Experimental studies on a mutant gene (p) causing premature death of Ambystoma mexicanum embryos.

The premature death (p) mutation is a recessive lethal, which, in the homozygous condition, gives rise to a complex of abnormalities. The mutant embryos develop only to stage 37, at which time disintegration of superficial tissue begins. Many of the abnormalities observed in sections of the stage-37 mutant embryo are related to its failure to establish a functioning circulatory system, or to the resulting edema and/or ascites that distend the abdomen and flanks. There are, however, abnormalities of heart, liver, gill and muscle development which cannot be attributed to lack of circulation and edema. All of these abnormalities can be indirectly related to the endoderm, particularly the anterior and dorsal endoderm. The findings, therefore, suggest that the mutation leads to a fairly general defect of the endoderm.

Diploid gynogenesis in the Mexican axolotl.

Gynogenetic diploid axolotls were produced by activating eggs with ultraviolet-inactivated sperm, and then subjecting the activated eggs to heat shock. Optimal conditions for ultraviolet inactivation of the sperm, and for suppression of the second meiotic division by heat shock, were established. Gynogenetic diploids produced by these procedures included progeny homozygous for recessive alleles carried by a heterozygous mother. Gynogenesis could, therefore, be used to uncover new mutations more rapidly than by conventional inbreeding techniques. However, some difficulty was encountered in recognizing mutant phenotypes because of the high incidence of abnormalities and deaths. Defective embryos probably resulted from a combination of heat-shock-induced damage to the eggs and the expression of deleterious recessive alleles carried by the mother.