A Study in the Theology of Christian Social Action

In this paper I have attempted to present a summary of my exposition of the theology of Rauschenbusch and Niebuhr, and of my own understanding of the issues of Christian Social Action. I have tried to reproduce in this short space the thought of these men, in a manner which should make it comprehensible and which should relate it to the larger questions of social action. This year’s work as a Senior Scholar has proved invaluable because of the discipline of self-directed study which the work taught, and because of myriad possibilities of future investigation which it has suggested. I hope that someday this present manuscript may be expanded into something more substantial. The personal value of such a project, in my opinion, must be measured by the contribution which the project makes to the individual’s general experience, and not merely by the written work which is produced. Therefore, although this manuscript is rather brief, it represents a great deal of value which I feel that I can measure only by my own experience.

The role of TaABF1 in abscisic acid-mediated suppression of -amylase gene expression in cereal grains

The phytohormones gibberellin (GA) and abscisic acid (ABA) regulate important developments events in germinating seeds. Specifically, GA induces the expression of hyrolase genes, like the α-amylase gene Amy32b, which mobilizes starch reserves to be used by the embryo, and ABA suppresses this induction. Recent advancements identified ABA and GA receptors and key components in the signaling pathways, however, the mechanism of crosstalk between the hormones remains largely unknown. To further elucidate the mechanism of ABA suppression of GA-induced genes, we focused on the transcription factor TaABF1, a member of the ABA response element binding factor family. TaABF1 has been shown to physically interact with the SnRK2 kinase PKABA1 and overexpression of TaABF1 or PKABA1 can suppress Amy32b. We carried out particle bombardment experiments to investigate how TaABF1 suppresses Amy32b and how TaABF1 is activated by ABA. The role of TaABF1 in ABA-mediated suppression of Amy32b is more complicated than hypothesized. Unlike PKABA1, overexpression of TaABF1 did not cause a decrease of GAMyb expression and in fact resulted in an increase of GAMyb expression. When TaABF1 and GAMyb were simultaneously overexpressed in aleurone, the GAMyb induction of Amy32b was unaffected, indicating that the target of TaABF1 action must be upstream of GAMyb. Furthermore, TaABF1 and ABA demonstrated an additive effect on the suppression of Amy32b. Based on our findings, we propose a model in which PKABA1 activates two separate targets, one being TaABF1 which then modifies an unknown target upstream of GAMyb and the other being an unknown transcription factor that suppresses GAMyb transcription.