Susceptibility to enterotoxigenic Escherichia coli with fimbriae F4ac is dominantly inherited in the pig. A three-generation pedigree was created to refine the position of F4acR on chromosome 13 comprising 202 pigs: eight parents, 18 F1 and 176 F2 pigs. The 17-point analysis indicates that F4acR lies between Sw207 and S0283. Recombinant offspring specify that the most probable order is Sw207-S0075-F4acR-Sw225-S0283. We observed six phenotypes for the three fimbrial variants F4ab, F4ac and F4ad. The two missing phenotypes F4abR-/F4acR+/F4adR+ and F4abR-/F4acR+/F4adR- indicate that pigs susceptible to F4ac are always susceptible to F4ab. Furthermore, a weak and a strong adhesion of F4ab and F4ad bacteria was observed. The weak receptor F4abR (F4abRw) was present only in pigs devoid of the receptor F4acR (F4abR+/F4acR-). In contrast, in pigs with the phenotype F4abR+/F4acR+, F4ab bacteria adhered to the majority of enterocytes. F4abRw constitutes a frequently observed phenotype whose inheritance is still unclear. Strong adhesion of F4ab and F4ac bacteria is most likely influenced by the same receptor that we name F4bcR. The number of F4ad bacteria that adhered to enterocytes was very variable in the adhesion test. Moreover, expression of F4adR was independent of age. Our segregation analyses indicated a dominant inheritance of F4adR, although the number of susceptible pigs was smaller than expected. We examined four genes as candidates for the F4acR locus: the transferrin receptor gene (TFRC) and three genes members of the glucosyl/galactosyltransferase family (B3GnT5, B3GALT3 and B4GALT4). Comparison of sequences from resistant and homozygous susceptible F4ac pigs did not reveal any causative single nucleotide polymorphism in the four genes. Two silent mutations at the positions 295 (C/T) and 313 (T/C) in B3GALT3 were found. Using the somatic cell hybrid panel, B3GnT5 and B3GALT3 were assigned to the chromosomal region SSC13q23-q41. No mutations were found in the cDNA sequences of these genes associated with the F4acR genotypes.

The aim of this study was to refine the localization of the receptor locus for fimbriae F4ac. Small intestinal enterocyte preparations from 187 pigs were phenotyped by an in vitro adhesion test using two strains of Escherichia coli representing the variants F4ab and F4ac. The three-generation pedigree comprised eight founders, 18 F1 and 174 F2 animals, for a total of 200 pigs available for the linkage analysis. Results of the adhesion tests on 171 F2 pigs slaughtered at 8 weeks of age show that 23.5% of the pigs were adhesive for F4ab and non-adhesive for F4ac (phenotype F4abR+/F4acR-; R means receptor). Pigs of this phenotype were characterized by a weak adhesion receptor for F4ab. No pigs were found expressing only F4acR and lacking F4abR. Receptors for F4ab and F4ac (F4abR+/F4acR+) were expressed by 54.5% of the pigs. Animals of this phenotype strongly bound both F4ab and F4ac E. coli. In the segregation study, the serum transferrin (TF) gene and 10 microsatellites on chromosome 13 were linked with F4acR (recombination fractions (theta) between 0.00 and 0.11 and lod score values (Z) between 11.4 and 40.4). The 11-point analysis indicates the F4acR locus was located in the interval S0068-Sw1030 close to S0075 and Sw225, with recombination fractions (theta) of 0.05 between F4acR and S0068, 0.04 with Sw1030, and 0.00 with S0075 and Sw225. The lack of pigs displaying the F4abR-/F4acR+ phenotype and the presence of two phenotypes for F4abR (a strong receptor present in phenotype F4abR+/F4acR+ and a weak receptor in phenotype F4abR+/F4acR-) led us to conclude that the receptor for F4ac binds F4ab bacteria as well, and that it is controlled by one gene localized between S0068 and Sw1030 on chromosome 13.

The objective of this study was to evaluate the effect of a GnRH-vaccine in the ram lamb. Experiments were performed using 20 male lambs, randomly divided into a test (GnRH-immunization) and control group (physiological NaCl-solution). At a body weight of 20 kg (age 2-3 months) and three weeks later, all animals of the test group received 2 ml of Improvac (CSL Limited, Parkville, Victoria, Australia). The body weight as well as the blood testosterone concentration were measured weekly for 16 weeks. Thereafter, blood samples for testosterone analysis were taken monthly in immunized lams only. After the booster injection testicular growth was suppressed and plasma testosterone remained at low values < 0.1 ng/ml for at least 12 weeks. The mean corresponding testosterone concentrations for the control lambs ranged between 0.1 and 0.9 ng/ml plasma. An increase of testosterone was observed in 8 of 10 immunized animals between 3 to 7 months after the booster dose. The control lambs showed a tendency for better growth rate than vaccinated animals, but the difference was not significant. Our results demonstrate that in prepubertal ram lambs two immunizations with Improvac, three weeks apart, can suppress testosterone secretion and testicular growth at least for three months after the booster injection. For a suppression of reproductive function longer than three months after the second vaccination, a third immunization is needed at this time or when testicular growth is beginning.

Arachnomelia in Brown Swiss cattle is a monogenic autosomal recessive inherited congenital disorder of the skeletal system giving affected calves a spidery look (OMIA ID 000059). Over a period of 20 years 15 cases were sampled in the Swiss and Italian Brown cattle population. Pedigree data revealed that all affected individuals trace back to a single acknowledged carrier founder sire. A genome scan using 240 microsatellites spanning the 29 bovine autosomes showed homozygosity at three adjacent microsatellite markers on bovine Chr 5 in all cases. Linkage analysis confirmed the localization of the arachnomelia mutation in the region of the marker ETH10. Finemapping and haplotype analysis using a total of 34 markers in this region refined the critical region of the arachnomelia locus to a 7.19-Mb interval on bovine Chr 5. The diseaseassociated IBD haplotype was shared by 36 proven carrier animals and allows marker-assisted selection. As the corresponding human and mouse chromosome segments do not contain any clear functional candidate genes for this disorder, the mutation causing arachnomelia in the Brown Swiss cattle might help to identify an unknown gene in bone development.

Vitamin C deficient pigs, when fed a diet lacking L-ascorbic acid (AscA), manifest deformity of the legs, multiple fractures, osteoporosis, growth retardation and haemorrhagic tendencies. This trait was shown by others to be controlled by a single autosomal recessive allele designated as od (osteogenic disorder). The inability of AscA biosynthesis in primates and guinea pigs that exhibit similar symptoms, when they are not supplemented with AscA in the food, was traced to the lack of L-gulono-gamma-lactone oxidase, which catalyzes the terminal step in the biosynthesis of AscA. The non-functional GULOP was mapped to human chromosome 8p21 that corresponds to an evolutionarily conserved segment on either porcine chromosome 4 (SSC4) or 14 (SSC14). We investigated linkage between OD and SSC4- and 14-specific microsatellite loci in order to map the OD locus. Twenty-seven informative meioses in families from one sire and three dams revealed linkage of od with microsatellites SW857 and S0089, located in the subcentromeric region of SSC14. We isolated part of the GULO gene of the pig by screening a porcine genomic library using a pig GULO cDNA as a probe, and mapped it to SSC14q14 by fluorescence in situ hybridization (FISH). Thus, the porcine GULO gene is both a good physiological and positional candidate gene for vitamin C deficiency in pigs.