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. The mutant carries a single base substitution in the PHYA gene that is genetically inseparable from the mutant phenotype. This substitution is predicted to direct the replacement of a conserved Ala in an N-terminal region of PHYA that is highly divergent between phyA and other phytochromes. This result identifies a region of the phyA photoreceptor molecule that may play an important role in its fate after photoconversion.

Mutations in Aero1 promote the silver flecking (aeromaculata) commonly seen on wild‐type pea (Pisum sativum L.) leaves, resulting in a phenotype known as supaeromaculata. We show here the MIII/122 line carries a supaeromaculata mutation allelic to the type aero allele (aero1‐1). MIII/122 (aero1‐10) and aero1‐1 were also found to attain an adult leaf form, flower and undergo apical arrest earlier than their wild‐type progenitor, cv. Virtus and cv. Torsdag, respectively. Principal component analyses indicated that in both cases these characteristics co‐segregated with the supaeromaculata phenotype. These results suggest that Aero1 is associated with the timing of plant development. Plants carrying an aero1 mutation become fully adult and reproductively competent sooner than their wild‐type counterparts, suggesting Aero1 is required to delay these aspects of plant development. Thus, Aero1 represents a previously unrecognized heterochronic gene in the garden pea.

The bushy mutant of pea (Pisum sativum L.) is characterized by short, thin stems, very small leaves and profuse branching. The bushy phenotype is conferred by a dominant allele, termed bsh. Here we show that bushy plants contain lower levels of free indole‐3‐acetic acid (IAA) than wild‐type (WT) plants. On emergence from the growth medium, bushy seedlings do not immediately display the mutant phenotype, and the effect of bsh on IAA content is small. After 10–14 days, the bushy phenotype begins to develop, and while the IAA content rises in WT plants, it falls in the mutant. The resulting difference in IAA level between WT and mutant can be up to 12‐fold. Although there is a deficiency of free IAA in bushy plants, the total IAA content (including free and conjugated forms) was not reduced in comparison with the WT. Furthermore, in bushy plants, the level of the main IAA conjugate in pea, IAAsp, was not reduced to the same extent as that of IAA, and metabolism studies indicated that faster IAA deactivation might contribute to IAA deficiency in the mutant. Application of IAA to bushy plants did not result in a WT phenocopy. However, the short internodes and profuse branching of bushy plants is consistent with classical views on how IAA affects plant development.

Our studies on two branching mutants of pea (Pisum sativum L.) have identified a further Ramosus locus, Rms6, with two recessive or partially recessive mutant alleles: rms6-1 (type line S2-271) and rms6-2 (type line K586). Mutants rms6-1 and rms6-2 were derived from dwarf and tall cultivars, Solara and Torsdag, respectively. The rms6 mutants are characterized by increased branching from basal nodes. In contrast, mutants rms1 through rms5 have increased branching from both basal and aerial (upper stem) nodes. Buds at the cotyledonary node of wild-type (WT) plants remain dormant but in rms6 plants these buds were usually released from dormancy. Their growth was either subsequently inhibited, sometimes even prior to emergence above ground, or they grew into secondary stems. The mutant phenotype was strongest for rms6-1 on the dwarf background. Although rms6-2 had a weak single-mutant phenotype, the rms3-1 rms6-2 double mutant showed clear transgression and an additive branching phenotype, with a total lateral length almost 2-fold greater than rms3-1 and nearly 5-fold greater than rms6-2. Grafting studies between WT and rms6-1 plants demonstrated the primary action of Rms6 may be confined to the shoot. Young WT and rms6-1 shoots had similar auxin levels, and decapitated plants had a similar magnitude of response to applied auxin. Abscisic acid levels were elevated 2-fold at node 2 of young rms6-1 plants. The Rms6 locus mapped to the R to Gp segment of linkage group V (chromosome 3). The rms6 mutants will be useful for basic research and also have possible agronomical value.

SQUAMOSA and APETALA1 are floral meristem identity genes from snapdragon (Antirrhinum majus) and Arabidopsis, respectively. Here, we characterize the floral meristem identity mutation proliferating inflorescence meristem(pim) from pea (Pisum sativum) and show that it corresponds to a defect in the PEAM4 gene, a homolog of SQUAMOSA and APETALA1. ThePEAM4 coding region was deleted in thepim-1 allele, and this deletion cosegregated with thepim-1 mutant phenotype. The pim-2 allele carried a nucleotide substitution at a predicted 5′ splice site that resulted in mis-splicing of pim-2 mRNA. PCR products corresponding to unspliced and exon-skipped mRNA species were observed. The pim-1 and pim-2 mutations delayed floral meristem specification and altered floral morphology significantly but had no observable effect on vegetative development. These floral-specific mutant phenotypes and the restriction ofPIM gene expression to flowers contrast with other known floral meristem genes in pea that additionally affect vegetative development. The identification of PIM provides an opportunity to compare pathways to flowering in species with different inflorescence architectures.

The fifth increased branching ramosus (rms) mutant, rms5, from pea (Pisum sativum), is described here for phenotype and grafting responses with four other rms mutants. Xylem sap zeatin riboside concentration and shoot auxin levels in rms5 plants have also been compared with rms1 and wild type (WT). Rms1 and Rms5 appear to act closely at the biochemical or cellular level to control branching, because branching was inhibited in reciprocal epicotyl grafts between rms5 or rms1 and WT plants, but not inhibited in reciprocal grafts between rms5 and rms1 seedlings. The weakly transgressive or slightly additive phenotype of the rms1 rms5 double mutant provides further evidence for this interaction. Like rms1, rms5 rootstocks have reduced xylem sap cytokinin concentrations, and rms5 shoots do not appear deficient in indole-3-acetic acid or 4-chloroindole-3-acetic acid. Rms1 and Rms5 are similar in their interaction with other Rms genes. Reciprocal grafting studies with rms1, rms2, and rms5, together with the fact that root xylem sap cytokinin concentrations are reduced in rms1 and rms5 and elevated in rms2 plants, indicates that Rms1 and Rms5 may control a different pathway than that controlled by Rms2. Our studies indicate that Rms1 and Rms5 may regulate a novel graft-transmissible signal involved in the control of branching.

The veg1 (vegetative) mutant in pea (Pisum sativum L.) does not flower under any circumstances and gi (gigas) mutants remain vegetative under certain conditions. gi plants are deficient in production of floral stimulus, whereas veg1 plants lack a response to floral stimulus. During long days in particular, these non-flowering mutant plants eventually enter a stable compact phase characterised by a large reduction in internode length, small leaves and growth of lateral shoots from the upper-stem (aerial) nodes. The first-order laterals in turn produce second-order laterals and so on in a reiterative pattern. The apical bud is reduced in size but continues active growth. Endogenous hormone measurements and gibberellin application studies with gi-1, gi-2 and veg1 plants indicate that a reduction in gibberellin and perhaps indole-3-acetic acid level may account, at least partially, for the compact aerial shoot phenotype. In the gi-1 mutant, the compact phenotype is rescued by transfer from a 24- to an 8-h photoperiod. We propose that in plants where flowering is prevented by a lack of floral stimulus or an inability to respond, the large reduction in photoperiod gene activity during long days may lead to a reduction in apical sink strength that is manifest in an altered hormone profile and weak apical dominance.

The spontaneous, single‐gene dominant, pea (Pisum sativum L.) mutant bushy is characterised by short, thin stems, tiny leaves and a proliferation of basal lateral branches. We symbolised the dominant mutant allele bsh and the recessive wild‐type allele BSH. Some effects were very large, e.g. the reduction in internode length was around 10‐fold in pure mutant plants. The effect on branching was qualitative under our conditions as the wild‐type did not branch and the mutant branched extensively. Analysis of epidermal cells indicated the reduction in internode length arose principally from a reduction in cell length. The bushy mutation also altered root morphology with a reduction in the number and length of lateral roots. Time to first open flower was increased but node of flower initiation was not affected. In a few cases, bushy plants died before producing an open flower even though tiny abortive flower buds were produced in the upper leaf axils. In pure mutant plants, individual seed weight was reduced by 30%, number of seeds per pod was reduced 3‐fold, and seed number per plant was reduced 4‐fold. However, pod size was essentially normal for a given seed content, and the flowers were fertile and of normal structure. Grafting studies showed the primary action of the bushy mutation occurred in the shoot. In summary, the reduced cell and shoot elongation, loss of apical dominance and a primary action in the shoot, all point toward auxin deficiency (or perceived deficiency) as a possible cause of the bushy phenotype. The overall characteristics of bushy make it a useful mutant for research on plant development.

Our results show flowering gene ppd in pea (Pisum sativum L.) is located between branching gene rms3 and isozyme locus Aatp near the IA end of a chromosome now known to include linkage groups IA and II. The ppd locus is about 3 cM from rms3 and 5 cM from Aatp. Two mutant alleles of Ppd are known, ppd-l and ppd-2. Both mutations result in early flowering and loss of ability to respond to photoperiod. In F(2) populations segregating for alleles Ppd and ppd-2 we found a significant deficiency of mutant segregants (on average, half the expected 25%). Reciprocal crosses were made between heterozygous Ppd ppd-2 and homozygous ppd2 ppd-2 plants. Segregation was in accordance with a 1:1 ratio when the hybrid plants were used as the female parent but a significant (P < .0001) deficiency of recessive plants occurred (only 24% were ppd-2) when the hybrid plants were used as the male parent. These results suggest that where Ppd and ppd-2 pollen are in competition there is selection against male gametes carrying the ppd-2 allele. The ppd-l mutation appears less severe than ppd-2 and segregation for ppd-l was not significantly disturbed.

Random amplified polymorphic DNA (RAPD) markers linked to two morphological markers ( fa and det), three ramosus genes (rms2, rms3 and rms4) and two genes conferring flowering response to photoperiod in pea (sn, dne) were selected by bulk segregant analysis on F2 populations. Two RAPD fragments were cloned and sequenced to generate the two SCAR markers V20 and S2 which are linked to rms3 and dne, respectively. All these genes, except rms2, were previously located on the pea classical linkage map. Rms2 mapped to linkage group IB which contains the afila gene. Precise genetic maps of the regions containing the genes were obtained and compared to the RAPD map generated from the recombinant inbred-lines population of the cross Térèse×K586. This cross was chosen because several mutants were obtained from cultivars Térèse and Torsdag (K586 was derived from Torsdag). This collection of isogenic lines was used for the construction of F2 mapping populations in which polymorphic RAPD markers were already known and mapped. Moreover, the well-known problem in pea of variability in the linkage associations between crosses was avoided. This work contributes to the precise integration between the classical map and the molecular maps existing in pea.