6
K. Sawamura
(e.g., sisterless-a, sisterless-b) and autosomes have putative denominator genes. It
is well-known that a maternal product (a transcription factor) of a second-linked
gene, daughterless, calculates the X/A ratio and regulates the ON/OFF state of a
key gene of sex determination, Sex-lethal (Cline 1993). If new genes are recruited
to the numerator/denominator system or each numerator/denominator element
evolves rapidly in independent populations, interspecific hybrids will show an imbalance of the system resulting in sex reversion. Because sex determination is related to dosage compensation of the X chromosome in some animals (see next
section), the failure of numerator/denominator count may also cause sex-specific
inviability of interspecific hybrids. Intersexuality accompanied with low viability
of flies produced from mothers of certain genotypes of the D. repleta/D. neorepleta
combination (Sturtevant 1946) may be an example of this.
Developmental bases of sexual reversion in mouse hybrids is well documented.
When the Y chromosome is introduced from wild mice of certain Mus domesticus
populations (e.g., the poschiavinlls chromosomal race) into a particular strain of
laboratory mouse, the chromosomal (XY) males develop as females or as hermaphrodites (Eicher et al. 1982; Nagamine et al. 1987). [Note that the laboratory mouse
strain (a genetic mixture of M. domesticlls and M. musculus) carries a Y chromosome of M. musculus origin (Bishop et al. 1985).] A testis-determining Y-linked
gene (Tdy = Sry) is believed to be involved in this phenomenon: the domesticus (or
poschiavinus) allele of the Sry gene does not function normally in the genetic background, homozygous for the laboratory mouse allele of testis-determining autosomal genes (tdal, tda2, and tda3) (Eicher and Washburn 1983; Coward et al. 1994;
Eicher et al. 1995, 1996). It has been shown that the sex-reversed fetuses have a
later onset of testicular development than the control fetuses (Taketo-Hosotani et
al. 1989; Taketo et al. 1991; Palmer and Burgoyne 1991). The Sry product, a transcription factor, is normally produced but its inactivation is delayed in the gonads
of sex-reversed fetuses. This delay seems to cause improper expression of genes
downstream of it, which results in the sex reversion (Lee and Taketo 1994). Recent
finding of high interspecific variability of the Sry gene sequences surprised molecular biologists (Whitfield et al. 1993; Tucker and Lundrigan 1993). Mammalian
geneticists tend to assume that this gene may playa key role in causing sex specific
defects in hybrids (Short 1997; Graves and O'Neill 1997). The incompatibility
between the Sry gene and some X-linked or autosomal genes may explain the paucity and/or sterility of heterogametic (XY) sex in interspecific mammalian hybrids,
the so-called Haldane's rule (Haldane1922).
2.3 Irregular Dosage Compensation
The X chromosome inactivation in female mammals, which compensates for the
dose difference of X-linked genes between sexes, is cell-autonomous: whether maternally derived X is inactivated or paternally derived X is inactivated is usually
determined at random (Lyon 1993). But this is not the case in some interspecific
hybrids: e.g., paternal X (of donkey origin) is preferentially inactivated in a female
K. Sawamura
(e.g., sisterless-a, sisterless-b) and autosomes have putative denominator genes. It
is well-known that a maternal product (a transcription factor) of a second-linked
gene, daughterless, calculates the X/A ratio and regulates the ON/OFF state of a
key gene of sex determination, Sex-lethal (Cline 1993). If new genes are recruited
to the numerator/denominator system or each numerator/denominator element
evolves rapidly in independent populations, interspecific hybrids will show an imbalance of the system resulting in sex reversion. Because sex determination is related to dosage compensation of the X chromosome in some animals (see next
section), the failure of numerator/denominator count may also cause sex-specific
inviability of interspecific hybrids. Intersexuality accompanied with low viability
of flies produced from mothers of certain genotypes of the D. repleta/D. neorepleta
combination (Sturtevant 1946) may be an example of this.
Developmental bases of sexual reversion in mouse hybrids is well documented.
When the Y chromosome is introduced from wild mice of certain Mus domesticus
populations (e.g., the poschiavinlls chromosomal race) into a particular strain of
laboratory mouse, the chromosomal (XY) males develop as females or as hermaphrodites (Eicher et al. 1982; Nagamine et al. 1987). [Note that the laboratory mouse
strain (a genetic mixture of M. domesticlls and M. musculus) carries a Y chromosome of M. musculus origin (Bishop et al. 1985).] A testis-determining Y-linked
gene (Tdy = Sry) is believed to be involved in this phenomenon: the domesticus (or
poschiavinus) allele of the Sry gene does not function normally in the genetic background, homozygous for the laboratory mouse allele of testis-determining autosomal genes (tdal, tda2, and tda3) (Eicher and Washburn 1983; Coward et al. 1994;
Eicher et al. 1995, 1996). It has been shown that the sex-reversed fetuses have a
later onset of testicular development than the control fetuses (Taketo-Hosotani et
al. 1989; Taketo et al. 1991; Palmer and Burgoyne 1991). The Sry product, a transcription factor, is normally produced but its inactivation is delayed in the gonads
of sex-reversed fetuses. This delay seems to cause improper expression of genes
downstream of it, which results in the sex reversion (Lee and Taketo 1994). Recent
finding of high interspecific variability of the Sry gene sequences surprised molecular biologists (Whitfield et al. 1993; Tucker and Lundrigan 1993). Mammalian
geneticists tend to assume that this gene may playa key role in causing sex specific
defects in hybrids (Short 1997; Graves and O'Neill 1997). The incompatibility
between the Sry gene and some X-linked or autosomal genes may explain the paucity and/or sterility of heterogametic (XY) sex in interspecific mammalian hybrids,
the so-called Haldane's rule (Haldane1922).
2.3 Irregular Dosage Compensation
The X chromosome inactivation in female mammals, which compensates for the
dose difference of X-linked genes between sexes, is cell-autonomous: whether maternally derived X is inactivated or paternally derived X is inactivated is usually
determined at random (Lyon 1993). But this is not the case in some interspecific
hybrids: e.g., paternal X (of donkey origin) is preferentially inactivated in a female