Ferrets (Mustela putoius furo) inefficiently convert beta-carotene to vitamin A.

The ferret has recently been used as a model to evaluate the absorption and metabolism of several carotenoids; however, little is known about the vitamin A (VA) requirements of this species or the ability of ferrets to convert dietary beta-carotene (betaC) to VA. Three studies were conducted to estimate the daily utilization of VA in ferrets and to determine the effect of prior VA status on the ability of ferrets to utilize betaC as a source of VA. Weanling male ferrets were fed a pelleted, low carotenoid, semipurified diet either with (+VA) or without VA (-VA) for 21- to 35-d prefeeding periods. Upon initiation of the experiments, several ferrets were killed to determine base-line VA status. The remaining ferrets were fed VA, betaC, or VA and betaC in pelleted feed (Studies 1-3) or liquid carrier (Study 3) for 16-21 additional days. Hepatic VA and betaC concentrations were used as the primary indicators of VA status, although serum and adrenal VA and betaC also were measured. The results showed the following: 1) provision of betaC at up to a 15:1 weight ratio of betaC to VA in pelleted feed or liquid carrier was not sufficient to maintain hepatic VA stores after a -VA prefeeding period; 2) the daily utilization rate of VA by ferrets ranged from 80 to 171 microg in the three studies; 3) the ferret was confirmed to be a species that has the majority of its serum VA in ester form; and 4) feeding -VA diets significantly reduced serum retinyl esters but had less effect on serum retinol. We conclude that although ferrets can convert betaC to VA, the process is inefficient. The ferret model can be most appropriately used when studying the biological effect of tissue betaC stores on VA status and is less appropriate for the evaluation of dietary betaC conversion to VA.

A male linkage map of the cattle (Bos taurus) genome.

A male linkage map of the cattle (Bos taurus) genome was constructed using nine large half-sib families. The map consists of 269 loci, of which 249 are microsatellites and 20 are structural genes. Among the 249 microsatellites, 140 are markers selected from other maps and 98 are new assignments. Chromosome assignment were established for 35 new markers by somatic cell hybrid analysis, of which 26 were confirmed by linkage analysis. Genome coverage is 1975 cM contained within terminal markers on all 29 autosomes. The average distance between adjacent loci is 9.7 cM, with 72.1% of the map intervals < or = 15 cM and 4.9% of the intervals > or = 25 cM. The inclusion of mapped markers permitted integration and comparisons with other maps, facilitating the identification of discrepancies in chromosome assignment, gene order, and map distance. The inclusion of Type I and blood group markers in the map was useful for comparative mapping, revealing possible blood group orthologies between humans and cattle. The map generated will serve as a useful tool for comparative mapping, mapping of quantitative trait loci and marker assisted selection.

Parental origin of the extra chromosome in Down's syndrome.

Chromosome 21 fluorescent heteromorphisms were studied in 42 patients with Down's syndrome, their parents and their siblings. Included in this number are two instances of an aunt and niece affected with trisomy 21, and one of affected siblings. One case has a de novo 21/21 translocation. Blood group, red cell and serum protein markers were also studied for linkage, gene exclusions, associations, and paternity testing. Thirty-one of the trisomy 21 cases were informative for parental origin of the extra chromosome and for stage of meiosis. The non-disjunctional event was of maternal origin in 24; 23 occurred in meiosis I, 1 in meiosis II. Seven were of paternal origin; 5 in meiosis I, and 2 in meiosis II. The translocation case was of paternal origin. A literature search revealed a total of 98 cases informative for the parent of origin of the extra chromosome, of greater than 347 families tested. In addition, 3 de novo translocation cases, of 7 tested, were informative. The data suggest that most cases result from an error in the first meiotic division in the mother, but that a significant proportion are paternal in origin.

Cytogenetic darkroom magic: now you see them, now you don't.

Customary procedures used to determine chromosomal inheritance do not disclose many of the chromosomal polymorphisms known to be present, resulting in uninformative families. The sequential printing of individual chromosomes presented here is a technique that has increased the number of informative families in our studies. This technique has revealed previously unseen heritable chromosome differences and allowed the designation of parental origin.

Parental origin of a ring 13 chromosome in a female with multiple anomalies.

A ring chromosome No. 13 was found in a 21-year-old female with multiple anomalies suggestive of 13q--syndrome. Chromosomes of the girl and her parents, studied by quinacrine staining, revealed the ring to be of paternal origin. Detailed study of the quinacrine banding pattern of the ring indicated loss of the most distal band of the long arm (13q34) and possible partial loss of the next adjacent long arm band (13q33). The short arm (13q11) was present but the stalk (13p12) and satellite (13p13) regions appeared to be missing.

Gene dosage: evidence for assignment of erythrocyte acid phosphatase locus to chromosome 2.

A child, trisomic for the distal short arm of chromosome 2 due to a familial 2/18 translocation, has elevated levels of activity of erythrocyte acid phosphatase [orthophosphoric-monoester phosphohydrolase (acid optimum), 3.1.3.2] Ferguson-Smith et al. [(1973) Nature New Biol. 243, 271-274] previously had found decreased levels of activity and loss of expression of an erythrocyte acid phosphatase allele in a subject who lacked one of the two homologous regions containing the distal three bands of chromosome 2. They suggested that the locus for erythrocyte acid phosphatase is located on that segment. Our findings provide further evidence for this assignment and also suggest an in vivo gene dosage effect of this autosomal locus, which depends on both the type and number of alleles present.