1. The Origin of Reproductive Isolation
9
2.6 Spermatogenic Defects
Evolutionary geneticists now have a consensus that spermatogenesis is one of the
most sensitive processes of development in interspecific hybrids (Wu and Davis
1993; Wu and Palopoli 1994; Carvajal et al. 1996; Forejt 1996; Hollocher and Wu
1996; True et al. 1996; Wu et al. 1996; Laurie 1997; Presgraves and Orr 1998;
Coyne et al. 1998; K. Sawamura, A. W. Davis and C.-I. Wu, submitted), and publication of papers dealing with this subject has burgeoned this decade. Here, I shall
cite a case where the molecular mechanism is characterized well. Recently, a gene
named Odysseus which causes male sterility when introduced from Drosophila
mauritiana into D. simulans was cloned (Ting et al. 1998; see also Perez et al.
1993; Perez and Wu 1995). This is the first sequenced gene of postzygotic reproductive isolation sensu stricto. Surprisingly, the gene encodes a paired-like
homeodomain protein which is highly conserved among nematodes, mice, and insects. Sequence analysis indicated that the homeobox domain of the gene evolved
rapidly between closely related species of Drosophila. It may be, speculatively, that
one of the redundant (duplicated) homeotic genes was recruited to the functional
regulation of spermatogenesis in this species group. Such an accelerated evolution,
presumably accompanied by an accessory function, in a particular species group of
Drosophila is also known in another homeotic gene, spalt (Reuter et al. 1989). It
has been assumed that genes involved in male sexual traits may evolve rapidly
because of sexual selection (Wu and Davis 1993; Wu et al. 1996; Tsaur and Wu
1997; Civetta and Singh 1998a, b; Tsaur et al. 1998).
2.7 Mitotic Defects
Mitotic chromosome loss in the early development of interspecific hybrids, which
sometimes results in inviability, is well-known since classical experiments. The
extensive literature on this subject, which deals particularly with echinoderms and
fishes, has been reviewed by Hertwig (1936) [for recent analyses see Bennet et al.
1976; Finch 1983; Fujiwara et al. 1997; references therein]. Endosymbiotic rickettsia, Wolbachia, are involved in some cases, e.g., in gynogenetic parasitic wasps
(Nasonia) produced by interspecific fertilization (Breeuwer and Werren 1990).
Wolbachia is well-known as an agent of cytoplasmic incompatibility responsible
for intraspecific hybrid inviability in the crosses between uninfected females and
infected males or between females and males infected by different strains (O'Neill
and Karr 1990). Nasonia may be a special case in which haploid zygotes that result
from the loss of the paternal genome can develop as males. A well-documented
mitotic defect is the loss of the paternal dot chromosome and resulting eye wrinkling in the hybrids between Drosophila virilis females and D. lummei males (Orr
1990; Braverman et al. 1992) [but see Heikkinen (1991, 1992) and references
therein]. Chromosome loss is also seen in mammalian somatic cell hybrids (Weiss
and Green 1967). It is interesting that paternal chromosomes are preferentially lost
9
2.6 Spermatogenic Defects
Evolutionary geneticists now have a consensus that spermatogenesis is one of the
most sensitive processes of development in interspecific hybrids (Wu and Davis
1993; Wu and Palopoli 1994; Carvajal et al. 1996; Forejt 1996; Hollocher and Wu
1996; True et al. 1996; Wu et al. 1996; Laurie 1997; Presgraves and Orr 1998;
Coyne et al. 1998; K. Sawamura, A. W. Davis and C.-I. Wu, submitted), and publication of papers dealing with this subject has burgeoned this decade. Here, I shall
cite a case where the molecular mechanism is characterized well. Recently, a gene
named Odysseus which causes male sterility when introduced from Drosophila
mauritiana into D. simulans was cloned (Ting et al. 1998; see also Perez et al.
1993; Perez and Wu 1995). This is the first sequenced gene of postzygotic reproductive isolation sensu stricto. Surprisingly, the gene encodes a paired-like
homeodomain protein which is highly conserved among nematodes, mice, and insects. Sequence analysis indicated that the homeobox domain of the gene evolved
rapidly between closely related species of Drosophila. It may be, speculatively, that
one of the redundant (duplicated) homeotic genes was recruited to the functional
regulation of spermatogenesis in this species group. Such an accelerated evolution,
presumably accompanied by an accessory function, in a particular species group of
Drosophila is also known in another homeotic gene, spalt (Reuter et al. 1989). It
has been assumed that genes involved in male sexual traits may evolve rapidly
because of sexual selection (Wu and Davis 1993; Wu et al. 1996; Tsaur and Wu
1997; Civetta and Singh 1998a, b; Tsaur et al. 1998).
2.7 Mitotic Defects
Mitotic chromosome loss in the early development of interspecific hybrids, which
sometimes results in inviability, is well-known since classical experiments. The
extensive literature on this subject, which deals particularly with echinoderms and
fishes, has been reviewed by Hertwig (1936) [for recent analyses see Bennet et al.
1976; Finch 1983; Fujiwara et al. 1997; references therein]. Endosymbiotic rickettsia, Wolbachia, are involved in some cases, e.g., in gynogenetic parasitic wasps
(Nasonia) produced by interspecific fertilization (Breeuwer and Werren 1990).
Wolbachia is well-known as an agent of cytoplasmic incompatibility responsible
for intraspecific hybrid inviability in the crosses between uninfected females and
infected males or between females and males infected by different strains (O'Neill
and Karr 1990). Nasonia may be a special case in which haploid zygotes that result
from the loss of the paternal genome can develop as males. A well-documented
mitotic defect is the loss of the paternal dot chromosome and resulting eye wrinkling in the hybrids between Drosophila virilis females and D. lummei males (Orr
1990; Braverman et al. 1992) [but see Heikkinen (1991, 1992) and references
therein]. Chromosome loss is also seen in mammalian somatic cell hybrids (Weiss
and Green 1967). It is interesting that paternal chromosomes are preferentially lost