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In yeast and other eukaryotes, the histone methyltransferase Set1 mediates methylation of lysine 4 on histone H3 (H3K4me). This modification marks the 5′ end of transcribed genes in a 5′-to-3′ tri- to di- to monomethyl gradient and promotes association of chromatin-remodeling and histone-modifying enzymes. Here we show that Ctk1, the serine 2 C-terminal domain (CTD) kinase for RNA polymerase II (RNAP II), regulates H3K4 methylation. We found that CTK1 deletion nearly abolished H3K4 monomethylation yet caused a significant increase in H3K4 di- and trimethylation. Both in individual genes and genome-wide, loss of CTK1 disrupted the H3K4 methylation patterns normally observed. H3K4me2 and H3K4me3 spread 3′ into the bodies of genes, while H3K4 monomethylation was diminished. These effects were dependent on the catalytic activity of Ctk1 but are independent of Set2-mediated H3K36 methylation. Furthermore, these effects are not due to spurious transcription initiation in the bodies of genes, to changes in RNAP II occupancy, to changes in serine 5 CTD phosphorylation patterns, or to "transcriptional stress." These data show that Ctk1 acts to restrict the spread of H3K4 methylation through a mechanism that is independent of a general transcription defect. The evidence presented suggests that Ctk1 controls the maintenance of suppressive chromatin in the coding regions of genes by both promoting H3K36 methylation, which leads to histone deacetylation, and preventing the 3′ spread of H3K4 trimethylation, a mark associated with transcriptional initiation. [ABSTRACT FROM AUTHOR]

Whilst the international community's focus has been on the region most devastated by HIV/ AIDS, namely sub-Saharan Africa, India now appears on the brink of a significant AIDS epidemic. In thinking about the implications of HIV/AIDS, considerable attention was initially drawn to its clinical aspects. More recently, other dimensions of HIV, including economic, have been explored. The primary objective of this review is to elaborate on the major elements of the national and international economic research to data on HIV/AIDS, and to infer lessons from it, for India. It also examines the evidence on the aggregate and household-level economic impacts of HIV, the economic roots that drive its transmission and the methods economists use to assess the efficacy of alternative interventions to address HIV and AIDS. Available evidence suggests that whereas aggregate impacts may be limited, the adverse household-level economic implications of AIDS may be serious; public resources that are available for health are also likely to be put under strain. Paucity of economic research on HIV and AIDS relating to India is highlighted.