Thomas G. Laffler

The PhysarumPhysarum Cell Cycle

Various aspects of the synchronous nuclear division cycle in Physarum polycephalum have been reviewed in detail recently (Holt, 1980; Tyson, 1982; Schedl et al., 1984b). In this chapter we shall concentrate on research published since 1982, particularly on reports discussed at the Workshop.

Thymidine-dependent growth of Physarum polycephalum amoebae treated with methotrexate in axenic culture

Abstract Low levels of methotrexate block the growth of Physarum amoebae in axenic culture. The block is readily reversed by adding thymidine to the medium.

Dissociation of Cellular and Humoral Immune Responsiveness to GAT

We have examined two aspects of cell-mediated Ir gene controlled responses to GAT in responder and nonresponder strains. First, levels of delayed-type hypersensitivity (DTH), T cell proliferative (Tprolf), and plaque-forming cell (PFC) responses in various mouse strains following subcutaneous immunization with GAT/CFA at the base of the tail were examined. Responders (H-2b,d,f) gave significant responses in all assays, while nonresponders were found to fall into two distinct response patterns. H-2q,s haplotype mice failed to respond to GAT in any assay system, while the B6.H-2 bm12 (bm12) mutant strain failed to show significant PFC or DTH responses, but responded at the same level as parental B6 (H-2b) in the Tprolf assay, suggesting that the site of the Ir defect in GAT nonresponders can lie at different points within the helper pathway. Secondly, we examined the help/suppression balance in GAT responders. IV injection of syngeneic GAT-coupled spleen cells (GAT-SC) into GAT responders led to the induction of antigen-specific tolerance of PFC, DTH, and Tprolf responses. Tolerant responder mice were found to contain antigen-specific Lyt 2+ suppressor T cells (Ts) which inhibited the induction of GAT-specific PFC and DTH, but not of Tprolf responses in recipient animals. A suppressor extract (TsF) prepared from these tolerant responders was found to inhibit the induction of primary GAT-specific PFC and DTH responses, but had no effect on either the induction or expression of GAT-specific Tprolf responses.