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Figure 8-1. Some different kinds of mating systems in single-celled organisms. (A) Mating in bacteria (e.g, E. coli), stages A-D; (B) mating in yeast (S. cerevesiae). Separate lines show switching from each of two states. For explanations see text. (B) redrawn from (Haber 1998).

Figure 8-1. Some different kinds of mating systems in single-celled organisms. (A) Mating in bacteria (e.g, E. coli), stages A-D; (B) mating in yeast (S. cerevesiae). Separate lines show switching from each of two states. For explanations see text. (B) redrawn from (Haber 1998).

regulatory sequences (EL, IL, ER, and IR) recognized by DNA-binding regulatory proteins, and a repressor switch (symbolized in the figure by a gray diamond), a copy is made of the derepressed donor gene, and the copy is inserted at MAT replacing what was there. A subsequence within HMLa or HMRa (Ya or Ya) codes for genes determining the different mating type. Haploid yeast of complementary mating types unite to form a diploid reproductive cell. The genetic mechanism for this switching, and the conditions under which diploid and haploid states occur or persist under different environmental circumstances, are highly variable among yeast species.

Many animals have sex determination in which males and females have different chromosomal complements. In mammals, females are homogametic and have two structurally identical X chromosomes, whereas males are heterogametic, with one X and one Y. The remaining chromosome sets, called autosomes, are structurally identical in each sex, although they may be differently modified in their respective somatic or gametic cells (see below), and of course may bear different alleles at any locus. Birds and nematodes have reversed male/female heterogamy.

Some species (e.g., some plants) produce diploid hermaphrodites, but closely related species may have obligatory sex-specific morphology and go through a haploid stage. In the haplodiploidy of social hymenopterans (ants and bees), males are haploid and come from unfertilized eggs, whereas workers and queens come from fertilized (and hence diploid) eggs. Queen development is environmentally induced by feeding larva on a special substance known as "royal jelly."

Factors in the environment can determine sex in some vertebrates. In many reptile species, such as turtles, sex determination is temperature-dependent. However, these environmental effects appear to work via genetic pathways similar to those used in descendant vertebrates, so that experimental sex-hormone manipulation can override the effect of temperature. From their presence in diverse living reptiles, we might infer that sex hormones already existed ancestrally for some purpose and may have been recruited to take over the role previously played by temperature, becoming regulated by genes linked to sex chromosomes.

Many plants can be male, female, or hermaphroditic. Flowering plants do not sequester a separate germ line, and cells at the shoot meristems (tips) can differentiate into male and female flowers, or flowers can be produced that bear both stamens and carpels, depending on patterns of regulatory gene expression. There can be location-specific sex determination, such as male tassels atop and female flowers along the axis of corn. Once committed, the designated cells undergo meiosis that is similar, although not identical, to meiosis in animals. Although some plants can self-fertilize, others have mechanisms that force them to crosspollinate using, for example, insects, birds, or wind. Darwin wrote an entire monograph on the devious ways this is achieved by orchids (Darwin 1862).

Some species form two sexes without a specific set of sex chromosomes. This can be achieved by quantitative polygenic contribution of genes on several chromosomes or (as in some reptiles) through environmental effects.

Some General Genetic issues

It is very interesting that, as important and pervasive as sexual reproduction is, its mechanisms are so highly variable and rapidly evolving. The mechanisms for sex specification differ greatly at the molecular level. Some species have sex chromosomes, but they work in different ways in different species. The genes on the sex chromosomes are responsible for some aspects of sex determination, but they typically induce developmental cascades using genes all over the genome to effect the wealth of differences in size, morphology, and behavior between males and females that go well beyond their respective gonadal differences.

Some of these effects are qualitative, but others are quantitative (e.g., Griffiths, Miller et al. 1996; Raff 1996). In mammals, the mechanism is dichotomous and sex-linked. The SRY regulatory gene, a member of the HMG/Sox chromatin-associated DNA binding protein family (see Table 7-6), binds and bends DNA in a critical region of the Y chromosome, presumably providing access to transcription factor (TF) activity that initiates a cascade to turn a gonad into a testis. Downstream activation includes a related gene, Sox9, which is involved in male determination in mammals and other tetrapods (but also having unrelated developmental functions). The sex-determining cascade also involves X-linked genes. However, germ cell differentiation and gonadal and morphological sex differences are not inherently connected (and there are developmental genetic differences, even between humans and mice).

By contrast, sex determination is more quantitative than dichotomous in flies (Schutt and Nothiger 2000). In a zygote with two X chromosomes and two sets of autosomes (A), the ratio of X- and A-linked gene products is roughly 1.0, a state that activates a TF, Sex lethal (Sxl), to initiate a female-producing downstream cascade of differentiation. The latter activates a gene known as Transformer (Tra) that activates the gene Doublesex (Dsx), which leads to female development. These appear to involve sex-specific splicing variants (e.g., Graham et al. 2003). In XY males, the X-to-A dosage ratio is less than 1.0, inactivating Sxl and producing a male. However, not all flies use the same control system for activating Dsx (Dubendorfer et al. 2002; Graham, Penn et al. 2003), suggesting that the lower-down mechanism was established initially and its control assumed by various genes during arthropod evolution. In many fly species tested, Sxl is not even involved in sex determination (it is not true that once you've seen one fly you've seen them all, nor that all flies are like Drosophila). In the species Ceratitis capitata the X-to-A ratio appears not to be involved either, but a separate Y-linked factor called M is.

The widely studied animal model nematode Caenorhabditis elegans also uses a dosage-sensing mechanism, with activity of the autosomal gene controlled by the sex-chromosome dosage. However, the controlling sex-determining gene, Xo1, is not homologous to Sxl, nor does the downstream cascade of genes that are on or off differently in male and female development bear much if any homology with the fly mechanism. Indeed, recent work suggests that even the clear-cut "mammalian" mechanism is not so clear-cut because mice and humans use SRY, and some other genes thought to be fundamental for sex determination, in different ways (Ostrer 2001; 2001). Furthermore, although they have a similar SRY mechanism, marsupials can be hormonally induced to form either sex, and gonadal development is determined by mechanisms separate from the sex-determining ones (Renfree and Shaw 2001).

The diverse sex-determining mechanisms appear to have evolved independently many times. However, some organisms, vertebrates and yeast for example, seem certainly to have had sexual reproduction ever since they shared a common ancestor;

therefore, the differences in mechanism seen today have probably arisen by pheno-genetic drift rather than via independent evolution from nonsexual forms.

Sex-Specific Chromosome Modification

Functions in the early zygote, from the single-cell stage onward, may be dominated by conditions inherited from the mother. This is especially true in species whose fertilized egg receives little besides DNA from the sperm. The nutrients and mRNA required for early development are produced by the mother. In mammals, maternally and paternally derived chromosomes arrive differently marked by imprinting, by methylation of the DNA (e.g., the Cs in CpG pairs) flanking the 5' start site of many vertebrate genes, which prevents promoter binding by TFs and thus represses transcription. In the formation of gametes, the parent resets its respective imprinting pattern.

How has this curious arrangement evolved? One explanation offered from a strongly darwinian behavioral-evolution perspective is that the fetus is a kind of parasite on the mother. It is related to the mother genetically but only by half, and she and the fetus compete for resources. The fetus could sap her of so much energy that she would not be able to reproduce again, which is against her interests, and conflicting with this is her clear interest in the health of the fetus.

Genes expressed in the trophoblast cells that form the extraembryonic tissues including the placenta are predominantly maternally derived, leading to a different possibility, that she is less likely to detect the implanted fetus as a foreign invader and destroy it. Sperm-derived chromosomes are generally more heavily imprinted and not expressed until somewhat later, and then in the cells that will form the embryo itself. Some imprinting signal does persist in the zygote, but differential imprinting cannot affect most autosomal genes, or at least not for long, because individuals typically show the expected equal inheritance proportion and effect of their autosomal alleles from both parents; for example, offspring from AA x aa matings typically manifest both A and a allelic effects. The known exceptions are notable for their rarity.

Gene Dosage and related issues

Diploid organisms must be able to function genetically in a haploid state, during early development as just mentioned, and the haploid germ cells must also be viable. However, heterogamic sexual reproduction raises an additional gene dosage problem. To the extent that gene products coded by autosomal and X-linked genes interact in a particular cell type, a female mammal has a double dose of autosomal and X-specific genes but a male has only one-half dose of the latter. In fact, this kind of dosage difference determines sex in flies, as described earlier.

In some species, there is upregulation (increased expression) of genes on the single chromosome in heterogametes, whereas in others, including mammals, there is downregulation. This is achieved by random X-inactivation in females. During embryogenesis, in each cell in females, one of the X chromosomes is inactivated so that the cell only expresses genes from a single of its two X chromosomes. This is achieved by an interesting mechanism. A gene called Xist is transcribed from an X-inactivation center, and the resulting Xist RNA "paints" (covers) that X chromo some (but not the other X chromosome in the cell) to block its genes from transcription at positions that may be signaled by the location of dispersed repeat elements (Bailey et al. 2000; Brockdorff 2002; Plath et al. 2002). The result is that, in males and females, protein interactions work at the same dose level. The genetic mechanisms used to inactivate the entire X in this process were already available as part of the general mechanisms used in selective gene silencing in differentiating cells.

Because of the random and differently timed nature of inactivation, a female is somatically mosaic, with approximately half of each tissue using the maternal and half the paternal X-linked genes. Furthermore, because the inactivation pattern is mitotically inherited, the time at which a given inactivation event occurred in development determines the nature and size of the downstream clone—the developmental lineage—of cells expressing the particular active chromosome. This long-known principle has been shown to be incomplete, however, in that some genes do appear to escape inactivation. Interestingly, humans and mice differ considerably in the details of their Xist systems (e.g., Daniels et al. 1997). In addition, both the X- and Y-linked copies of some genes are active in males; the gene Amelogenin that is involved in dental enamel production is an example, with an active copy of the gene on both X and Y chromosomes.

Sex-linked genes in some organisms, one example being Bombyx mori (silkworm), appear not to be dosage compensated, showing that, clearly, interactions among gene products can be adjusted. Both male and female gametes are similar and in some species essentially identical. Some parent-specific marking persists in life so that alleles identical in sequence function differently if they were inherited from the maternal or paternal line. A few instances of this have been discovered in inherited disease, when the genes were examined carefully. Angelman syndrome is a set of conditions including developmental, speech, and other behavioral disturbances that arises when maternally imprinted information in a region of chromosome 15 is lost through various mechanisms such as aberrant meiosis. Alternatively, if paternal imprinting pattern in that chromosome region is absent a different disorder, Prader-Willi syndrome results; Prader-Willi has very different symptoms, predominated by morbid obesity. Several other known diseases are preferentially inherited through one parental line, again for presumed imprinting reasons.

Variation Everywhere

Variation is everywhere in the sexual reproduction arena. And an arena it is, because of the behavioral complexities required for the two sexes to find each other. Add to this the variation involved in making different kinds of gametes, not to mention their delivery by various mechanisms as well as the diversity of genital organs, ges-tational systems, and the huge repertoire of associated appearance, behavior, and morphological differences between males and females. Indeed, it is too simple to think of sex as dichotomous (males and females). There are, for example, plants that make both sexes and may be self-fertilizing, reptiles that can be either sex depending on how hot they are (or were as eggs), and fish that can respond to environmental conditions by changing their sex. Many if not most aspects of sexual morphology are variable among closely related species (e.g., Renfree and Shaw 2001). We also have culturally based ideas about gender, that is male and female behavior, but we know that there are exceptions, both in our species and many others.

More importantly perhaps is that as cultural beings who monitor our own societies closely, we know that there are all sorts of morphological as well as behavioral gradations related to plumbing as well as sex-related morphology and gender. These are not all highly correlated and hence are likely to be genetically unlinked. Not all this variation is dysfunctional in reproductive terms, and while in many or most species mating behavior involves stereotypical components, wide ranges of subtleties in morphology and behavior are compatible with successful reproduction. This probably indicates the kind of variation with which evolution works as sexual mechanisms change over time.

Finally, all evolutionary explanations have a Kiplingesque Just So element in them. Bdelloid rotifers illustrate this in regard to sex. These are microscopic aquatic animals that have been around for a long time and are phylogenetically diverse. They reproduce entirely by parthenogenesis (either by laying eggs or "hatching" already formed young) (Judson and Normark 2000; Welch and Meselson 2000). How this "violation" of so important an evolutionary rule as having sexual reproduction (and yet surviving quite well) occurred is not known, but of course even to propose this as a conundrum is to build in assumptions about the importance of sexual reproduction.

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