ABSTRACT
The cloned breakpoint at 11q13.3 of the t(11;14)(q13.3;q32.3) in a B-cell lymphocytic leukemia (B-CLL) was used to analyze DNA from individuals with and without the rare folate-sensitive fragile site at 11q13.3. On Southern blots there were no discernible differences. Subclones of the ends of the leukemia breakpoint clone were prepared and used for in situ hybridization to chromosomes expressing fra(11)(q13.3). Both subclones hybridized distal to the fragile site. These experiments indicate that the breakpoints at 11q13.3 in B-CLL (and in a B-cell lymphoma) are not at the fragile site at 11q13.3.
Subject(s)
Chromosome Fragility , Chromosomes, Human, Pair 11 , Chromosomes, Human, Pair 14 , Leukemia, Lymphoid/genetics , Translocation, Genetic , B-Lymphocytes , Chromosome Banding , Chromosome Fragile Sites , DNA Restriction Enzymes , Genetic Markers , Humans , Karyotyping , Nucleic Acid HybridizationABSTRACT
Mu DNA, isolated from infected cells or minicells, has been shown to be held by proteins in twisted and open circular forms. Circularization does not require protein synthesis in the infected cells. A 64,000-dalton polypeptide is injected into the infected cell with Mu DNA and co-sediments with Mu DNA through sucrose gradients. Circularization of the infecting Mu DNA does not require removal of the Escherichia coli DNA sequences which are attached to both ends of the Mu genome in the viral particle.
