In the face of pressure from transnational social groups and increasingly influential human rights organizations the international community has quietly introduced provisions into four global human rights treaties that challenge the received wisdom in international relations. These individual petition mechanisms allow citizens to file complaints of human rights violations against their governments before global tribunals. International relations scholarship suggests that governments should be unlikely to ratify such provisions and accept UN oversight of their domestic human rights policies. Why do states ratify these mechanisms, particularly when ratification of the accompanying treaties does not require ratification of the individual petition Mechanism (IPM)? This work provides a quantitative analysis of ratification of individual petition mechanisms in the four global institutions that possess them and a qualitative analysis of ratification in two geographic regions. I argue that autocrats and democrats use ratification of individual petition mechanisms as a signaling device to attract aid. After regional political crises have ravaged their domestic economies I argue that state leaders will be more inclined to seek out ways to attract aid from western donors. Regional political crises intensify the need for aid and help to explain the timing of ratification. I find support for the link between regional political crises and ratification in the Racial Discrimination and Women's Discrimination Conventions in Chapter 2. Chapter 3 demonstrates that Slovak Prime Minister Meciar and Czech Prime Minister Zeman ratified Article 14 in the Racial Discrimination Convention to signal for aid. In Chapter 4 I demonstrate that autocratic leaders in Kyrgyzstan and Tajikistan accepted the oversight of the Human Rights Committee by ratifying the Optional Protocol to the ICCPR to signal for aid. In the short term leaders ratify IPM's insincerely and then clamp down particularly hard on their citizens' civil rights. However, in the long term, regional human rights groups latch onto the decisions of UN oversight committees and pressure governments, even the most entrenched autocrats, to make significant changes to their domestic human rights practices

The process of plant cell wall biosynthesis involves a complex series of biochemical processes involving many hundreds of proteins. Determining the function of a specific gene through functional genomics techniques have proved problematic due to genetic redundancies and undetectable changes. Common techniques have used mutant collections in forward genetic screens or reverse genetics to directly target and disrupt genes of interest. Since such techniques are heavily reliant on some phenotypic discrimination to asses gene function, the absence of a measureable difference often results in little useful information. Furthermore the complete absence of many genes produced by such techniques results in a lethal phenotype as the gene is absolutely required for normal function of the plant. A more subtle approach utilizes genetic differences in naturally occurring variants to provide important information about gene function and genetic diversity. In collaboration with the Joint Genome Institute we have sequenced two Arabidopsis accessions (Bay-0 and Sha-0) that have previously been shown to have measureable differences in Ara-Rha ratios in cell wall extracts. This genetic information and the utilization of recombinant inbred lines (RIL?s) will be used to map QTL?s identified in these and other Arabidopsis accessions to identify loci that contribute to functional differences in plant cell walls.

Genetic variation in different accessions of Arabidopsis thaliana has occurred through thousands of years of geographic spread and adaptation. As a result of this diversity, disparate accessions have phenotypic differences that can be used to identify genes that contribute to the biosynthesis and composition of cell walls. Forward and reverse genetic screens to identify single mutants often prove difficult for detection of genetic differences that may lead to more subtle phenotypes. Exploiting the inherent genetic variation in Arabidopsis accessions through quantitative trait analysis will allow for the detection of variation in cell wall biosynthesis and composition. We selected two methods for screening parental accessions: measuring monosaccharide composition by HPAEC and structural changes by Near Infrared (NIR) spectroscopy. From these analyses, we selected Ri-0 as the most different accession from the reference accession Col-0. Recombinant inbred lines (RILs) derived from Col-0 and Ri-0 parents were used to determine quantitative trait loci (QTL) that contribute to the differences observed in monosaccharide and pectin content and NIR spectroscopy. Two putative candidate genes encoding enzymes involved in nucleotide sugar conversion have been identified. We are currently determining differences between the parental versions of the genes and how any differences contribute to the observed phenotypes. Additionally, we have re-sequenced two Arabidopsis accessions, Bay-0 and Shahdara, in collaboration with the Joint Genome Institute. This effort has resulted in a collection of SNPs between these accessions and the reference Arabidopsis accession, Col-0. Re-seqeuencing efforts are being expanded to other accessions, beginning with Ri-0. Information obtained from resequencing will aid in QTL analysis and be of service to the general Arabidopsis community.

According to current dogma, there is little or no ongoing neurogenesis in the fully developed adult enteric nervous system. This lack of neurogenesis leaves unanswered the question of how enteric neuronal populations are maintained in adult guts, given previous reports of ongoing neuronal death. Here, we confirm that despite ongoing neuronal cell loss because of apoptosis in the myenteric ganglia of the adult small intestine, total myenteric neuronal numbers remain constant. This observed neuronal homeostasis is maintained by new neurons formed in vivo from dividing precursor cells that are located within myenteric ganglia and express both Nestin and p75NTR, but not the pan-glial marker Sox10. Mutation of the phosphatase and tensin homolog gene in this pool of adult precursors leads to an increase in enteric neuronal number, resulting in ganglioneuromatosis, modeling the corresponding disorder in humans. Taken together, our results show significant turnover and neurogenesis of adult enteric neurons and provide a paradigm for understanding the enteric nervous system in health and disease.