The role of the genome in the development of the haploid syndrome in Anura.

The problem of the factors involved in the development of the haploid syndrome in anuran embryos is as yet unsolved. It is known that about 90 % of all haploid frog embryos develop the haploid syndrome, which is characterized by the presence of oedema and sluggishness, by reduction in pigmentation and in the efficiency of the heart and circulation, and by a partial failure of the gut to coil and of muscle to differentiate. The two most favoured explanations of the development of the haploid syndrome have been nucleocytoplasmic imbalance, since a haploid nucleus is only half the size of a diploid nucleus in the same-sized egg, and unmasked recessive lethal genes. There is good evidence that an abnormal nucleocytoplasmic ratio is an important contributory factor in the development of the haploid syndrome. Briggs (1949) compared populations of haploids developing from large and small eggs and Subtelny (1958) compared the development of haploids and homozygous diploids which possessed a reduplicated set of haploid chromosomes. Both these workers found that the proportion of embryos developing the haploid syndrome was smaller when the nucleocytoplasmic ratio approached normal (i.e. in the small-egged haploids and the homozygous diploids) but was not reduced to such an extent that a genetic influence could be ruled out. Other evidence from grafting experiments (Hadorn, 1936; Baltzer, 1941) has shown that although lethal genes may be unmasked in haploids, they are not necessarily cell-lethal, and Hamilton (1963) also observed that haploid organs may become viable and functional in a diploid environment. The demonstration that the haploid syndrome can be mimicked by treatment of heterozygous diploids with lithium chloride and sodium thiocyanate (Hamilton, 1965), and that similar abnormalities are found in magnesium-starved and nucleolarless Xenopus (Brown & Gurdon, 1964), led to the conclusion that developmental stresses could give rise to the haploid syndrome in both haploid and diploid embryos but that the threshold was very much higher in heterozygous animals.