Uniparental chromosome elimination in the early embryogenesis of the inviable salmonid hybrids between masu salmon female and rainbow trout male

被引:103
作者
Fujiwara, A
Abe, S
Yamaha, E
Yamazaki, F
Yoshida, MC
机构
[1] HOKKAIDO UNIV,GRAD SCH ENVIRONM EARTH SCI,LAB CYTOGENET,SAPPORO,HOKKAIDO 060,JAPAN
[2] HOKKAIDO UNIV,FAC SCI,CHROMOSOME RES UNIT,SAPPORO,HOKKAIDO 060,JAPAN
[3] HOKKAIDO UNIV,FAC FISHERIES,NANAE FISH CULTURE EXPT STN,KAMEDA 04111,JAPAN
[4] HOKKAIDO UNIV,FAC FISHERIES,LAB BREEDING SCI,HAKODATE,HOKKAIDO 041,JAPAN
关键词
D O I
10.1007/s004120050223
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chromosome elimination through chromosome loss and partial deletion is known to be one of the causes of embryonic inviability in some salmonid interspecific hybrids. Using fluorescence in situ hybridization and related techniques, including whole chromosome painting and comparative genomic hybridization, parental origin of eliminated chromosomes was identified in the inviable hybrids between masu salmon (Ms, Oncorhynchus masou) female and rainbow trout (Rb, O. mykiss) male at the early embryonic stage prior to death. In these hybrids, the haploid Rb chromosome number decreased to nearly half, whereas the Ms chromosomes were retained as one or occasionally two full haploid complements. The Rb chromosomes were also involved in the frequently observed fragments and micronuclei. Whereas the occurrence of fragments was constant throughout the observed period, chromosome loss occurred mainly from just after fertilization to the blastulae stage. In tissue sections and cell spreads of late blastula, some Rb chromosomes were trapped in the midzone from ana- to telophase, resulting in micronuclei at the subsequent 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 present findings suggest that the paternal Rb chromosomes in the inviable hybrids are preferentially eliminated through mitotic abnormalities during early embryogenesis, owing to a possible incompatibility between the maternal Ms cytoplasm and paternal Rb genome.
引用
收藏
页码:44 / 52
页数:9
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