Perhaps the most critical test of Fisher's theory involves assessing the dominance of mutations in "artificial diploids" from a normally haploid species. Because heterozygotes do not exist in haploid species, it is impossible to select for reduced expression of mutations in heterozygotes; thus, Fisher's theory could not explain the recessivity of mutations in haploid species. Unfortunately, the well-known recessivity of most mutations in bacteria and fungi, although suggestive, does not cleanly settle the issue: bacterial cells are "polykaryotic"-that is, they normally carry several copies of a chromosome (9, 10). Thus, each time a mutation recurswhich must be very often given the enormous size of bacterial populations-it spends several generations as a heterozygote and is exposed to Fisherian selection for recessivity. Many fungi are also polykaryotic: the compartments of haploid hyphae are frequently multinucleate (11). Furthermore, fungi do not possess true cells; instead, the gene products of adjacent compartments freely mix (11). Thus, mutations essentially arise as heterozygotes, just as in diploid organisms. Natural selection-even weak selection acting for only several generations each time a mutation arises-can then render these mutations increasingly recessive over long periods -of time. Last, fungi have a diploid sexual stage in which Fisherian selection might occur.
Chlamydomonas escapes most of these difficulties and so provides nearly ideal material for testing Fisher's theory. Chlamydomonas, which can reproduce vegetatively for an apparently endless number of generations, spends the overwhelming proportion of its time as a haploid (12, 13). Moreover, its haploid cells are truly monokaryotic-i.e., they carry only one copy of each chromosome (12). Thus, mutations arise as hemizygotes, not heterozygotes, and so are not subjected to Fisherian selection. Although Chlamydomonas can enter into a diploid zygotic state, this stage is brief and dormant (12). Most important, as discussed below, many characters are expressed only in the haploid stage.
The dominance of Chlamydomonas mutations has been tested in two ways. First, one can form temporary dikaryons: when two haploid gametes fuse to form a prozygote, one can observe the phenotype of the cell immediately prior to nuclear fusion (13, 14). Second, one can screen for rare diploid vegetative cells. In the laboratory, zygotes occasionally (0.2-3.0%o) divide mitotically instead of meiotically, yielding temporary vegetative diploids (15, 16). These diploids represent evolutionary dead-ends: they are mitotically unstable and difficult to maintain and apparently cannot undergo imeiosis (12, 17, 18).
I surveyed the literature for information on the dominance of Chlamydomonas mutations using Harris' (12, 19) mutant lists as guides. To ensure that mutations having similar phenotypes represent alleles at separate loci, only mutations that were mapped to a known linkage group were included. Because its evolutionary history is unclear, mutations mapping to the unusual circular UNI chromosome (12) were excluded; inclusion of these loci would not, however, qualitatively change the present results.
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