MHC and Non-MHC genetic influences on rous sarcoma metastasis in chickens

The B ⁵/B ⁵ genotype, in Leghorns, was associated with a high degree of metastasis of Rous sarcoma virus-induced tumors, but in combination with a Leghorn-New Hampshire background markedly less metastasis occurred. Initially, four mating types were used: B ⁵/B ⁵ × B ⁵/B ⁵ chickens from the F₅ generation of the cross of Leghorn lines 6₁ and 15₁, B ²⁴/B ²⁴ × B ²⁴/B ²⁴ chickens from line UNH 105 (New Hampshires), and reciprocal crosses of B ⁵/B ⁵ × B²⁴/B²⁴ chickens. Subsequently, F₂ generation progeny of the cross of B⁵/B⁵ and B ²⁴/B ²⁴ breeders, as well as B ²⁴/B ²⁴ line UNH 105 and B ⁵/B ⁵ (6₁ × 15₁)F₂ chickens, were used. Six-week-old chickens were inoculated in the wingweb with Rous sarcoma virus. Chickens dying during a 10-week period after inoculation were necropsied and suspect metastatic lesions examined histologically. Among 234 terminal chickens from the initial four mating types the incidence of metastasis associated with B ⁵/B ⁵ Leghorns (66%) was substantially higher than for B ²⁴/B ²⁴ New Hampshires (12%) and B ⁵/B ²⁴ progeny of reciprocal Leghorn-New Hampshire crosses (19 and 24%). Subsequently, among 524 terminal hosts in the Leghorn-New Hampshire F₂ population, B genotype significantly influenced tumor dissemination. However, among 52 concurrently challenged B ⁵/B ⁵ hosts from the (6₁ × 15₁)F₂ population the incidence of metastasis (60%) was significantly higher than among 122 B ⁵/B ⁵ hosts from the Leghorn-New Hampshire F₂ population (31%), indicating a non-major histocompatibility complex genetic effect on metastasis.     

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.     

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.     

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.     

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.     

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.     

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.     

Digestive and metabolic utilization of lauric,myristic and stearic acid in cows,and associated effects on milk fat quality

A study was carried out to examine the effect of dietary supplementation of oregano essential oil on performance of broiler chickens experimentally infected with Eimeria tenella at 14 days of age. A total of 120 day-old Cobb-500 chicks separated into 4 equal groups with three replicates each, were used in this study. Two groups, one infected with 5·10⁴ sporulated oocysts of E. tenella and the other not, were given a basal diet and served as controls. The other two groups also infected with E. tenella were administered diets supplemented with oregano essential oil at a level of 300 mg/kg, or with the anticoccidial lasalocid at 75 mg/kg. Following this infection, survival rate, bloody diarrhoea and oocysts excretion as well as lesion score were determined. Throughout the experimental period of 42 days, body weight gain and feed intake were recorded weekly, and feed conversion ratios were calculated. Two weeks after the infection with E. tenella supplementation with dietary oregano oil resulted in body weight gains and feed conversion ratios not differing from the non-infected group, but higher than those of the infected control group and lower than those of the lasalocid group. These parameters correspond with the extent of bloody diarrhoea, survival rate, lesion score and oocyst numbers and indicated that oregano essential oil exerted an anticoccidial effect against E. tenella, which was, however, lower than that exhibited by lasalocid.     

Role of the immune-response region of the B complex in the control of the graft-vs-host reaction in chickens

The relative importance of the B and IR regions of the chicken B complex were compared as to their role in the graft-versus-host (GVH) reaction. Spleen enlargement (splenomegaly) on 19-day-old embryos, inoculated 5 days earlier with immune competent leukocytes, served as the test for the GVH reaction. The B blood group locus was the marker of the B region, and the Ir-GAT gene was the marker of the immune response (Ir) region of the B complex, the major histocompatibility system (MHS) of chickens. The test stocks consisted of B¹B¹ GAT-Low (1-Low) and B¹⁹B¹⁹ Gat-High (19-High) birds of our S1 Leghorn line plus the recombinant genotypes B¹B¹ Gat-High (1-High) and B¹⁹B¹⁹ GAT-low (19-Low). A dosage of 0.1 ml of donor white blood cells was injected into each of 191 recipient embryos on day 14, and the spleens were removed and weighed on day 19. Of 16 combinations of (donor blood)-(host embryos), arranged with respect to the four genotypes listed above, four were compatible, e. g., (1-Low)-(1-Low). There were four incompatible combinations at the B locus, four at the GAT locus, and four at both the B and GAT loci. All 16 combinations were replicated. Results were expressed as a splenomegaly index (SI), that is, the ratio of incompatible to compatible spleen weights corrected for differences in embryo weight. If (SI-1) is greater than 0, the GVH reaction is considered positive within sampling errors. The mean (SI-1) indexes obtained were: incompatible at GAT-0.5±0.07; incompatible at B-1.34±0.10. Thus, both GAT and B contributed to the GVH reaction, but the B region was much stronger than the IR region. The results were strongly asymmetrical: maximal stimulation occurred when the host embryo was B¹⁹B¹⁹ GAT-high and donor leukocytes were B¹B¹ GAT-Low. The parental donor-host paired combinations gave stronger GVH reactions than did the recombinant pairs. Effects of incompatibilities at the two regions proved additive when compared with two-locus differences of parental genotypes. In general, the results proved that the IR region, as specifically defined by recombinants obtained in our S1 line of Leghorns, plays a significant, but minor, role in the GVH reaction compared with the region of the B complex identified with the B blood-group locus.     

Studies on construction of a recombinant Eimeria tenella SO7 gene expressing Escherichia coli and its protective efficacy against homologous infection

Eimeria spp. are the causative agents of coccidiosis, a major disease affecting the poultry industry. A recombinant non-antibiotic Escherichia coli that expresses the Eimeria tenella SO7 gene was constructed and its protective efficacy against homologous infection in chickens was determined. The three-day-old chickens were orally immunized with the recombinant non-antibiotic SO7 gene expressing E. coli and boosted two weeks later. Four weeks after the second immunization, the chickens were challenged with 5 × 10⁴ homologous sporulated oocysts. The protective effects of the recombinant non-antibiotic E. coli were determined by measuring body weight change, mortality, histopathology, lesion scores, oocyst counts, the specific antibody response and the frequency of CD4⁺ and CD8⁺ lymphocytes in peripheral blood. The results showed that immunization with SO7 expressing E. coli resulted in significantly improved body weight gain, reduced lesion scores and oocyst shedding in immunized chickens compared to controls. Furthermore, administration of recombinant SO7 expressing E. coli leads to a significant increase in serum antibody, CD4⁺ and CD8⁺ T cells in peripheral blood of chickens. These results, therefore, suggest that the recombinant non-antibiotic E. coli that expresses the SO7 gene is able to effectively stimulate host protective immunity as evidenced by the induction of development of both humoral and cell-mediated immune responses against homologous challenge in chickens.     

Effect of various environmental factors on the viability of Cryptosporidium parvum oocysts

Aims: To evaluate individual and combined effects of temperature (4, 18 and 25°C), pH (7 and 10), ammonia (5 and 50 mg l^?1) and exposure time (1, 2, 4 and 6 days) on the viability of Cryptosporidium parvum oocysts in water. Methods and Results: The viability of oocysts was evaluated using the fluorogenic vital dyes assay (4′,6‐diamidino‐2‐phenylindole and propidium iodide). All the factors analysed (temperature, pH, ammonia and exposure time) and their interaction were statistically significant (P < 0·005). Exposure of oocysts to pH 10 for 6 days at 25°C reduced oocyst viability from ～80% to 51%. Similarly, the exposure of C. parvum oocysts to 5 mg NH₃ l^?1 and 50 mg NH₃ l^?1 for 4 days reduced their viability from between ～80% to 41·5% and 14·8%, respectively. Conclusions: The interaction between pH, temperature and exposure time may have adverse effects on the survival of C. parvum oocysts in water. Low concentrations of ammonia, as commonly found in alga‐based wastewater systems, over a long period of time can produce high C. parvum oocyst inactivation rates. Significance and Impact of the Study: This study provides relevant data on the inactivation of C. parvum oocysts in alga‐based wastewater‐treatment systems in the northwest of Spain.     

Genetic variability of resistance to Eimeria acervulina and E. tenella in chickens

Summary The genetic variability of 18 sire families of the Athens-Canadian randombred population infected with coccidiosis was assessed by examining the response variables of weight gain, packed red blood cell volume, mortality and coccidial lesions. A significant gain and PCV depression and high lesion scores for Eimeria tenella and E. acervulina were produced in the infected group compared to the noninfected group. Significant variation among the sire families was observed for all of the response variables except E. acervulina lesions and a significant sex x sire interaction was observed for weight gain. The heritability (h²) estimates for the response variables revealed that resistance to coccidiosis in chickens is moderately heritable. The h² estimates for gain and PCV increased with the coccidial infections indicating that maximum progress in selecting for resistance should be made when the population was exposed to coccidial infection. Gain was positively correlated to the other measures of resistance and thus selecting for coccidial resistance should not reduce growth rates. PCV was similarly correlated but had higher positive correlation with E. tenella lesion. Percent mortality which is the selection parameter in most coccidial selection programs was correlated with resistance to coccidiosis. The phenotypic and genotypic correlations demonstrated that chickens susceptible to E. tenella were also susceptible to E. acervulina. Total lesion scores were moderately to highly correlated with the other variables and would be a suitable variable to use in coccidiosis experimentation including a genetic selection program for resistance. This study shows that progress could be made in selecting for resistance to coccidiosis in chickens using one or a combination of these response variables.     

Influence of non-MHC T lymphocyte alloantigens on regression of rous sarcomas in the chicken

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 7₂, although these lines are identical for the major histocompatibility complex (MHC, B complex). They differ, however, at two independent autosomal loci, Ly-4 and Th-1, which determine surface alloantigens of partly overlapping subsets of T lymphocytes. Association of genotypes at these loci with quantitative variation in ability to regress Rous sarcomas was tested in segregating progeny derived from crosses of lines 6₃ and 7₂. In the F4 generation chickens of the Ly-4 ^a /Ly-4 ^a , Th-1 ^a /Th-1 ^a genotype (symbolized aa/aa) had significantly higher regressor ability than any of the other three double homozygous genotypes. In F5, all nine genotypes formed by combinations of homozygotes and heterozygotes were tested, and higher regressor ability was shown by the aa/aa, ab/aa, and aa/ab genotypes. These results indicate that higher regression is associated with: (1) interaction between the line 6₃ Ly-4 ^a and Th-1 ^a alleles in homozygous form; and (2) dominance x dominance interaction, in that the a allele at each locus is dominant for higher regression only within the homozygous aa genotype at the other locus.     

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.     

Fine‐mapping of a locus on linkage group 23 for sex determination in Nile tilapia (Oreochromis niloticus)

Genetic markers in tilapia species associated with loci affecting sex determination (SD), sex‐specific mortality or both were mapped to linkage groups (LG) 1, 2, 3, 6 and 23. The objective of this study was to use these markers to fine‐map the locus with the greatest effect on SD in Oreochromis niloticus. Our parental stock, full‐sibs of Nile tilapia (Swansea origin), were divided into three groups: (i) untreated, (ii) feminized by diethylstilbestrol and (iii) masculinized by 17α‐methyltestosterone. We analysed the first group for association of microsatellite markers representing these five LGs. The strongest association with gender was found on LG23 for marker UNH898 (χ²; P = 8.6 × 10^?5). Allele 276 was found almost exclusively in males, and we hypothesized that this allele is a male‐associated allele (MAA). Sex‐reversed individuals were used for mating experiments with and without the segregating MAA. Mating of individuals lacking the MAA resulted in all‐female progeny. Mating of two heterozygotes for MAA gave rise to 81 males and 30 females. Analysis of association between gender and genotypes identified the MAA in 98.6% of males as opposed to 8.0% of females (χ²; P = 2.5 × 10^?18). Eight markers that flank UNH898 were genotyped to map the locus on LG23 within a confidence interval of 16–21 cM. Mating of homozygous individuals for MAA is underway for production of all‐male populations.     

Genetic control of immune responses in chickens

The immune response of inbred lines of chickens to the terpolymer poly(glu⁶⁰ala³⁰tyr¹⁰) and copolymer poly(glu⁶⁰ala⁴⁰) was determined. Of six lines immunized, one (line 7) contained birds that either did not respond or were low responders to two injections of 1 mg each of the polymers in Freund's complete adjuvant. As indicated by radioimmunoelectrophoresis, low responders produced a 7S response, although the switch from 17S (high molecular weight immunoglobulin) to 7S antibody production was slower than in high-responder lines. Analysis of the distribution of responders and nonresponders in F₂ generations produced byinter se mating of F₁ hybrids of line 7 with high-responder lines, showed that immune responses were clearly determined by certain alloalleles of theB blood group locus, the major histocompatibility system in the chicken.     

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     

Intestinal Transit Time During Infection with Eimeria nieschulzi in Rats*

SYNOPSIS. Experiments were designed to test whether or not intestinal transit time increases significantly during severe coccidiosis in the rat. Intraduodenal catheters were surgically implanted into 25 rats. Six to 12 days after surgery 11 rats were inoculated orally with 10⁴ sporulated oocysts of Eimeria nieschulzi Dieben, and 11 were inoculated with 10⁶ oocysts; 3 rats were retained as uninfected controls. At 2, 4, 8, 9, and 16 days postinoculation (PI) Na₂⁵¹CrO₄ was injected through the catheter into the duodenum of fasted rats and allowed to progress through the small bowel for 15 min, at which time the rats were killed. The distribution of ⁵¹Cr in the gut was plotted as a function of gut length. The leading edge of radioactivity traversed 70% of the gut length in controls, and ～ 50–60% in parasitized rats on days 2, 4, 8, and 9 PI. Also, a reflux of gut contents, as evidenced by radioactivity in the stomach, occurred early (PI days 2 & 4) in rats infected with 10⁴ oocysts and throughout patency in rats infected with 10⁶ oocysts. A 2nd study was undertaken to determine if chemically induced suppression of gut transit time during early infection would enhance infectivity as measured by increased parasite fecundity. Nine rats were injected subcutaneously with an antidiarrheal agent, Loperamide®, known to slow small bowel motility significantly. Another group of 9 control rats was injected with the ethanol-propylene glycol solvent. Ten min after injection, all rats were inoculated per os with 10⁴E. nieschulzi oocysts. The daily number of oocysts discharged/rat was followed from PI days 5–11. Patency began for all rats on PI day 7. The total number of oocysts discharged by the drugged rats as compared with controls was not significantly different.     

Genetic resistance to fowl cholera is linked to the major histocompatibility complex

Chickens of the Iowa State S1 line have been selected for ability to regress Rous sarcoma virus-induced (RSV) tumors, humoral immune response to GAT (Ir-GAT), and erythrocyte antigen B. Sublines homozygous at the major histocompatibility complex (MHC), as well as F₁ heterozygotes and F₂ segregants, were tested for resistance to fowl cholera by challenge with Pasteurella multocida strain X73. Control of the response at high doses was associated in a preliminary study with Ir-GAT and response to RSV tumors. Genetic control of resistance to low doses of P. multocida was demonstrated via sublines and F₂ segregants to be linked with genes of the B-G region. Thus, genetic control of resistance to fowl cholera in chickens after exposure to Pasteurella multocida was shown to be linked to the major histocompatibility B complex, in this first demonstration of MHC-linked resistance to bacterial disease challenge.     

Expression of cycloheximide resistance in carrot somatic hybrids and their segregants

Cycloheximide resistance (CH^r) was shown to be a function expressed in differentiated plant tissues, but not in unorganized callus tissues. A variant, WCH105, expressing CH^r in the callus, as well as in regenerated plantlets, was isolated from a cell line derived from a wild carrot plant. The plantlets regenerated from WCH105 are green, but do not produce normal, dissected leaves. Protoplasts of WCH105 were fused with that of a cycloheximidesensitive (CH^s) cell line derived from an albino, domesticated carrot. Hybrid selection was based on (1) irreversible growth inhibition of WCH105 protoplasts by iodacetamide, and (2) restoration of green plants producing dissected leaves.——Analysis of the CH^r trait as an unselected marker in the callus cells of the somatic hybrids indicated that it behaved as a recessive. The combined recessive and resistant phenotype of this trait allowed the recovery of CH^r segregants from CH^s hybrids at a frequency of 10^-4, 1000 times higher than the spontaneous frequency of CH^r. The recovery of CH^r somatic segregants confirmed the recessiveness of the CH^r trait.