.     

H-2-associated control of natural cytotoxicity and hybrid resistance against RBL-5

(C57B1 × DBA)F₁ hybrids were more resistant to the inoculation of 10³ Rauscher virus-induced, serially propagated RBL-5 cells than syngeneic C57Bl recipients. Resistance was linked toH-2^di in the C57Bl backcross. Spleen cells from nonimmune (C57Bl × DBA)F₁ hybrids were significantly more reactive against RBL-5 in the natural killer (NK) cytotoxicity test in vitro than were C57Bl spleen cells. In the C57Bl backcross,H-2^dH 2^b heterozygotes were more cytotoxic than theH- 2^B homozygotes. Along with RBL-5, they were also more cytotoxic to the Moloney virus-induced YAC lymphoma (of strain A origin) and to the human ALL-derived MOLT-4 line.     

Paramagnetic 1H NMR spectroscopy of the reduced, unbound Photosystem I subunit PsaC: sequence-specific assignment of contact-shifted resonances and identification of mixed-and equal-valence Fe-Fe pairs in [4Fe-4S] centers FA − and FB −

A and F_B. The g-tensor orientation of F_A ⁻ and F_B ⁻ is believed to be correlated to the preferential localization of the mixed-valence and equal-valence (ferrous) iron pairs in each [4Fe-4S]⁺ cluster. The preferential position of the mixed-valence and equal-valence pairs, in turn, can be inferred from the study of the temperature dependence of contact-shifted resonances by ¹H NMR spectroscopy. For this, a sequence-specific assignment of these signals is required. The ¹H NMR spectrum of reduced, unbound PsaC from Synechococcus sp. PCC 7002 at 280.4 K in 99% D₂O solution shows 18 hyperfine-shifted resonances. The non-solvent-exchangeable, hyperfine-shifted resonances of reduced PsaC are clearly identified as belonging to the cysteines coordinating the clusters F_A ⁻ and F_B ⁻ by their downfield chemical shifts, by their temperature dependencies, and by their short T ₁ relaxation times. The usual fast method of assigning the ¹H NMR spectra of reduced [4Fe-4S] proteins through magnetization transfer from the oxidized to the reduced state was not feasible in the case of reduced PsaC. Therefore, a de novo self-consistent sequence-specific assignment of the hyperfine-shifted resonances was obtained based on dipolar connectivities from 1D NOE difference spectra and on longitudinal relaxation times using the X-ray structure of Clostridium acidi urici 2[4Fe-4S] cluster ferredoxin at 0.94 Å resolution as a model. The results clearly show the same sequence-specific distribution of Curie and anti-Curie cysteines for unbound, reduced PsaC as established for other [4Fe-4S]-containing proteins; therefore, the mixed-valence and equal-valence (ferrous) Fe-Fe pairs in F_A ⁻ and F_B ⁻ have the same preferential positions relative to the protein. The analysis reveals that the magnetic properties of the two [4Fe-4S] clusters are essentially indistinguishable in unbound PsaC, in contrast to the PsaC that is bound as a component of the PS I complex. Received: 1 February 2000 / Accepted: 20 March 2000     

Genetic interaction between Non-MHC T- and B-cell alloantigens in response to rous sarcomas in chickens

Chickens of Regional Poultry Research Laboratory (RPRL) inbred line 6₃ regress sarcomas induced by Bryan high-titer Rous sarcoma virus to a greater extent than chickens of line RPRL 100, although these lines are identical for the major histocompatibility B complex. They differ, however, at three independent autosomal loci: Ly-4 and Th-1 determine the surface alloantigens of partly overlapping subsets of T lymphocytes, and Bu-1 determines a surface alloantigen of B lymphocytes. The association of genotypes at these loci with quantitative variation in their ability to regress Rous sarcomas was tested in segregating F₄ generation progeny derived from crosses of lines 100 and 6₃. The Ly-4 and Bu-1 genotypes showed association with Rous sarcoma regression, but the Th-1 genotype did not. Chickens of the Ly-4 ^a/Ly-4 ^a, Bu-1 ^b/Bu-1 ^b and Ly-4 ^b/Ly-4 ^b, Bu-1 ^a/Bu-1 ^a genotypes had a significantly higher regressor ability than the other two double homozygous genotypes. These results indicate that higher regression is associated with (1) interaction between the Ly-4 and Bu-1 loci, and (2) complementation between either the line 6 Ly-4 ^a allele and the line 100 Bu-1 ^b allele, or the line 100 Ly-4 ^b allele and the line 6 Bu-1 ^a allele.     

Increased growth of RSV-induced tumors in chickens partially tolerant to MHC alloantigens

Chickens withB ² B ² MHC genotypes were made partially tolerant to B₅ MHC cell-surface antigens and the fate of their Rous-sarcoma-virus (RSV)-induced tumors was determined.B ² B ² chickens partially tolerant to viable or lysed white blood cells (WBC) or viable red blood cells (RBC) fromB ⁵ B ⁵ chickens had a significantly higher incidence of tumor progression than untreated, PBS-treated, orB ² B ² chickens inoculated with WBC from otherB ² B ² chickens. The criteria for tolerance were absence of antibody titer to the cell type inoculated and acceptance of allografts fromB ⁵ B ⁵ donors byB ² B ² chickens. Graft-vs-host reactions occurred only inB ² B ² chickens inoculated with viable WBC fromB ⁵ B ⁵ chickens. It appears thatB ² B ² chickens partially tolerant to B₅ antigens failed to mount a successful immune response to RSV-induced tumors partly because a B₅ MHC antigen(s) cross-reacted with a tumor associated antigen(s) thereby severely limitingB ² B ² host recognition of the tumor as foreign. Since WBC and RBC cell-surface antigens appear to contribute similarly to the effect, theB-F- region of the MHC may be involved.     

Anti-Rous sarcoma response of major histocompatibility (B) complex haplotypes B23, B24 and B30

Responses to Rous sarcoma virus (RSV) induced tumours were studied in UNH 105, a non-inbred line of New Hampshire chickens. Six single male matings encompassing a total of 50 dams produced 345 progeny which segregated for B complex genotypes B23/B23, B23/B24, B23/B30, B24/B24, B24/B30 and B30/B30. Six-week-old chicks were wingweb inoculated with a pseudotype of Bryan high titre Rous sarcoma virus, BH RSV (RAV-1). Tumours were scored for size six times over a 10-week period post-inoculation. Each chick was assigned a tumour profile index (TPI) as an indicator of immunological response. The number of days to death (DTD) was recorded for 148 chicks with terminal tumours. Genotypes B23/B23, B23/B24 and B23/B30, with TPIs of 1.8, 1.7 and 2.0 respectively, did not differ significantly from each other, suggesting dominance of response of B23 over B24 and B30 haplotypes. B24/B30 chicks with the highest TPI (3.4) and shortest DTD (34.6) were significantly different from B30/B30 (2.8; 41.6) but not from B24/B24 (3.1; 34.9) suggesting dominance of response of the B24 haplotype over B30 in the absence of B23.     

Synergistic promotion of gibberellin and cytokinin on direct regeneration of floral buds from in vitro cultures of sepal segments in sinningia speciosa hiern

Summary This study reports the direct regeneration of flower buds from cultured sepal segments of Sinningia speciosa Hiern. Two types of floral bud regeneration were observed: regeneration of floral buds only (designed as B^F) and regeneration of both floral and vegetative buds (designed as B^F+V). The capacity of B^F regeneration was closely related to the location of sepal segments and the concentration of exogenous gibberellin (GA₃) and cytokinin in the medium. On the medium containing 1.0mgl^&#x2212;1 GA₃, the addition of 6-benzyladenine (BA) significantly increased the frequency of total flower bud (B^F+B^F+V) formation, with the frequency up to 91.5% in the presence of 0.4mgl^&#x2212;1 BA. On the medium containing 0.1mgl^&#x2212;1 BA, the addition of GA₃ also increased the frequency of total flower bud regeneration, with the frequency up to 74.3% in the presence of 1.0mgl^&#x2212;1 GA₃, but no further increase in regeneration was observed when the GA₃ concentration was higher than 1.0mgl^&#x2212;1. The capacity of B^F regeneration from different locations of sepal segments was differential. The adaxial part of sepal segments gave rise to the highest frequency of 56.7 and 84.3% for B^F and B^F+B^F+V, respectively.     

Dietary arginine influences Rous sarcoma growth in a major histocompatibility B complex progressor genotype.

L-Arginine (L-Arg) can serve as a substrate for the production of reactive nitrogen intermediates. One of these metabolites, nitric oxide, has been shown to possess significant antitumor properties in vitro. To investigate the importance of this system in vivo, we have examined the dietary L-Arg host tumor interaction in the chicken. Since chickens are incapable of de novo L-Arg synthesis, concentration of this amino acid is readily controlled by diet. Line UNH 105 New Hampshire chickens having the major histocompatibility complex genotype, B24/B24, were used to study in vivo effects of dietary L-Arg on Rous sarcoma growth. After 5 weeks on a standard diet, 119 chicks were fed either a basal (0.92% L-Arg) diet or a high arginine (2.40% L-Arg) diet. One week later, chicks were wing-web inoculated with subgroup A Rous sarcoma virus. Tumor growth was monitored weekly for 12 weeks after inoculation. Plasma L-Arg levels and body weights from birds on each dietary treatment were analyzed. Neither body weight gains nor latent period for tumor development was affected by diet. However, plasma L-Arg levels were significantly different between dietary treatments (basal, 0.245 +/- 0.01 mumol/ml; high, 0.738 +/- 0.03 mumol/ml). In addition, mean tumor size scores were significantly (P less than 0.05) lower over time in chickens fed the high L-Arg diet. The results suggest that dietary L-Arg in excess of the amount required for growth reduces tumor load.     

Expression of Thinopyrum distichum NORs in wheat×Thinopyrum amphiploids and their backcross generations

Summary The C-banding pattern of the satellited chromosomes in Thinopyrum distichum and Triticum durum was established. Both T. durum and Th. distichum contained two pairs of satellited chromosomes, which could be distinguished from one another. In the amphiploids [T. durum×Th. distichum (2x=56)] and in the backcross T. durum/(T. durum×Th. distichum)², BC₁F₃, and BC₁F₅ (2n = 42) the satellite was visible on only 1B and 6B of T. durum. The vector pTa 71 containing the rRNA gene from wheat hybridized to two pairs of chromosomes (four hybridization sites) in T. durum and Th. distichum, to eight sites in the amphiploid hybrid (2n=56), and to six sites in the backcross populations BC₁F₁. BC₁F₃, and BC₁F₅ (2n=42). The two satellite pairs in Th. distichum could be distinguished by the chromosomal location of the rRNA site (median or subterminal) and by the centromere position. One copy of each pair was present in the BC₁F₁, but in the BC₁F₃ and BC₁F₅ populations the pair with the subterminal location of rRNA genes was absent. Silver nitrate staining indicated that the rRNA genes of T. durum did not completely suppress those of Th. distichum. The octoploid amphiploid (2n = 56) contained a maximum of four large and four small nucleoli and the hexaploid BC₁s (2n=42), four large and two small nucleoli.     

Genetic linkage between immune response to GAT and the fate of RSV-induced tumors in chickens

Recent studies suggest that the gene locus controlling the fate of tumors induced by Rous sarcoma virus (RSV) is linked to theB histocompatibility complex. Birds carrying the dominant allele regress the tumor; homozygous recessives being unable to do so, develop large tumors and die. These are called progressors.The Bryan strain of RSV was inoculated into 220 6 week old Leghorns homozygous forB ¹ B ¹,B ² B ², orB ¹⁹ B ¹⁹ of which the percentages of progressors were 79, 22 and 56, respectively. The balance of each were regressors and survived.TheB ¹ B ¹ test birds were derived from special matings, i.e., high and low immune responders to the amino acid polymer, GAT. Of 67 tests progeny of theB ¹ B ¹ GAT-low mating, 63 or 94% proved to be progressors, and 6% were regressors. Of 84 test progeny of theB ¹ B ¹ GAT-high matings, 67% were progressors, and 33% were regressors. The difference between the high and low GAT responders is highly significant and indicates that the locus controlling the fate of RSV-induced tumors is closely linked to the locus controlling immune response to GAT. The latter maps within theIr region of theB histocompatibility complex.     

Bu-1 andTh-1, two loci determining surface antigens of B or T lymphocytes in the chicken

Alloantisera were prepared by reciprocal immunizations with bursal or thymic lymphoid cells between chickens of two inbred lines identical at theB major histocompatibility locus. In cytotoxic assays, antibursa sera were specific for donor-line bursa cells without absorption; antithymus sera were similarly specific for donor-line thymus cells. Both types of sera cytolyzed some peripheral lymphoid cells from spleen, bone marrow, and blood. Absorption of either type of serum with peripheral blood leukocytes removed all cytotoxic reactivity for central lymphoid cells. The inheritance of the alloantigens detected by these specific antisera was studied in F₁, F₂, and backcross progeny from the two lines. Phenotypes were determined by a method in which antisera preabsorbed with progeny leukocytes were reacted against⁵¹Cr-labeled bursal or thymic cells from chickens of both lines. The results established two independent autosomal loci-Bu-1 andTh-1-determining antigens expressed, respectively, on bursal cells and peripheral B lymphocytes or on thymic cells and peripheral T lymphocytes. Cytotoxic testing of bursal or thymic cells from chickens of other inbred lines and F₁ populations led to the tentative conclusion that the number of alleles atBu-1 is restricted, whileTh-1 exhibits considerable multiple allelism.     

Molecular studies of FIme resistance plasmids, particularly in epidemic Salmonella typhimurium.

Summary The molecular sizes of F₁ me resistance plasmids from strains of Salmonella typhimurium, S. wien and S. typhi were within the range 87.9–102.6×10⁶ daltons. DNA reassociation studies indicated that the plasmids from these hosts had at least 80% of their nucleotide sequences in common. A high proportion of F₁ me plasmids cannot mediate their own transfer. The non-autotransferring property of such plasmids is the result of DNA deletion; a non-autotransferring F₁ me plasmid was about 10×10⁶ daltons shorter than autotransferring representatives of the group, and its DNA showed 100% homology with them. Plasmids of the F₁ me group are incompatible with the F factor and with F₁R factors. F₁ me plasmids are incompatible with the fi ⁺ MP10 plasmid of S. typhimurium, whereas F and F₁ factors are compatible with MP10 (Anderson et al., 1977). There was no significant DNA homology between members of the F₁ me group and MP10, and these plasmids may share only a small region of DNA responsible for their incompatibility. The F₁ me R factors examined had 29–37% DNA homology with the F factor, and 50–58% homology with the F₁ resistance plasmid, R162. Molecular examination therefore supports the genetic differentiation of members of the F₁ me group from other F-like plasmids. Both types of investigation can thus be used in epidemiological studies of bacterial strains carrying resistance or other plasmids.     

Genome-scan analysis for quantitative trait loci in an F<Subscript>2</Subscript> tilapia hybrid

We searched for genetic linkage between DNA markers and quantitative trait loci (QTLs) for innate immunity, response to stress, biochemical parameters of blood, and fish size in an F₂ population derived from an interspecific tilapia hybrid ( Oreochromis mossambicus × O. aureus). A family of 114 fish was scanned for 40 polymorphic microsatellite DNA markers and two polymorphic genes, covering ~80% of the tilapia genome. These fish had previously been phenotyped for seven immune-response traits and six blood parameters. Critical values for significance were P <0.05 with the false discovery rate (FDR) controlled at 40%. The genome-scan analysis resulted in 35 significant marker-trait associations, involving 26 markers in 16 linkage groups. In a second experiment, nine markers were re-sampled in a second family of 79 fish of the same species hybrid. Seven markers ( GM180, GM553 , MHC-I , UNH848 , UNH868 , UNH898 and UNH925) in five linkage groups (LG 1, 3, 4, 22 and 23) were associated with stress response traits. An additional six markers ( GM47, GM552 , UNH208 , UNH881 , UNH952 , UNH998) in five linkage groups (LG 4, 16, 19, 20 and 23) were verified for their associations with immune response traits, by linkage to several different traits. The portion of variance explained by each QTL was 11% on average, with a maximum of 29%. The average additive effect of QTLs was 0.2 standard deviation units of stress response traits and fish size, with a maximum of 0.33. In three linkage groups (LG 1, 3 and 23) markers were associated with stress response, body weight and sex determination, confirming the location of QTLs reported by several other studies.Communicated by G. Reuter