UNIPARENTAL CHROMOSOME ELIMINATION IN THE EARLY EMBRYOGENESIS OF THE INVIABLE SALMONID HYBRIDS BETWEEN MASU SALMON FEMALE AND RAINBOW-TROUTMALE

Citation
A. Fujiwara et al., UNIPARENTAL CHROMOSOME ELIMINATION IN THE EARLY EMBRYOGENESIS OF THE INVIABLE SALMONID HYBRIDS BETWEEN MASU SALMON FEMALE AND RAINBOW-TROUTMALE, Chromosoma, 106(1), 1997, pp. 44-52
Citations number
32
Categorie Soggetti
Genetics & Heredity
Journal title
ISSN journal
00095915
Volume
106
Issue
1
Year of publication
1997
Pages
44 - 52
Database
ISI
SICI code
0009-5915(1997)106:1<44:UCEITE>2.0.ZU;2-W
Abstract
Chromosome elimination through chromosome loss and partial deletion is known to be one of the causes of embryonic inviability in some salmon id interspecific hybrids. Using fluorescence in situ hybridization and related techniques, including whole chromosome painting and comparati ve genomic hybridization, parental origin of eliminated chromosomes wa s identified in the inviable hybrids between masu salmon (Ms, Oncorhyn chus masou) female and rainbow trout (Rb, O. mykiss) male at the early embryonic stage prior to death. In these hybrids, the haploid Rb chro mosome number decreased to nearly half, whereas the Ms chromosomes wer e retained as one or occasionally two full haploid complements. The Rb chromosomes were also involved in the frequently observed fragments a nd micronuclei. Whereas the occurrence of fragments was constant throu ghout the observed period, chromosome loss occurred mainly from just a fter fertilization to the blastulae stage. In tissue sections and cell spreads of late blastula, some Rb chromosomes were trapped in the mid zone from ana- to telophase, resulting in micronuclei at the subsequen t interphase. Micronuclei and mitotic abnormalities were also observed in the androgenetic haploid hybrids. However, such abnormalities were seldom or never observed in the viable reciprocal hybrids. The presen t findings suggest that the paternal Rb chromosomes in the inviable hy brids are preferentially eliminated through mitotic abnormalities duri ng early embryogenesis, owing to a possible incompatibility between th e maternal Ms cytoplasm and paternal Rb genome.