A Pollen Chase Experiment; Examining Varying Levels of Embryonic Inbreeding Depression

A pollen chase experiment was performed upon three Costa Rican populations of Witheringia solanacea to examine the breakdown of genetically enforced self incompatibility (SI) and the extent of embryonic inbreeding depression. Self-pollen was applied in the bud, with outcross pollen applied one day later, and outcross pollinations at both intervals as a control. A variety of responses were found among the populations. BOHS readily accepted self pollen and suffered from very low inbreeding depression. Monteverde and Las Cruces both have lower fruit set with self-pollination precedence indicating that bud pollinations can overcome the self-incompatibility response and that embryonic death due to inbreeding depression causes fruit failure. The treatment:control fruit set is higher for the Las Cruces plants indicating stronger SI response Self-precedence seeds from the Las Cruces plants are likely to be outcrossed. Self-precedence seeds from Monteverde are likely selfed.

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.