A dominant mutation in the pea PHYA gene confers enhanced responses to light and impairs the light-dependent degradation of phytochrome A.

Phytochrome A (phyA) is an important photoreceptor controlling many processes throughout the plant life cycle. It is unique within the phytochrome family for its ability to mediate photomorphogenic responses to continuous far-red light and for the strong photocontrol of its transcript level and protein stability. Here we describe a dominant mutant of garden pea (Pisum sativum) that displays dramatically enhanced responses to light, early photoperiod-independent flowering, and impaired photodestruction of phyA.

Brassinosteroid deficiency due to truncated steroid 5alpha-reductase causes dwarfism in the lk mutant of pea.

The endogenous brassinosteroids in the dwarf mutant lk of pea (Pisum sativum) were quantified by gas chromatography-selected ion monitoring. The levels of castasterone, 6-deoxocastasterone, and 6-deoxotyphasterol in lk shoots were reduced 4-, 70-, and 6-fold, respectively, compared with those of the wild type. The fact that the application of brassinolide restored the growth of the mutant indicated that the dwarf mutant lk is brassinosteroid deficient.

Uncoupling brassinosteroid levels and de-etiolation in pea.

The suggestion that brassinosteroids (BRs) have a negative regulatory role in de-etiolation is based largely on correlative evidence, which includes the de-etiolated phenotypes of, and increased expression of light-regulated genes in, dark-grown mutants defective in BR biosynthesis or response. However, we have obtained the first direct evidence which shows that endogenous BR levels in light-grown pea seedlings are increased, not decreased, in comparison with those grown in the dark. Similarly, we found no evidence of a decrease in castasterone (CS) levels in seedlings that were transferred from the dark to the light for 24 h.

Control of gibberellin levels and gene expression during de-etiolation in pea.

Gibberellin A(1) (GA(1)) levels drop significantly in wild-type pea (Pisum sativum) plants within 4 h of exposure to red, blue, or far-red light. This response is controlled by phytochrome A (phyA) (and not phyB) and a blue light receptor. GA(8) levels are increased in response to 4 h of red light, whereas the levels of GA(19), GA(20), and GA(29) do not vary substantially.

Molecular characterization of the brassinosteroid-deficient lkb mutant in pea.

The brassinosteriod-deficient lkb mutant of garden pea (Pisum sativum L.) is characterized by an erectoides phenotype (reduced internode length, thickened stems, epinastic leaves), which is rescued by application of exogenous brassinolide. We show that the LKB gene is the Arabidopsis DIMINUTO/DWARF-1 (DIM/DWF1) homologue of pea.

Interaction of phytochromes A and B in the control of de-etiolation and flowering in pea.

The interactions of phytochrome A (phyA) and phytochrome B (phyB) in the photocontrol of vegetative and reproductive development in pea have been investigated using null mutants for each phytochrome. White-light-grown phyA phyB double mutant plants show severely impaired de-etiolation both at the seedling stage and later in development, with a reduced rate of leaf production and swollen, twisted internodes, and enlarged cells in all stem tissues. PhyA and phyB act in a highly redundant manner to control de-etiolation under continuous, high-irradiance red light.

Evidence that auxin promotes gibberellin A1 biosynthesis in pea.

In shoots of the garden pea, the bioactive gibberellin (GA1) is synthesised from GA20, and the enzyme which catalyses this step (a GA 3-oxidase -- PsGA3ox1) is encoded by Mendel's LE gene. It has been reported previously that decapitation of the shoot (excision of the apical bud) dramatically reduces the conversion of [3H]GA20 to [3H]GA1 in stems, and here we show that endogenous GA1 and PsGA3ox1 transcript levels are similarly reduced. We show also that these effects of decapitation are completely reversed by application of the auxin indole-3-acetic acid (IAA) to the 'stump' of decapitated plants.

Characterization of the gene encoding the apoprotein of phytochrome B2 in tomato, and identification of molecular lesions in two mutant alleles.

The structure of the gene encoding the apoprotein of tomato phytochrome B2 (PHYB2) has been determined from genomic and cDNA sequences. The coding region is organized into four exons, like almost every other angiosperm phytochrome (phy). The deduced phyB2 apoprotein (PHYB2) consists of 1121 amino acids, with 82, 74 and 70% identity to tomato PHYB1, Arabidopsis PHYB, and Arabidopsis PHYD, respectively.

Molecular analysis of PHYA in wild-type and phytochrome A-deficient mutants of tomato.

Tomato (Lycopersicon esculentum Mill., recently redesignated Solanum lycopersicum L.), an agronomically important crop plant, has been adopted as a model species complementary to Arabidopsis in which to characterize the phytochrome family.

A Temporarily Red Light-Insensitive Mutant of Tomato Lacks a Light-Stable, B-Like Phytochrome.

We have selected four recessive mutants in tomato (Lycopersicon esculentum Mill.) that, under continuous red light (R), have long hypocotyls and small cotyledons compared to wild type (WT), a phenotype typical of phytochrome B (phyB) mutants of other species. These mutants, which are allelic, are only insensitive to R during the first 2 days upon transition from darkness to R, and therefore we propose the gene symbol tri (temporarily red light insensitive).

Far-red light-insensitive, phytochrome A-deficient mutants of tomato.

We have selected two recessive mutants of tomato with slightly longer hypocotyls than the wild type, one under low fluence rate (3 mumol/m2/s) red light (R) and the other under low fluence rate blue light. These two mutants were shown to be allelic and further analysis revealed that hypocotyl growth was totally insensitive to far-red light (FR). We propose the gene symbol fri (far-red light insensitive) for this locus and have mapped it on chromosome 10.