Flowering Responses to Altered Expression of Phytochrome in Mutants and Transgenic Lines of Arabidopsis thaliana (L.) Heynh

Abstract

l h e long-day plant Arabidopsis tbaliana (L.) Heynh. flowers early in response to brief end-of-day (EOD) exposures to far-red light (FR) following a fluorescent short day of 8 h. FR promotion of flowering was nullified by subsequent brief red light (R) EOD exposure, indicating phytochrome involvement. The EOD response to R or FR is a robust measure of phytochrome action. Along with their wild-type (WT) parents, mutants deficient in either phytochrome A or B responded similarly to the EOD treatments. Thus, neither phytochrome A nor B exclusively regulated flowering, although phytochrome B controlled hypocotyl elongation. Perhaps a third phytochrome species is important for the EOD responses of the mutants and/or their flowering is regulated by the amount of the FR-absorbing form of phytochrome, irrespective of the phytochrome species. Overexpression of phytochrome A or phytochrome B resulted in differing photoperiod and EOD responses among the genotypes. The day-neutra1 overexpressor of phytochrome A had an EOD response similar to all of the mutants and WTs, whereas R EOD exposure promoted flowering i n the overexpressor of phytochrome B and FR EOD exposure inhibited this promotion. The comparisons between relative flowering times and leaf numbers at flowering of the overexpressors and their WTs were not consistent across photoperiods and light treatments, although both phytochromes A and B contributed to regulating flowering of the transgenic plants.

Phytochrome RNAi enhances major fibre quality and agronomic traits of the cotton Gossypium hirsutum L

“…The multiple-fold overexpression of cotton PHYE (as well as PHYB in line T 3 -1_7) in PHYA1 RNAi plants might result in increased yield potential, as has been seen in tobacco 15 and potato 16 since PHYE is most closely related to PHYB, both functionally and phylogenetically [1][2][3] . This hypothesis is supported by the observation that both the potato PHYB-overexpressing lines 16 and our cotton PHYA1 RNAi suppression lines showed markedly increased anthocyanin production, particularly close to the time of senescence.…”

“…Phytochrome genes play key regulatory roles in a wide range of plant developmental processes [1][2][3] . As such, the manipulation of phytochrome gene function has long been considered as a promising avenue for the modification of economically important traits in crops 13,14 .…”

“…It affects virtually all aspects of plant growth, from seed germination to vegetative morphology, floral initiation, control of circadian rhythms, regulation of gene expression, gravitropism and phototropism [1][2][3] . Plants respond to light through several photoreceptor systems.…”

Fluence and Wavelength Requirements for Arabidopsis CAB Gene Induction by Different Phytochromes

“…For instance, far-red induction of the homeotic gene Athb-2 is mediated mainly by phytochrome(s) other than PhyA and PhyB (Carabelli et al, 1996). Bagnall et al (1995) suggested the possibility of the involvement of phytochrome(s) other than PhyA and PhyB in the end-of-day far-red response of flowering. It was also reported that the phyA/pkyB double mutant displays an inhibition of petiole elongation accompanied by elongated internodes and an early-flowering response to end-of-day far-red treatment.…”

Floral transition mutants in Arabidopsis

“…The involvement of phytochrome in flowering of Arabidopsis was derived from studies using different R/FR ratios during development (Halliday, Koornneef & Whitelam 1994;Johnson et al 1994), end of day red (EOD R) and far-red (EOD FR) treatments (Bagnall et al 1995), daylength extension with low fluences of FR and R (Bagnall et al 1995), phytochromedeficient mutants (Goto et al 1991;Johnson et al 1994;Reed et at. 1994) and transgenic plants overexpressing phytoehrome proteins (Bagnall et al 1995). From these studies it appears that the low fluenee rate FR-enriehed promotive daylength extension effeet is eaused by phytochrome A (phyA), since phyA mutants do not respond to this treatment (Johnson et al 1994).…”