MODELING POTENTIAL TIGER HABITAT IN HUPINGSHAN-HOUHE ANDMANGSHAN-NANLING NATIONAL NATURE RESERVES, CHINA

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Modeling Potential Tiger Habitat in Hupingshan-Houhe and Mangshan-Nanling National Nature Reserves, China

After declining steadily for several decades, the South China tiger (Panthera tigris amoyensis) is now thought to be extinct in the wild. However, there is some hope of reintroduction, with Hupingshan-Houhe and Mangshan-Nanling National Nature Reserves in southern China seeming to hold the most promise. Our study used slope, elevation, vegetation, and landcover variables to construct a rough habitat suitability index for tigers in these two parks. According to our model, there are areas of suitable habitat within both parks. However, there are some important variables that we were unable to include in our model, such as human population density and prey availability. Considerable in-depth research will be necessary to evaluate the suitability of these locations before reintroduction is considered.

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.