• Jennifer A. Marshall Graves

      Articles written in Journal of Genetics

    • Genome instability in interspecific cell hybrids I. Unstable expression of genes in divergent cell hybrids

      Jennifer A. Marshall Graves

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      Somatic cell hybrids between cells of widely divergent mammalian species display a range of chromosomal and genetic anomalies which may be the equivalent of the “genomic shock” phenomena observed in many plant and animal interspecific hybrids. Mouse-kangaroo hybrids show extreme segregation and fragmentation of the kangaroo chromosomes. Here 1 show that, in addition to the chromosomal instability, some hybrids display unstable expression of three genes borne on the kangaroo active maternal X chromosome. These genes (HPRT, G6PD andPGK) may be co-ordinately inactivated at high frequency, then reactivated once more. I suggest that this reversible inactivation in interspecific hybrids may be the result of an unstable change at an X inactivation centre located in the kangaroo Xq.

    • Genomic instability in interspecific cell hybrids III. Repression of Colcemid resistance in hybrids suggests preferential β-tubulin expression

      Paula A. Zelesco Jennifer A. Marshall Graves

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      A Colcemid-resistant Chinese hamster line with an altered form of β-tubulin was used in studies of the expression of spindle proteins in interspecific cell hybrids. Eight hybrids between this line, and a Colcemid-sensitive mouse cell line, were studied. The altered hamster β-tubulin was not expressed as an increased resistance to Colcemid in any hybrid. Since the complete hamster chromosome complement was represented among the hybrids, the absence of altered β-tubulin is not due to segregation of the mutant hamster β-tubulin gene. We suggest either that the hamster β-tubulin gene is repressed in hybrids, or that hamster β-tubulin is excluded from the spindle in hybrid cells. We compare these findings with previous reports of the repression of other highly active, moderately repeated constitutive genes in interspecific hybrids.

    • Suppression of position-effect variegation inDrosophila melanogaster by fatty acids and dimethylsulphoxide: implications for the mechanism of position-effect variegation

      John Michailidis Jennifer A. Marshall Graves Neil D. Murray

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      Position-effect variegation refers to the inactivation, in clones of somatic cells, of genes contained in a euchromatic region relocated to near heterochromatin. On the basis of suppression of variegation byn-butyrate (a fatty acid whose effects include inhibition of histone deacetylase activity), it has been suggested that histone deacetylation is involved in inactivation of the variegating loci. We confirm the effect of butyric (and propionic) acid in suppressing variegation of the white eye gene in maleIn (1)wm4 flies, and demonstrate that this effect is independent of the effects of these agents on pH and on development time. However, we find that fatty acids have no effect on variegation in femaleIn(1)wm4 flies. We also show that 0.05 M dimethylsulphoxide has an even greater suppressive effect, such that virtually all treated flies (males and females) have a fully revertanl wild type phenotype. Dimethylsulphoxide has no known effect on histone deacetylase activity, but this agent, as well as butyrate, has multiple effects on gene expression in other systems. Thus either histone deacetylation is not involved, and both agents interfere with another inactivation process (e.g. chromatin condensation or DNA modification), or alternatively, DMSO and fatty acids affect different steps of a multi-step inactivation pathway.

    • Genomic instability in mammalian cell hybrids. IV. Is mutation frequency elevated in hybrid cells?

      Robert Center Jaclyn M. Watson Lynne Mckay Rosalia Bruzzese Jennifer A. Marshall Graves

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      In this study, we set out to determine whether the mutation frequency in cell hybrids is increased over the frequencies in the two parental lines, and whether this increase is related to the evolutionary divergence of the cell parents. Two test loci were chosen: forward mutation at the HPRT locus and mutation to resistance to the drug emetine. We conclude that while some cell combinations do seem to produce hybrids with higher mutation frequencies, this is not consistently so, and, indeed, mutation rates in hybrids may be higher, lower or very similar to rates in the parental lines. Further, evolutionary divergence between the parental lines does not appear to correlate to mutation frequency in the hybrids.

    • Weird mammals provide insights into the evolution of mammalian sex chromosomes and dosage compensation

      Jennifer A. Marshall Graves

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      The deep divergence of mammalian groups 166 and 190 million years ago (MYA) provide genetic variation to explore the evolution of DNA sequence, gene arrangement and regulation of gene expression in mammals. With encouragement from the founder of the field, Mary Lyon, techniques in cytogenetics and molecular biology were progressively adapted to characterize the sex chromosomes of kangaroos and other marsupials, platypus and echidna—and weird rodent species. Comparative gene mapping reveals the process of sex chromosome evolution from their inception 190 MYA (they are autosomal in platypus) to their inevitable end (the Y has disappeared in two rodent lineages). Our X and Y are relatively young, getting their start with the evolution of the sex-determining 𝑆𝑅𝑌 gene, which triggered progressive degradation of the Y chromosome. Even more recently, sex chromosomes of placental mammals fused with an autosomal region which now makes up most of the Y. Exploration of gene activity patterns over four decades showed that dosage compensation via X-chromosome inactivation is unique to therian mammals, and that this whole chromosome control process is different in marsupials and absent in monotremes and reptiles, and birds. These differences can be exploited to deduce how mammalian sex chromosomes and epigenetic silencing evolved.

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