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Distribution of genetic diversity among disjunct populations of the rare forest understory herb, Trillium reliquum.

We assessed genetic diversity and its distribution in the rare southeastern US forest understory species, Trillium reliquum. In all, 21 loci were polymorphic (PS=95.5%) and the mean number of alleles per polymorphic locus was 3.05. However, genetic diversity was relatively low (Hes=0.120) considering the level of polymorphism observed for this outcrossing species. A relatively high portion of the genetic diversity (29.7%) was distributed among populations. There was no relationship between population size and genetic diversity, and we did not detect significant inbreeding. These results are best explained by the apparent self-incompatibility of this species, its longevity and clonal reproduction. To address questions regarding the history of T. reliquum's rarity, we compared results for T. reliquum with that of its more common and partially sympatric congener, T. cuneatum. Despite shared life history traits and history of land use, we observed significant genetic differences between the two species. Although T. cuneatum contains slightly lower polymorphism (Ps=85%), we detected significantly higher genetic diversity (Hes=0.217); most of its genetic diversity is contained within its populations (GST=0.092). Our results suggest that not only is there little gene flow among extant T. reliquum populations, but that rarity and population isolation in this species is of ancient origins, rather than due to more recent anthropogenic fragmentation following European colonization. The Chattahoochee River was identified as a major barrier to gene exchange.

Cluster Analysis↗

The Drosophila UBC9 homologue lesswright mediates the disjunction of homologues in meiosis I.

BACKGROUND: In Saccharomyces cerevisiae and other organisms, the UBC9 (ubiquitin-conjugating 9) protein modifies the function of many different target proteins through covalent attachment of the ubiquitin-like protein SMT-3/SUMO. RESULTS: Using a second-site suppression screen of a mutation in the nod locus with a variable meiotic phenotype, we have identified mutations in the Drosophila melanogaster UBC9 homologue, encoded by the gene lesswright (lwr). lwr mutations dominantly suppress the nondisjunction and cytological defects of female meiotic mutations that affect spindle formation. The lwr lethal phenotype is rescued by a Drosophila UBC9/lwr transgene. CONCLUSIONS: We suggest that LWR mediates the dissociation of heterochromatic regions of homologues at the end of meiotic prophase I. Our model proposes that when there is less LWR protein, homologues remain together longer, allowing for more normal spindle formation in mutant backgrounds and therefore more accurate meiotic chromosome segregation.

Alleles↗

Minding the gap: some theory-practice disjunctions in nursing education research.

Nursing and nurse education are currently experiencing 'turbulence' as a result of the rapid, unpredictable and often divergent forces in the macro- and micro-institutional settings. Research-based knowledge seeks to 'smooth-over' this 'turbulence', which the literature cites as 'gaps' between the rhetorical ideals and practical realities. This paper deconstructs three influential ENB-sponsored research projects. It is argued that these research reports introduce forms of 'Utopianism', reinserting theory-practice gaps they sought to close down. Finally, as a result of the idealism revealed by the deconstruction, five key issues for future development in nursing research are discussed. These issues are of significance to educationalists since educational policy and practice in nursing are often developed from research findings.

Clinical Competence↗

Meiotic disjunction of circular minichromosomes in yeast does not require DNA homology.

Circular plasmids containing an autonomously replicating sequence (ARS) and a centromeric DNA sequence (CEN) segregate as independent linkage groups during meiosis in Saccharomyces cerevisiae. If two genetically marked plasmids are present in the same diploid cell, their segregation during meiosis may be determined relative to each other. It has been observed that for centromere plasmids containing some DNA sequences in common, these plasmids tend to segregate away from each other at the first meiotic division [Clarke, L. & Carbon, J. (1980) Nature (London) 287, 504-509; Clarke, L., Fitzgerald-Hayes, M., Buhler, J.-M. & Carbon, J. (1981) Stadler Genet. Symp. 13, 9-23]. Here we show that nonhomologous plasmids, having no detectable DNA sequence cross-hybridization, also tend to disjoin from each other at the first meiotic division. Therefore, this nonrandom segregation to opposite poles can occur by mechanisms that do not involve DNA sequence homology. This process may be an active nonhomologous pairing system or it may reflect unknown physical restraints on the meiotic segregation of the two plasmids. In either case, this process cannot be used as a possible assay for homologous meiotic pairing.

Centromere↗

Spo12 is a limiting factor that interacts with the cell cycle protein kinases Dbf2 and Dbf20, which are involved in mitotic chromatid disjunction.

The DBF2 and DBF20 genes of the budding yeast Saccharomyces cerevisiae encode a pair of structurally similar protein kinases. Although yeast with either gene deleted is viable, deletion of both genes is lethal. Thus, the Dbf2 and Dbf20 proteins are functional alternatives for an essential activity. In contrast to deletions, four different mutant alleles of DBF2 are lethal. Thus, the presence of a nonfunctional Dbf2 protein, rather than the lack of function per se, is inhibitory. Here we present genetic evidence that nonfunctional mutant Dbf2 protein blocks the function of Dbf20 protein by sequestering a common interacting protein encoded by SPO12. Even a single extra copy of SPO12 is sufficient to suppress the dbf2 defect. Since SPO12 appears to encode a limiting factor, it may be a rate limiting cofactor that is involved in the regulation of the Dbf2 and Dbf20 protein kinases. A corollary to the finding that one extra copy of SPO12 can suppress dbf2, is that the acquisition of an extra chromosome VIII, which carries the SPO12 locus, will also suppress dbf2. Indeed, physical analysis of chromosome copy number in dbf2 revertants able to grow at 37 degrees showed that the frequency of chromosome VIII acquisition increased when cells were incubated at the restrictive temperature, and reached a frequency of more than 100-fold the amount in wild-type yeast. This suggested that the dbf2 mutation was not only suppressed by an extra copy of chromosome VIII but also that the dbf2 mutation actually caused aberrant chromosomal segregation. Conventional assays for chromosome loss confirmed this proposal.

Cell Cycle↗