Effect Maternal Control

Transcription from the genome of a zygote does not usually begin until several cleavage divisions have taken place. The early cleavage divisions, and often much of early embryogenesis, are accomplished by RNAs and proteins deposited in the unfertilized egg by the maternal genome during oogenesis. The early patterning of the embryo is also dependent on maternal positional information in the unfertilized egg. For example, both the anterioposterior and dorsoventral axes of Drosophila are determined by maternally acting genes (1-3). The extent of maternal control of early development has been most characterized in Drosophila melanogaster using mutations that alter development. Mutations that act in the mother to alter the development of progeny are called maternal effect mutations.

Maternal effect mutations that cause the death of all progeny are a special type of female sterile mutation, called maternal effect lethal mutations. The severity of the defects in the dead progeny can be independent of their genotype (nonrescuable by the paternal gene delivered by the sperm), or can be less severe in zygotes that receive a wild-type gene from the father (partially rescued). When the progeny are completely rescued by the wild-type paternally derived gene, the maternal-effect mutation is not classified as a female sterile. One example is the cinnamon (cin) mutation of Drosophila (4). Homozygous cin mutant progeny from homozygous mutant mothers die during embryogenesis. However, progeny of cin mutant mothers that receive a wild-type allele from the father survive. Most screens for maternal-effect mutations in Drosophila have not been designed to identify mutations that are completely rescued by the paternally contributed allele, and the frequency of this type of gene is not known. Most screens would also miss maternal-effect mutations in which the progeny die later than embryogenesis. Because the zygotic genome becomes transcriptionally active relatively early in embryogenesis, few maternal-effect mutations are expected to cause death later than embryogenesis. An estimate of the proportion of the genome that can mutate to give maternal-effect lethal mutations can be made from the work of Schüpbach and Wieschaus (5). They recovered female-sterile mutations at about 8% of the frequency of lethal mutations. Of these female-sterile mutations, about 25% produced normal eggs that were fertilized but the embryos died during early development. This suggests that about 72 genes in Drosophila should mutate to maternal-effect lethality. As many of the female-sterile mutations are single alleles of genes that usually mutate to zygotic lethality (6), this estimate is probably somewhat low.

The study of maternal control using maternal-effect mutations is limited by the ability to recover mutations that are not lethal to the zygotes that carry them. This problem has been circumvented by the use of genetic mosaics. One method is to transplant germ cells from embryos homozygous for lethal mutations into wild-type embryos. These mutant germ cells are included in the developing ovary, and the resulting females have wild-type somatic cells, but mutant germ cells. This approach is limited by the difficulty and time involved in the transplantation techniques. Mitotic recombination in the germ cells of females heterozygous for recessive lethal mutations can also be used to produce homozygous mutant germ cells. The use of a dominant female-sterile mutation to prevent the formation of normal eggs from all of the germ cells except those homozygous for the mutation of interest has greatly facilitated this approach (7). Female germ cells heterozygous or homozygous for the ovo^D1 mutation are blocked early in oogenesis. Mitotic recombination in females heterozygous for this mutation produces germ cells that are homozygous for the wild-type allele (they lack the mutant allele), are no longer blocked in oogenesis, and can produce wild-type eggs. If the chromosome that carries the wild-type allele of ovo also carries a recessive lethal mutation, the germ cells that lose the mutant ovo^D1 allele also lose the wild-type allele for the recessive lethal mutation. Extensive experiments using this technique suggest that at least 70% of the zygotic lethal mutations in Drosophila have maternal effects (8).

References

1. D. Morisato and K. V. Anderson (1995) Annu. Rev. Genet. 29, 371–399. 

2. C. Nüsslein-Volhard (1993) Cancer 71, 3189–3193. 

3. S. Roth, F. S. Neuman-Silberbert, G. Barcelo, and T. Schüpbach (1995) Cell 81, 967–978. 

4. B. S. Baker (1973) Dev. Biol. 33, 429–440. 

5. T. Schüpbach and E. Wieschaus (1989) Genetics 121, 101–117.  

6. N. Perrimon and A. P. Mahowald (1986) In Gametogenesis and the Early Embryo (J. Gall, ed.), Alan R. Liss, New York, pp. 221–235. 

7. N. Perrimon, L. Engstrom, and A. P. Mahowald (1984) Dev. Biol. 105, 404–414. 

8. Reference 6, p. 225.

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The Serendipitous Discovery of trp Enzyme Hypersynthesis

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