Identification of parental chromosomes and changes of artificial, inter-generic F-1 hybrid between Dendranthema horaimontana and Nipponanthemum nipponicum by fluorescence genomic in situ hybridization (GISH) and fluorescence in situ hybridization (FISH)

El-Twab, M.-Hussein-Abd; Kondo, K.

Chromosome Science 8(3): 71-79


Accession: 012173919

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The maternal Dendranthema horaimontana (2n = 18) and the paternal Nipponanthemum. nipponicum (2n= 18) were artificially crossed and produced F-1 hybrid plants of which the strains' embryo rescued and axenic cultured in vitro and later acclimatized in vivo. Genomic it? situ hybridization (GISH) distinguished respective genome for the two parents in the chromosome complement of the F-1 hybrid plants and showed the time largest chromosomes were related to N. nipponicum while the nine smallest chromosomes were related to D. horaimontana. Some of the hybrid plants showed a non-reciprocal translocation in certain somatic chromosomes of N. nipponicum, which could occur during the process of somatic cell division after the fertilization without any progress of the meiosis. Simultaneous bicolor of GISH and fluorescence in situ hybridization (FISH) using the digoxigenin-labelled total genomic DNA of X nipponicum and biotin-labeled probes of pTa71 of 45S rDNA and 5S rDNA distinguished the chromosomes of NOR and 5S rDNA in the genome of respective species in the chromosome complement of the F-1 hybrid. One FISH signal of 45S and that of 5S rDNA were hybridized in separated sites with each probe in two of the nine chromosomes of D. horaimontana, while the FISH signals of 45S and 5S rDNA were hybridized and co-localized at the 45S rDNA site in one or the nine chromosomes of N. nipponicum in the chromosome complement of their F-1 hybrid. The FISH signal of the 5S rDNA showed instability between existence and disappearance in the chromosomes of N. nipponicum in the F-1 hybrid plants. GISH showed that the chromosomes of D. horaimotana and N. nipponicum were in spatial separation in chromosomal domains during the intherphase and mitotic cell division.