B-cell non-Hodgkin's lymphoma cell line (Karpas 1106) with complex translocation involving 18q21.3 but lacking BCL2 rearrangement and expression.

A B-cell non-Hodgkin's lymphoma (B-NHL) cell line (Karpas 1106) with an unusual three-way translocation involving 18q21.3 has been derived from a patient with mediastinal lymphoblastic B-NHL. Although conventional cytogenetics showed a derivative 18q-identical to that seen in cases with t(14;18)(q32.3;q21.3), no translocations of either chromosome 14 could be detected. Instead fluorescent in situ hybridization analysis using a chromosome-18 paint showed that the segment 18q21.3-18qter had become sandwiched on a derivative chromosome X between segments Xqter-c-Xq28 and 13q12-qter, with the centrometric site of 18q21.3 subband juxtaposed to the X sequences. Pulsed-field DNA blots failed to detect rearrangement of the BCL2 gene. Conventional DNA blots using a variety of restriction digests and both 5' and 3' BCL2 and FVT 1 probes also failed to detect rearrangement in Karpas 1106. A rearranged fragment seen only in HindIII digests with 5' BLC2 probes may represent a local microalteration, which is either a mutation or small deletion involving the HindIII site as seen in other cases of B-NHL. Neither BCL2 RNA nor BCL2 protein expression were detected. These and other data suggest that genes at 18q21.3, other than BCL2 and FVT1, may be targets for translocation in certain subgroups of B-NHL.

In vitro transforming capacities of mouse c-jun:junD chimeric genes.

Among the murine Jun family of transcription factors, c-Jun and JunD are closely-related proteins with similar dimerization, DNA binding and transactivating properties. However, when expressed from a self-replicating retroviral RCAS vector, c-jun, but not junD, transforms chick embryo fibroblasts. We attempted to map the regions of c-jun which are important for transformation by constructing hybrids between c-jun and junD. Using common restriction sites, we prepared six different chimeric molecules. All of these c-jun:junD hybrids code for transactivators of AP1-containing promoters. An N-terminal segment of 79 amino acids of c-Jun converts JunD into a strong transforming protein, while other segments of c-Jun contribute to a lesser extent. Contrary to what has been reported with rat embryo fibroblasts, a c-Jun derivative with serines substituted by alanines in positions 63 and 73 still transforms CEFs efficiently.

Evidence for common epitopes among proteins of the membrane skeleton of a ciliate, an euglenoid and a dinoflagellate.

The cytoskeleton of many protists comprises an extensive submembranous epiplasm which contributes to cell shape and integration of cell membranes with underlying structures according to the species-specific cortical architecture. Using various extraction procedures, epiplasm-enriched fractions have been isolated from the ciliate Pseudomicrothorax dubius, the euglenoid Euglena acus and the dinoflagellate Noctiluca scintillans. Comparative gel electrophoretic analysis of such preparations reveals heterogeneity of protein composition, the major polypeptides differing in size. Antibodies raised against epiplasmic proteins from these three organisms have permitted the confirmation of submembranous localization of the antigens by immunoelectron microscopy. Heterologous reactions performed by means of combined immunocytochemical and immunoblotting procedures indicate the existence of common epitopes among major proteins making up the bulk of the epiplasm of the three species examined. These findings suggest that proteins of the epiplasm have significantly diverged during evolution while conserving structural domains essential for their cytoskeletal function. It is postulated that these common domains may underly the ability of epiplasmic proteins to assemble into an ordered spatial organization, typical of the highly differentiated cortex of unicellular micro-organisms.

Concanavalin A induces germinal vesicle breakdown in Barnea candida (Mollusca, Pelecypoda) oocytes.

Treatment of Barnea candida oocytes with 5 micrograms/ml Con A or above elicits germinal vesicle breakdown (GVBD), the timing for this event being dose dependent. At 100 micrograms/ml, GVBD occurs within 20 to 30 min, a lag time corresponding to that observed after fertilization. Con A-induced GVBD requires the presence of 2 mM external calcium during all the treatment period while at 10 mM external Ca2+, the calcium-dependent period is slightly reduced. It is sensitive to low pH Na-acetate sea water, 50 microM trifluoperazine, 20 microM D-600 or 2,4-dinitrophenol, as well as to 10 micrograms/ml cytochalasin B. A straightforward interpretation of these data would be that Con A-induced maturation is sustained by an energy-requiring effector mechanism involving intracellular contractile proteins.