RESUMEN
In Rosa canina (2n = 5x = 35), the pollen and ovular parents contribute, respectively, seven and 28 chromosomes to the zygote. At meiosis I, 14 chromosomes form seven bivalents and 21 chromosomes remain as univalents. Fluorescent in situ hybridization to mitotic and pollen mother cells (PMC) of R. canina showed that 10 chromosomes (two per genome) carry ribosomal DNA (rDNA) loci. Five chromosomes carry terminal 18S-5.8S-26S rDNA loci; three of these also carry paracentric 5S rDNA loci and were designated as marker chromosomes 1. Five chromosomes carry only 5S rDNA loci and three of these were designated as marker chromosomes 2. The remaining four of the 10 chromosomes with rDNA loci were individually identifiable by the type and relative sizes of their rDNA loci and were numbered separately. At PMC meiosis, two marker chromosomes 1 and two marker chromosomes 2 formed bivalents, whereas the others were unpaired. In a gynogenetic haploid of R. canina (n = 4x = 28), obtained after pollination with gamma-irradiated pollen, chromosomes at meiosis I in PMC remained predominantly unpaired. The data indicate only one pair of truly homologous genomes in R. canina. The 21 unpaired chromosomes probably remain as univalents through multiple generations and do not recombine. The long-term evolutionary consequence for the univalents is likely to be genetic degradation through accumulated mutational change as in the mammalian Y chromosome and chromosomes of asexual species. But there is no indication that univalents carry degenerate 5S rDNA families. This may point to a recent evolution of the R. canina meiotic system.
Asunto(s)
ADN Ribosómico/análisis , Meiosis , Poliploidía , Rosa/genética , Bandeo Cromosómico , Cromosomas de las Plantas , ADN de Plantas/análisis , Rayos gamma , Hibridación Fluorescente in Situ , Mitosis , Polen , ARN Ribosómico 18S , ARN Ribosómico 28S , ARN Ribosómico 5.8S , Rosa/efectos de la radiaciónRESUMEN
We report a familial case of Waardenburg syndrome. A four and a half year old boy had displacement of the canthi, a white forelock, perceptive deafness, and a congenital heart defect. The mother and younger brother had the same syndrome. Usually, cases of Waardenburg syndrome are divided into types I and II according to whether lateral displacement of the inner canthi is present or absent. Uni or bilateral perceptive deafness is found in 13 to 28% of type I cases and 53% of type II cases. The white forelock is a feature in 30% of cases and should suggest the diagnosis. Several other abnormalities have been reported in this syndrome. Inheritance of Waardenburg syndrome is autosomal dominant with variable penetrance. We discuss the possibility that one or both of the children we report were homozygous for a dominant gene.