1. The Origin of Reproductive Isolation
7
mule (Hamerton et al. 1969). Such an irregularity is also seen in gray vole (Microtus) hybrids: the X chromosome with a heterochromatin block is preferentially inactivated in this case (Zakian et al. 1987, 1991). Improper dosage compensation, if
any, is potentially responsible for abnormal development of hybrids, e.g., hybrid
inviability and sterility. This should not be restricted to the X-linked genes. For
example, if the maternal allele is active in one species but the paternal allele is
active in the other at the early stages of embryogenesis (genomic imprinting)
(Cattanach and Beechey 1990), hybrids may show improper expression of the loci
resulting in hybrid inferiority.
Dosage compensation in insects is somewhat different from that in mammals,
but it can also be involved in postzygotic reproductive isolation. The equalization
of X-linked gene expression in male and female Drosophila is brought about by
doubling the activity of the single X loci in males (Lucchesi 1998). If speciesspecific systems (e.g., cis-acting sequence differences) operate in the dosage compensation, hybrids may show improper gene expression resulting in abnormal development. Although proper dosage compensation has been shown in many cases
of interspecific Drosophila (Dobzhansky 1957; Lakhotia et al. 1981; Mutsuddi et
al. 1984; see also Orr 1989), there is at least one case of improper dosage compensation in D. azteca/D. athabasca hybrids. Males carrying the D. azteca X chromosome are larger ('hybrid giant males'), while those carrying the D. athabasca X are
smaller and have low viability (,hybrid dwarf males'), if compared with their parents and sisters (Sturtevant and Dobzhansky 1936). The replication of the hemizygous X chromosome is asynchronized from autosomes in the hybrid giant males,
and as a result their poly ten chromosomes undergo one more endoreplication (Meer
1976, 1980).
2.4 Nucleolar Dominance
Nucleolar dominance is a phenomenon usually seen in interspecific hybrids in which
an allele of nucleolar organizer (rRNA coding gene) derived from one of the parental species is transcriptionally inactivated. This is observed in various crosses of
plants and animals [for reviews see Wallace and Langridge (1971), Rieger et al.
(1979), Reeder (1984)]. Its molecular basis is well documented in amphibian (Xenopus) hybrids. The X. laevis/X. borealis hybrid embryos express only ribosomal
genes of the former species (Honjo and Reeder 1973; Cassidy and Blacklar 1974).
This is the consequence of competition between enhancers of ribosomal genes from
two species (Reeder and Roan 1984): X. laevis has more copies of an enhancer
element for the ribosomal gene promoter in the spacer region (La Volpe et al.
1983). It is, however, not always true that nucleolar dominance is a manifestation
of a simple "allelic repression". It is assumed in mouse-human somatic hybrids that
nucleolar dominance is due to the loss or inactivation of the gene for a specificity
factor required to recognize the species-specific ribosomal gene promoter, since
extracts from cell lines in which some of the human chromosomes are lost cannot
initiate transcription of human ribosomal genes (Onishi et al. 1984; Miesfeld et al.
7
mule (Hamerton et al. 1969). Such an irregularity is also seen in gray vole (Microtus) hybrids: the X chromosome with a heterochromatin block is preferentially inactivated in this case (Zakian et al. 1987, 1991). Improper dosage compensation, if
any, is potentially responsible for abnormal development of hybrids, e.g., hybrid
inviability and sterility. This should not be restricted to the X-linked genes. For
example, if the maternal allele is active in one species but the paternal allele is
active in the other at the early stages of embryogenesis (genomic imprinting)
(Cattanach and Beechey 1990), hybrids may show improper expression of the loci
resulting in hybrid inferiority.
Dosage compensation in insects is somewhat different from that in mammals,
but it can also be involved in postzygotic reproductive isolation. The equalization
of X-linked gene expression in male and female Drosophila is brought about by
doubling the activity of the single X loci in males (Lucchesi 1998). If speciesspecific systems (e.g., cis-acting sequence differences) operate in the dosage compensation, hybrids may show improper gene expression resulting in abnormal development. Although proper dosage compensation has been shown in many cases
of interspecific Drosophila (Dobzhansky 1957; Lakhotia et al. 1981; Mutsuddi et
al. 1984; see also Orr 1989), there is at least one case of improper dosage compensation in D. azteca/D. athabasca hybrids. Males carrying the D. azteca X chromosome are larger ('hybrid giant males'), while those carrying the D. athabasca X are
smaller and have low viability (,hybrid dwarf males'), if compared with their parents and sisters (Sturtevant and Dobzhansky 1936). The replication of the hemizygous X chromosome is asynchronized from autosomes in the hybrid giant males,
and as a result their poly ten chromosomes undergo one more endoreplication (Meer
1976, 1980).
2.4 Nucleolar Dominance
Nucleolar dominance is a phenomenon usually seen in interspecific hybrids in which
an allele of nucleolar organizer (rRNA coding gene) derived from one of the parental species is transcriptionally inactivated. This is observed in various crosses of
plants and animals [for reviews see Wallace and Langridge (1971), Rieger et al.
(1979), Reeder (1984)]. Its molecular basis is well documented in amphibian (Xenopus) hybrids. The X. laevis/X. borealis hybrid embryos express only ribosomal
genes of the former species (Honjo and Reeder 1973; Cassidy and Blacklar 1974).
This is the consequence of competition between enhancers of ribosomal genes from
two species (Reeder and Roan 1984): X. laevis has more copies of an enhancer
element for the ribosomal gene promoter in the spacer region (La Volpe et al.
1983). It is, however, not always true that nucleolar dominance is a manifestation
of a simple "allelic repression". It is assumed in mouse-human somatic hybrids that
nucleolar dominance is due to the loss or inactivation of the gene for a specificity
factor required to recognize the species-specific ribosomal gene promoter, since
extracts from cell lines in which some of the human chromosomes are lost cannot
initiate transcription of human ribosomal genes (Onishi et al. 1984; Miesfeld et al.