Contextualising Apartheid at the End of Empire: Repression, ‘Development’ and the Bantustans

This article examines the global dynamics of late colonialism and how these informed South African apartheid. More specifically, it locates the programmes of mass relocation and bantustan ‘self-government’ that characterised apartheid after 1959 in relation to three key dimensions. Firstly, the article explores the global circulation of idioms of ‘development’ and trusteeship in the first half of the twentieth century and its significance in shaping segregationist policy; secondly, it situates bantustan ‘selfgovernment’ in relation to the history of decolonisation and the partitions and federations that emerged as late colonial solutions; and, thirdly, it locates the tightening of rural village planning in the bantustans after 1960 in relation to the elaboration of anti-colonial liberation struggles, repressive southern African settler politics and the Cold War. It argues that, far from developing policies that were at odds with the global ‘wind of change’, South African apartheid during the 1960s and 1970s reflected much that was characteristic about late colonial strategy

Bcl-3 and NF kappa B p50-p50 homodimers act as transcriptional repressors in tolerant CD4(+) T cells

The transcriptional events that control T cell tolerance are still poorly understood. To investigate why tolerant T cells fail to produce interleukin (IL)-2, we analyzed the regulation of NFkappaB-mediated transcription in CD4(+) T cells after tolerance induction in vivo. We demonstrate that a predominance of p50-p50 homodimers binding to the IL-2 promoter kappaB site in tolerant T cells correlated with repression of NFkappaB-driven transcription. Impaired translocation of the p65 subunit in tolerant T cells was a result from reduced activation of IkappaB kinase and poor phosphorylation and degradation of cytosolic IkappaBs. Moreover, tolerant T cells expressed high amounts of the p50 protein. However, the increased expression of p50 could not be explained by activation-induced de novo synthesis of the precursor p105, which was constitutively expressed in tolerant T cells. We also demonstrate the exclusive induction of the IkappaB protein B cell lymphoma 3 (Bcl-3) in tolerant T cells as well as its specific binding to the NFkappaB site. These results suggest that the cellular ratio of NFkappaB dimers, and thus the repression of NFkappaB activity and IL-2 production, are regulated at several levels in tolerant CD4(+) T cells in vivo