By Sebastian Fugmann
This ebook covers the present figuring out of the function of activation-induced cytidine deaminase (AID) within the iteration of antibody reaction to antigenic problem. because the discovery of relief, and the genetic demonstration of its position in somatic hypermutation and class-switch recombination of antibody genes, a lot has been discovered concerning the biochemistry of this enzyme. besides the fact that, a few key questions stay hotly contested, comparable to: how does this enzyme get to the antibody locus leaving the remainder of the genome intact, and why are DNA fix pathways which regularly fix deamination occasions co-opted into truly solving mutations into the genome? those questions, between others, may be addressed during this monograph from quite a few views. Being prime specialists of their respective fields, the individuals of this hugely valued name summarize present study within the box of reduction and placed forth hypotheses which will supply a platform for destiny experiments.
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Extra resources for DNA Deamination and the Immune System: AID in Health and Disease (Molecular Medicine and Medicinal Chemistry)
2008; Lamond and Spector, 2003). , 2008). One solution to the enigma of AID targeting could be that AID and Ig genes are coordinately sequestered to the same transcriptionally-permissive nuclear subcompartment to the exclusion of non-Ig genes. , 2009). , 2007), the splicing factor CTTNBL1 is concentrated there with its interaction partner AID to produce focused mutagenesis. The next iteration of AID studies is likely to be informative and exciting in equal measure. ). The authors have no competing financial interests.
They do not confer expression of a functional Igκ chain. Thus such transgenes do not interfere with B cell development, are not subject to selective forces during germinal center responses and are thought to solely act as reporters for SHM. , 1995). , 2004). Thus, the search for cis-acting targeting elements focused on the noncoding sequences within the Igκ locus. As transcription and SHM are intimately linked, the importance of two well-characterized transcriptional control elements for SHM was tested.
Mammalian S regions are uniquely rich with clusters of G nucleotides on the nontranscribed strand, and repetitive hotspot motifs for AID deamination, WGCW (W = A or T; Stavnezer and Amemiya, 2004). , 2007). R loops in S regions (Fig. , 2007). , 2004). , 2004). , 2009). However, a causal relationship between R-loops and RNAP II enrichment awaits direct experimental demonstration. , 1997). , 2001), strongly implicating promoter proximal transcription with inducing AID-dependent mutations. Based on these observations Peters and Storb postulated that a mutator (now known to be AID) associates with the transcription initiation apparatus, tracks with the transcription elongation complex and dissociates stochastically to produce mutations (Peters and Storb, 1996).