10
K. Sawamura
in most of the cases. This may be caused by the incompatibility between maternally
supplied proteins and paternal chromosomes (see also next section).
A mitotic defect is also seen in the larval lethal hybrid males from the crosses
between Drosophila melanogaster females and males of its sibling species (D.
simulans, D. mallritiana, or D. sechellia). The male larvae show a typical pathology of mitotic mutants and show a failure of chromatin condensation (Orr et al.
1997). Normal mitotic figures can be seen in hybrids which are rescued from the
inviability by a mutation, Hybrid male rescue (Hutter and Ashburner 1990). The
loss of the X chromosome of sibling species origin is frequently detected as mosaics
in hybrid females (XX//XO), which may result from a milder mitotic defect than in
the brothers. And, importantly, the XO clones (produced with a trick) are mostly
seen in the abdomen not in the head nor the thorax. As Orr et al. (1997) speculate,
maternally supplied products necessary for mitosis in the hybrids might be used up
gradually and imaginal disc cells may be less tolerant than larval histoblast cells
(the latter mainly forms abdominal cuticle).
2.8 Maternal/Zygotic Transition Failure
Proteins and mRNAs necessary for the very early stage of development are generally supplied from mothers. Interspecific hybrids have one set of genome derived
from paternal species, so the maternally supplied transcription factors may not be
able to regulate zygotic gene actions of the incompatible species. In such cases,
hybrid embryos will die before the onset of zygotic transcriptions. In species groups
of male heterogamety (i.e., XX females, XY males), an X chromosome of patcrnal
origin exists in hybrid females but not in hybrid males. So, only hybrid females
should suffcr from the incompatibility, if the paternal X chromosome has a dominant incompatible gene(s). This could result in the exceptions to Haldane's rule
(Sawamura et al. 1993a, c; Wu and Davis 1993; Wu et al. 1996; Sawamura 1996;
Huttcr 1997; Laurie 1997).
A well-known example is the embryonic inviability of hybrid females from the
crosses between Drosophila melanogaster males and fcmales of its sibling species
(D. simulans, D. mauritiana, or D. sechellia) [for a rcview see Sawamura ct al.
(1993b); other examples listed in Sawamura (1996)]. The lethal embryos show a
typical pathology of maternal/zygotic transition failure (K. Sawamura, C.-I Wu
and T. L. Karr, unpublished observation). Two genetic components involved in the
inviability have been detected as rescue mutations: one is a maternally acting gene
located on the second chromosomc of D. simulans (maternal hybrid rescue: mhr),
and the other is a zygotic acting gene located on the X chromosome of D.
melanogaster (zygotic hybrid rescue: zhr) (Sawamura et al. 1993a, c). Orr (1996)
has described a dominant rescue gene(s) segregating in natural populations of D.
simulans, which is potentially allelic to mhr. Its dominance may depend on the D.
melanogaster strains employed, although further examination is necessary. Apparently, natural popUlations of D. melanogaster have a variation in the strength of the
K. Sawamura
in most of the cases. This may be caused by the incompatibility between maternally
supplied proteins and paternal chromosomes (see also next section).
A mitotic defect is also seen in the larval lethal hybrid males from the crosses
between Drosophila melanogaster females and males of its sibling species (D.
simulans, D. mallritiana, or D. sechellia). The male larvae show a typical pathology of mitotic mutants and show a failure of chromatin condensation (Orr et al.
1997). Normal mitotic figures can be seen in hybrids which are rescued from the
inviability by a mutation, Hybrid male rescue (Hutter and Ashburner 1990). The
loss of the X chromosome of sibling species origin is frequently detected as mosaics
in hybrid females (XX//XO), which may result from a milder mitotic defect than in
the brothers. And, importantly, the XO clones (produced with a trick) are mostly
seen in the abdomen not in the head nor the thorax. As Orr et al. (1997) speculate,
maternally supplied products necessary for mitosis in the hybrids might be used up
gradually and imaginal disc cells may be less tolerant than larval histoblast cells
(the latter mainly forms abdominal cuticle).
2.8 Maternal/Zygotic Transition Failure
Proteins and mRNAs necessary for the very early stage of development are generally supplied from mothers. Interspecific hybrids have one set of genome derived
from paternal species, so the maternally supplied transcription factors may not be
able to regulate zygotic gene actions of the incompatible species. In such cases,
hybrid embryos will die before the onset of zygotic transcriptions. In species groups
of male heterogamety (i.e., XX females, XY males), an X chromosome of patcrnal
origin exists in hybrid females but not in hybrid males. So, only hybrid females
should suffcr from the incompatibility, if the paternal X chromosome has a dominant incompatible gene(s). This could result in the exceptions to Haldane's rule
(Sawamura et al. 1993a, c; Wu and Davis 1993; Wu et al. 1996; Sawamura 1996;
Huttcr 1997; Laurie 1997).
A well-known example is the embryonic inviability of hybrid females from the
crosses between Drosophila melanogaster males and fcmales of its sibling species
(D. simulans, D. mauritiana, or D. sechellia) [for a rcview see Sawamura ct al.
(1993b); other examples listed in Sawamura (1996)]. The lethal embryos show a
typical pathology of maternal/zygotic transition failure (K. Sawamura, C.-I Wu
and T. L. Karr, unpublished observation). Two genetic components involved in the
inviability have been detected as rescue mutations: one is a maternally acting gene
located on the second chromosomc of D. simulans (maternal hybrid rescue: mhr),
and the other is a zygotic acting gene located on the X chromosome of D.
melanogaster (zygotic hybrid rescue: zhr) (Sawamura et al. 1993a, c). Orr (1996)
has described a dominant rescue gene(s) segregating in natural populations of D.
simulans, which is potentially allelic to mhr. Its dominance may depend on the D.
melanogaster strains employed, although further examination is necessary. Apparently, natural popUlations of D. melanogaster have a variation in the strength of the