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D L Hartl

Publications and source records attributed to D L Hartl.

191 records · Page 11Linked to original sources
PubMed1973

Complementation analysis of male fertility among the segregation distorter chromosomes of Drosophila melanogaster.

The fecundities of 55 genotypes of the form SD(i)/SD(j) generated by 11 different SD chromosomes have been examined. Five of the genotypes are lethal The fecundities of the rest fall into a pattern of fertility and sterility that is highly suggestive of intracistronic complementation. The complementation leading to male fertility is only partial complementation: the fecundity of most fertile genotypes is less than half that of controls. The three components of the SD system, the Sd locus, the Ac locus, and the modifiers in 2R, were examined separately, and it appears that the complementation is a phenomenon associated with the Sd locus. A hypothesis of the molecular events involved in segregation distortion is formulated in the light of these observations. The model is based on the assumption that the Sd locus produces a multimeric molecule that regulates the activity of the Ac(=Rsp) locus during spermatogenesis.

Alleles↗
PubMed1969

Dysfunctional sperm production in Drosophila melanogaster males homozygous for the segregation distorter elements.

Drosophila males heterozygous for the segregation distorter chromosome show a reduction in fecundity which is correlated with the degree of distortion of their segregation ratio. When males are made homozygous for the segregation distorter elements, their fecundity is lowered to just that extent expected if each SD were independently causing the sperms carrying the other to dysfunction. In three cases tested, Sd Ac/Ac, Sd Ac/Sd Ac, and Sd Ac St/Sd Ac St, the fecundity of the males is consistent with the dysfunction model, whereas the females are normal. The Sd Ac St/Sd Ac St males are almost completely sterile. They do produce sperms, however, which are motile and which look morphologically normal in the phase contrast microscope. They are transferred to the female during copulation and are stored in apparently normal numbers in the seminal receptacle and spermathecae.

Animals↗
PubMedDate not supplied

Pseudogene evolution and natural selection for a compact genome.

Pseudogenes are nonfunctional copies of protein-coding genes that are presumed to evolve without selective constraints on their coding function. They are of considerable utility in evolutionary genetics because, in the absence of selection, different types of mutations in pseudogenes should have equal probabilities of fixation. This theoretical inference justifies the estimation of patterns of spontaneous mutation from the analysis of patterns of substitutions in pseudogenes. Although it is possible to test whether pseudogene sequences evolve without constraints for their protein-coding function, it is much more difficult to ascertain whether pseudogenes may affect fitness in ways unrelated to their nucleotide sequence. Consider the possibility that a pseudogene affects fitness merely by increasing genome size. If a larger genome is deleterious--for example, because of increased energetic costs associated with genome replication and maintenance--then deletions, which decrease the length of a pseudogene, should be selectively advantageous relative to insertions or nucleotide substitutions. In this article we examine the implications of selection for genome size relative to small (1-400 bp) deletions, in light of empirical evidence pertaining to the size distribution of deletions observed in Drosophila and mammalian pseudogenes. There is a large difference in the deletion spectra between these organisms. We argue that this difference cannot easily be attributed to selection for overall genome size, since the magnitude of selection is unlikely to be strong enough to significantly affect the probability of fixation of small deletions in Drosophila.

Animals↗