Genetic studies of photoreceptor signal transduction in Arabidopsis.

摘要

Photoperiodic flowering in plants is regulated by photosensory receptors including the red/far-red light receptors phytochromes and the blue/UV-A light receptors cryptochromes. In this thesis describe a molecular genetic characterization of the functions and the genetic interactions among the Arabidopsis cry1, cry2, phyA, and phyB photoreceptors in the regulation of flowering time. The function of cryptochromes in floral induction was investigated, showing that in addition to the phyB-dependent function, cry2 also acts redundantly with cry1 to promote floral initiation in a phyB-independent manner. A photoperiod-dependent diurnal rhythm of protein abundance of the cry2 and phyA photoreceptors was found, suggesting a mechanism for direct daylength perception in Arabidopsis. Genetic analyses of Arabidopsis photoreceptor mutants demonstrated the specific roles of individual photoreceptors, including cry2, phyA, and phyB, and functional interactions of different photoreceptors in the control of floral initiation. Together with the discovery of a light spectrum-specific photoperiodic sensitivity of Arabidopsis, and previous studies of the photoperiod-dependent circadian rhythmic expression of flowering-time genes, these results suggest a molecular explanation of how photoreceptors regulate photoperiodic flowering in Arabidopsis.; An integrated bioinformatics-driven whole-genome approach was developed and implemented to identify candidate genes encoding Arabidopsis photoreceptor signal transduction proteins from three well-established classes of signaling proteins—transcription factors, protein kinases and phosphatases. T-DNA insertion mutations were identified for several hundred of these candidate genes, and analyses of these mutants identified several novel putative Arabidopsis photoreceptor signaling mutations that affect hypocotyl elongation, chloroplast development, and photoperiodic flowering.; The t&barbelow;all in &barbelow;far-r&barbelow;ed 1 (tfr1) gain-of-function mutation of Arabidopsis disrupts phyA-mediated inhibition of hypocotyl elongation in FR, the phyA-mediated promotion of flowering by FR, and circadian regulation of seedling leaf movements. TFR1 encodes a casein kinase I-like serine/threonine protein kinase that is homologous to the Drosophila double-time (DBT) and mammalian TAU/casein kinase I epsilon proteins that function as circadian clock components in animals. In wild-type plants the TFR1 transcript's of very low abundance and shows multiple splicing anomalies.