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1. The ladykiller (lk) gene has been located on the sex chromosome of the fowl. It is 4.2 map units distant from the feathering rate locus (k) and 11.2 map units distant from the dwarf (dw) locus. 2. Most of the embryonic mortalities associated with this gene occurred between 3 and 4 d of incubation.
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The bacteriophage T3 promoter can be selectively transcribed by the corresponding RNA polymerase in eukaryotic cells. A toxic gene can in principle be linked to this promoter in a "dormant" and innocuous transgene in a transgenic animal. In this scheme, the activating strain expresses the RNA polymerase. When expression of the gene is needed in the progeny, the 2 lines are crossed. However, when a single molecule is sufficient to kill the cell--as with the diphtheria toxin--transcriptional "leakage" from the promoter may not be tolerated by the cell, even when extremely weak. Therefore, prior to more elaborate studies, diphtheria toxin, as a prototype of a gene toxic to the organism, has been linked to the bacteriophage T3 promoter in a T3-E-DTA construct. The T3-E-DTA plasmid has been transiently transfected into human embryonic kidney derived cells together with a lacZ plasmid. By co-transfection, the T3-E-DTA cells can be readily identified as lacZ positive, and their fate followed by the production of beta-galactosidase at the single cell or overall population level. In spite of the extreme toxicity of the toxin, the cells tolerate the presence of the T3-E-DTA construct, and are only killed--with a high efficiency--when the T3 RNA polymerase is present. Transactivation is usually restricted to the auxiliary factors of transcription. With this study, the promoter and the polymerase are revealed as potential and efficient inducible and activating elements of a very simple binary system.
Effects of a second chromosome male-specific lethal gene, maleless (mle), of Drosophila melanogaster were further studied. It was shown that, although no maternal effect was seen with respect to the male-specific lethality, the lethal stage was influenced by whether parental females were homozygous or heterozygous for mle. Thus, in the former mle/mle males died mostly in the late third instar larval stage, while in the latter practically all males survived to the pupal stage. In the dying mle/mle male pupae complete differentiation of adult external head and thorax structures was often observed but that of abdominal structures was incomplete forming only a few segments in most cases. Imaginal discs from third instar mle/mle male larvae which were produced by mle/mle mothers and were destined to die as larvae were able to differentiate into adult structures upon transplantation into normal third instar larval hosts. A somewhat elaborated version of the previously presented hypothesis (FUKUNAGA, TANAKA and OISHI 1975) was discussed as to the possible presence of a class of sex-specific lethals which are not related to the process of primary sex differentiation.
Linear regressions have been used extensively for the calculation of lethal gene equivalents in human populations. There are considerable theoretical and practical objections to the use of the method for this purpose.
Through examination of all available data on lethal and inversion frequencies on the second chromosome in natural populations of Drosophila melanogaster, we have discovered that there is a clear negative correlation between the two quantities. Lethal genes are located more densely on the regions of standard gene arrangement than the inverted regions, and this accounts for the negative correlation. To reveal the underlying mechanism of the phenomena, we have carried out an experiment and found that effect of EMS-induced mutations on the inversion-carrying chromosome is more severe than that on the standard chromosome. We interpret these results as evidence for coadaptation or position-effect within the inversion chromosomes. New mutations within the coadapted gene complex are quickly eliminated from the population and polymorphic inversions are kept free of mutants through selective elimination.
A range of mathematical models and error distributions was used to examine the validity of linear regression methods for the calculation of lethal gene equivalents. Because of the restricted span of inbreeding coefficient F values available in human studies and the limited number of data points, equivalent results were obtained with all combinations tested. It was concluded that linear regressions should be employed only for the detection of significant inbreeding effects in man and that their application to the estimation of lethal gene equivalents was not warranted.
We have shown that the Sex-lethal (Sxl) gene, which controls morphological aspects of sex determination in Drosophila melanogaster, also regulates sexual behavior. Chromosomal males that are hemizygous for a deletion of the entire Sxl locus perform normal courtship and synthesize the two courtship-inhibiting pheromones that normal males make. However, ectopic expression of female-specific Sex-lethal gene products drastically alters chromosomal males' ability to perform and elicit courtship and increases the probability that they will synthesize a courtship-stimulating pheromone or fail to synthesize one of the inhibitory pheromones. These observations suggest that male sexual behavior is a consequence of the Sxl gene's being functionally inactive in haplo-X flies.