No description available.

Human cutaneous malignant melanoma progresses through well-defined stages, culminating in metastatic melanoma. The underlying genetic changes have not be n identified. The aim of this work was to identify activated transforming genes in human melanoma samples. Transfection assays have been used to identify potential transforming genes in melanoma samples, and transmissable transforming activity was demonstrated in several cases. A secondary transfectant obtained following transfection of DNA from the cell line NKI4 retained a single human repeat sequence-containing EcoRI fragment of approximately 16 kb. This fragment was molecularly cloned and analysis revealed the presence of human sequences corresponding to a novel human gene, which was designated MEL. Homologous sequences were also present in mouse DNA. The MEL gene was expressed in human melanoma cell lines and NIH 3T3 mouse fibroblasts, and cDNA clones were isolated from a normal human fibroblast cDNA library. The human MEL gene was localised to a region of chromosome 19 (p13. 2) implicated in some human malignancies. However the clone isolated from the secondary transfectant lacked transforming activity, and was not retained in either tertiary transformants or additional primary transformants. A related sequence was isolated from the cell line NKI4, which was capable of transforming NIH 3T3 cells. This sequence also detected a restriction fragment length polymorphism in human melanoma cell lines. To conclusively identify the transforming gene in NKI4, transfectant DNA was "tagged" with a selectable marker, G418 resistance (neo). The sequences adjacent to the "tag" on one side were cloned and analysed, from which it was deduced that the transforming gene must lie on the other side of the "tag". Melanoma cell lines and tumour biopsies were analysed for the presence of activated RAS genes, using a combination of biological (transfection) and biochemical (restriction enzyme polymorphisms, PCR and sequence specific oligonucleotide hybridisation) assays. Mutations were detected in all three RAS genes (K12, H12, N61), at all stages of melanoma development, including benign naevi.

No description available.

Polyploidy is widely acknowledged as a widespread mechanism in the evolution and speciation of the majority of flowering plants. Allopolyploid forms through interspecific hybridization and whole genome duplication. While allopolyploids may display increased vigor relative to their progenitors, they can also face challenges to fertility following hybridization. Genetic changes in allopolyploids result from recombination between the hybridized subgenomes, which can influence phenotype and ultimately determine fitness of future generations. To study dynamic changes that follow allopolyploid formation, Brassica napus lineages were derived by hybridizing Brassica oleracea and Brassica rapa. Two lineages of B. napus were analyzed for genetic and phenotypic changes in the S2, S7, and S12 generations. Although these lineages were genetically identical at the time of hybridization, divergence was apparent by the S2 generation. There was a significant increase in sequence loss across generations within both lineages. Four of six generations from both lineages displayed no significant differences to each other in sequence loss relative to the parental generation. In both lineages, there was a bias towards losing sequences from the B. olereacea subgenome. Some individual plants showed novel phenotypes; however, there was no correlation between the examined genetic changes and selected phenotypes.