ABSTRACT
Flowering is one of the most important progresses for most plants during the transition from vegetative growth to reproductive growth. There are many factors that affect the flowering, including two main external factors, light and temperature, and the internal factors such as gibberellin acid (GA) and autonomous elements. At present, the late-flowering mutants are fallen into four pathways: photoperiod pathway, vernalization pathway, autonomous pathway and GA pathway according to factors described above. Through several floral integrators, such as SOC1, FT and LFY, the multiple flowering regulatory pathways control the flowering finely under the variable environmental condition and physiological condition.
ABSTRACT
Plant programmed cell death (PCD) plays an important role in plant growth and development as well as defensive response against biotic and abiotic stresses. Fumonisin B1 (FB1) is a fungi toxin, which is a competitive inhibitor of ceramide synthase in de novo sphingolipid biosynthesis. FB1 can induce PCD in both animal and plant cells. To dissect this pathway, a genetic screen for fumonisin B1 resistant (fbr) mutants, and identified 11 fbr mutants was carried out. Genetic analysis showed that these 11 mutants belonged to 9 complementary groups or genetic loci. Here a detailed phenotypic analysis of fbr136 was reported. In addition to the resistance to FB1, fbr136 also showed resistance other PCD-inducing compounds, including H2O2 and paraquat. Furthermore, FB1-induced PR1 expression was reduced in fbr136, suggesting that a PCD pathway is likely impaired in the mutant. When stained with nitroblue tetrazolium (NBT), fbr136 showed a reduced accumulation of reactive oxygen species (ROS) induced by FB1. The fbr136 mutation was roughly mapped onto chromosome Ⅲ, where no other fbr mutants have been previously identified. It is proposed that FBR136 may act as an important regulator in a sphingolipid-mediated PCD pathway, involved in the generation of ROS.