Oncogenic allelic interaction inXiphophorushighlights hybrid incompatibility

Mixing genomes of different species by hybridization can disrupt species-specific genetic interactions that were adapted and fixed within each species population. Such disruption can predispose the hybrids to abnormalities and disease that decrease the overall fitness of the hybrids and is therefore named as hybrid incompatibility. Interspecies hybridization between southern platyfish and green swordtails leads to lethal melanocyte tumorigenesis. This occurs in hybrids with tumor incidence following progeny ratio that is consistent with two-locus interaction, suggesting melanoma development is a result of negative epistasis. Such observations makeXiphophorusone of the only two vertebrate hybrid incompatibility examples in which interacting genes have been identified. One of the two interacting loci has been characterized as a mutant epidermal growth factor receptor. However, the other locus has not been identified despite over five decades of active research. Here we report the localization of the melanoma regulatory locus to a single gene,rab3d, which shows all expected features of the long-sought oncogene interacting locus. Our findings provide insights into the role ofegfrregulation in regard to cancer etiology. Finally, they provide a molecular explainable example of hybrid incompatibility.

MUTATIONS IN POLYPLOID CEREALS: IV. A SEGMENTAL CHROMOSOME DEFICIENCY DETERMINING AN α SERIES RATIO IN A SPELTOID WHEAT

The C chromosome of beardless Triticum vulgare carries epistatic inhibitors, about 30 crossover units apart on the longer arm of the chromosome, which prevent the expression of the bearded-speltoid complex of genes. It has earlier been shown that het speltoid mutants may lack one of the two sets of inhibitors through the loss of the entire C chromosome, or its longer arm, or an interstitial segment of this arm. The first determines Series β segregation (1 normal: ca. 5 het speltoids: ca. 0.03 speltoids), the last two Series γ (1: 1: ca. 0.05). A third type of progeny ratio, α, is a distortion of a 1: 2: 1 caused by a greater or lesser deficiency of speltoids and, less markedly, of het speltoids. Some workers regard α ratios as resulting from mutation of the epistatic inhibitors to their recessive state; others as due to chromosome aberration similar to, but less extensive than, that observed in typical γ strains. The latter interpretation is proved correct herein. That deviations from the ratios characteristic of the three Series are determined by the degree of pollen certation superimposed on the proportion in which normal and mutant ovules are formed has been shown by analyses involving natural hybrids and crosses made with other types. The extent of certation in α and γ Series may be measured from their progeny ratios—normal pollen = N + H − Sp: mutant pollen = 2 × Sp. A rough correlation has been established between the length of the mutant C chromosome, percentage conjugation with C, proportion of N: Sp progeny, percentage β het Sp progeny, and the coefficient of certation. The percentage het Sp of Series β expected as secondary mutants in the het Sp progeny of α and γ het Sp approximates to [Formula: see text].