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SPA1: A New Genetic Locus Involved in Phytochrome A- Specific Signal TransductionUte Hoeckera,b, Yong Xu1,a,b, and Peter H. Quaila,ba Department of Plant and Microbial Biology, University of California, Berkeley, California 94720 b U.S. Department of Agriculture, Plant Gene Expression Center, 800 Buchanan Street, Albany, California 94710 Correspondence to: Peter H. Quail, quail{at}nature.berkeley.edu (E-mail), 510-559-5678 (fax).
To identify mutants potentially defective in signaling intermediates specific to phytochrome A (phyA), we screened for extragenic mutations that suppress the morphological phenotype exhibited by a weak phyA mutant (phyA-105) of Arabidopsis. A new recessive mutant, designated spa1 (for suppressor of phyA-105), was isolated and mapped to the bottom of chromosome 2. spa1 phyA-105 double mutants exhibit restoration of several responses to limiting fluence rates of continuous far-red light that are absent in the parental phyA-105 mutant, such as deetiolation, anthocyanin accumulation, and a far-red light-induced inability of seedlings to green upon subsequent transfer to continuous white light. spa1 mutations do not cause a phenotype in darkness, indicating that the suppression phenotype is light dependent. Enhanced photoresponsiveness was observed in spa1 seedlings in a wild-type PHYA background as well as in the mutant phyA-105 background but not in a mutant phyA null background. These results indicate that phyA is necessary in a non-allele-specific fashion for the expression of the spa1 mutant phenotype and that phyB to phyE are not sufficient for this effect. Taken together, the data suggest that spa1 mutations specifically amplify phyA signaling and therefore that the SPA1 locus encodes a component that acts negatively early in the phyA-specific signaling pathway.
Through the process of photosynthesis, sunlight is the primary source of energy for most plants. Therefore, it is essential that plants adapt their growth and development to ambient light conditions. Several informational photoreceptors have evolved that allow constant monitoring of light intensity, light quality, the direction of the incoming light, and light periodicity (day length). There are three major classes of such photoreceptors: the red light (R)- and far-red light (FR)-sensing phytochromes, the blue/UV-A light-responsive cryptochromes, and the UV-B light-sensing UV-B receptors. Of these, the phytochromes are the most extensively characterized and are known to regulate many aspects of plant development, including induction of seed germination, seedling deetiolation (opening of apical hook and cotyledons, chloroplast biogenesis, and inhibition of hypocotyl elongation), stem elongation, and floral induction (
The Arabidopsis phytochromes are encoded by a small family of five genes (PHYA to PHYE) (
phyA is highly abundant in dark-grown seedlings, accumulating to a level ~50-fold higher than that of phyB (
The light-stable phyB, in contrast, is the primary phytochrome responsible for deetiolation in response to R (
Despite intense research efforts, it is not known by which molecular mechanism Pfr transduces the perceived light signal downstream. One powerful approach to this problem is the isolation of mutants defective in normal light signaling (reviewed in
An alternate strategy has been to isolate mutants that display reduced sensitivity to light. Apart from photoreceptor mutants, these screens identified a recessive signaling mutant, hy5, that is likely to be deficient in a positively acting component of light signaling (
With the goal of identifying very early signaling intermediates, possibly specific to a single photoreceptor, screens for mutants have been conducted that selected for a defect in a phyA- or phyB-specific response, such as deetiolation in FRc or Rc or delay of flowering under short-day conditions. In these screens, mutants that appeared to be specifically affected in either phyA signal transduction (fhy1 and fhy3;
We were interested in identifying additional phyA-specific signal transduction intermediates. To this end, we conducted a screen for extragenic mutations that are capable of suppressing the deficiencies exhibited by a phyA mutant. Because our goal was to recover suppressors that function in a phyA-dependent fashion rather than constitutively like mutations at COP/DET/FUS-like loci, we used a weak phyA mutant (phyA-105;
Isolation of Extragenic, FRc-Dependent phyA-105 Suppressors In 24 of the 48 lines, the PHYA gene was sequenced in the region of the phyA-105 mutation to determine whether suppression of the phyA-105 mutant phenotype occurred by reversion of the phyA-105 mutation to the PHYA wild-type sequence. One true revertant was found and eliminated from further analysis. To distinguish between intragenic and extragenic suppressors among the remaining 47 lines, we determined linkage of the suppressing mutation to the phyA-105 gene: homozygous mutant suppressor plants were crossed to wild-type plants (ecotype RLD), and segregation in the F2 generations was analyzed in FRc. Thirty-one of 36 lines tested segregated only short seedlings with fully opened cotyledons, indicating that the suppressor mutation is tightly linked to the phyA-105 gene. These lines are therefore very likely to represent intragenic suppressors or revertants. This result was confirmed for five lines in which the PHYA gene was sequenced, and single missense mutations were detected in addition to the maintained phyA-105 mutation. Five lines, in contrast, segregated tall seedlings in the F2 generations derived from the respective crosses to the wild type, indicating that the phyA-105 gene and the mutant suppressor gene segregated independently. These lines are therefore extragenic suppressors of phyA-105. In all five lines, the segregation ratio in the F2 generation was in close agreement with a recessive, unlinked mutation conferring the suppressor phenotype (data not shown).
The Suppressor Mutations Are Recessive and Allelic To determine the map position of spa1, two mapping populations were generated: spa1 plants (RLD) were crossed to phyA plants of the Columbia (Col) or Landsberg erecta (Ler) ecotypes, respectively (phyA-211 or phyA-203). In the F2 generations, linkage analysis of the spa1 mutant phenotype to polymerase chain reaction (PCR)-based polymorphic markers mapped the SPA1 locus to the bottom of chromosome 2 (Figure 1). This map position indicates that spa1 mutants are not allelic to any previously isolated and mapped photomorphogenic mutants.
spa1 Mutations Partially Suppress Multiple Parameters of the Phenotype Caused by the phyA-105 Missense Allele
In contrast, when grown in darkness, spa1 phyA-105 double mutants were indistinguishable from phyA-105 or the wild type: all genotypes exhibited an elongated hypocotyl of similar length, a closed apical hook, and closed, unexpanded cotyledons (Figure 2C and Figure 2D). Hence, suppression of etiolated growth in spa1 phyA-105 double mutants is FRc conditional.
Lack of an FRc-Preconditioned Block of Greening In an effort to characterize the effects of spa1 mutations more fully, we tested whether these mutations restore the FRc-preconditioned block of greening in the phyA-105 mutant. As shown in Figure 3A, phyA-105 seedlings that were exposed to intermediate fluence rates of FRc for 3 days retained the ability to green upon subsequent illumination with Wc, resulting in accumulation of chlorophyll to amounts similar to those in a phyA null mutant (phyA-101). Hence, under these light conditions, phyA-105 is insensitive to FRc. In contrast, spa1 phyA-105 seedlings failed to green when transferred from FRc to Wc. These seedlings accumulated negligable amounts of chlorophyll that were indistinguishable from those produced by wild-type seedlings (Figure 3A). Thus, with respect to the FRc-preconditioned block of greening under the conditions used, spa1 mutations appear to restore completely a wild-type phenotype in the phyA-105 mutant. Restoration of a block of greening was not a constitutive response but was dependent on preillumination with FRc before transfer to Wc: spa1 phyA-105 double mutants that were kept in darkness for 3 days before exposure to Wc accumulated chlorophyll at levels similar to the phyA-105 mutant, although the accumulation was slightly lower than in the wild type grown under the same conditions (Figure 3B). Thus, spa1 phyA-105 double mutants retain the competence to green when grown in darkness.
Lack of Anthocyanin Accumulation in FRc
Effect of spa1 Mutations on Adult Growth
spa1 Mutations Confer Hypersensitivity to FRc in the Presence of Wild-Type phyA As shown in Figure 5a, the spa1-3 single mutant exhibited a significantly reduced hypocotyl length compared with the RLD wild type over a range of FRc fluence rates tested. Moreover, spa1-3 seedlings opened their cotyledons at a lower FRc fluence rate than did RLD wild-type seedlings. At an FRc fluence rate of 1 µmol m-2 sec-1, cotyledons of wild-type seedlings were closed or only partially opened, whereas most spa1-3 seedlings exhibited fully opened and expanded cotyledons at this fluence rate (Figure 5b). In dark-grown seedlings, in contrast, the spa1-3 mutation had no effect on hypocotyl length or cotyledon phenotype (Figure 5a and Figure 5b). The alleles spa1-1 and spa1-2 were outcrossed into a wild-type PHYA background as well and caused a phenotype very similar to that caused by the spa1-3 allele (data not shown).
These results indicate that spa1 single mutants show an increased sensitivity to FRc. This FRc-hypersensitive phenotype segregated in F2 generations at the expected Mendelian ratio (data not shown), indicating that the phenotype is caused by a monogenic recessive mutation at the SPA1 locus. Consistent with this result, progeny of a homozygous wild-type segregant (SPA1(+)) that was identified in a population segregating for the spa1-3 mutation exhibited a hypocotyl length and a cotyledon phenotype similar to that of the RLD wild type (Figure 5a and Figure 5b). We further tested whether FRc-induced accumulation of anthocyanins is affected in spa1 single mutants. As shown in Figure 6A, spa1 single mutants (spa1-1, spa1-2, and spa1-3) accumulated higher levels of anthocyanins in FRc than did the RLD wild type or available progeny of respective homozygous wild-type control segregants (SPA1-2(+) and SPA1-3(+)). In dark-grown seedlings, in contrast, spa1 mutations did not cause a significant increase in anthocyanin levels (Figure 6B). These results indicate that spa1 single mutants are hypersensitive to FRc with respect to anthocyanin accumulation in addition to deetiolation.
Because spa1 mutations did not cause any apparent phenotype in dark-grown seedlings, we predicted that expression of FRc hypersensitivity in spa1 single mutants is strictly dependent on the presence of phyA, the only phytochrome that senses FRc. Indeed, spa1-2 phyA-101 seedlings, which produce no phyA, exhibited a hypocotyl length similar to that of the phyA null mutant phyA-101 and progeny of a homozygous SPA1(+) phyA-101 control segregant when grown under FRc (Figure 7a). Also, spa1-2 phyA-101 seedlings had closed cotyledons in FRc and thus were indistinguishable in appearance from phyA-101 seedlings (Figure 7b). Hence, in contrast to the spa1-2 single mutant that is hypersensitive to FRc (Figure 7a and Figure 7b), the spa1-2 phyA-101 double mutant was fully insensitive to FRc. The increase in sensitivity to FRc caused by spa1 mutations therefore requires light perception through the photoreceptor phyA.
Strictly Dependent on phyA, spa1 Mutations Also Confer Hypersensitivity to Rc
We considered at least two possibilities to explain the observed lack of wavelength specificity. First, spa1 mutations might alter the function or signal transduction capacity of other phytochromes, such as phyB, in addition to phyA. Second, spa1 mutations might specifically affect phyA sensory specificity or signal transduction capacity. In this latter scenario, the increased sensitivity of spa1 mutants to FRc as well as to Rc would be caused by enhancing the light signal perceived and transduced by phyA. To distinguish between these two possibilities for SPA1 function, we tested the effect of spa1 mutations on Rc responsiveness in a phyA null (phyA-101) background. This allowed us to determine whether phyA is required for the Rc hypersensitive phenotype in the spa1 mutants. Figure 8C shows that no difference in hypocotyl length was observed between the spa1-2 phyA-101 double mutant and the genotypes phyA-101 and RLD wild type. As an additional control, we determined hypocotyl length of the progeny of a segregant that was determined to be homozygous wild type at the SPA1 locus and homozygous phyA-101 at the PHYA locus. Seedlings of this line (SPA1(+) phyA-101) also exhibited a hypocotyl length in Rc similar to that of spa1-2 phyA-101 seedlings (Figure 8C). Thus, no Rc hypersensitive phenotype was observed in the spa1-2 phyA-101 double mutant. In contrast, the spa1-2 single mutant exhibited the previously described significant reduction in hypocotyl length in Rc (Figure 8C). Similar results were obtained for the spa1-3 phyA-101 double mutant (data not shown). Hence, expression of increased sensitivity to Rc in spa1 mutants strictly depended on the presence of wild-type phyA or the partially functional phyA-105. These results suggest therefore that spa1 mutations specifically alter phyA function or signal transduction.
spa1 Mutations Do Not Alter phyA Protein Levels
We further tested the possibility that the Rc hypersensitive phenotype observed in spa1 mutant seedlings might be caused by an increase in protein stability of PfrA. As shown in Figure 9B, illumination of seedlings with Rc caused a rapid decrease in phyA levels that is similar in the SPA1 wild type and all tested spa1 mutants, both in the mutant phyA-105 and the wild-type PHYA backgrounds. Hence, spa1 mutations did not cause a detectable increase in phyA protein levels in Rc-grown seedlings.
It is well established that phytochromes A and B exhibit contrasting photosensory specificity in the control of seedling deetiolation (
The Effects of spa1 Mutations Are Light Dependent
The Enhanced Photoresponsiveness Caused by the spa1 Mutations Is phyA Dependent Although epistatic interactions between phyA and phyC, phyD, or phyE are not known, these findings argue against an involvement of phytochromes other than phyA in the spa1 mutant phenotype. In particular, the observation that no detectable Rc-induced seedling hypocotyl phenotype was observed in spa1 phyA null double mutants strongly suggests that phyB function and signal transduction are not affected by spa1 mutations. That spa1 mutations did not cause any clearly visible effects on additional phyB-mediated responses, such as petiole elongation and flowering time, is consistent with this interpretation.
spa1 Mutations Amplify phyA Signal Transduction
Because spa1 mutations increased light responsiveness in both mutant phyA-105 and wild-type PHYA backgrounds, it is evident that the effects of spa1 mutations are not specific to the phyA-105 allele. These findings suggest that spa1 mutations are likely to increase phyA signaling in the PHYA and phyA-105 backgrounds via the same mechanism and that this mechanism does not specifically rescue the defect caused by the phyA-105 mutation. Moreover, spa1 mutations caused a higher FRc and Rc responsiveness in the wild-type PHYA background than in the mutant phyA-105 background, in which only a partially functional phyA is expressed. Hence, it appears that spa1 mutations cause a general amplification of signaling through the phyA pathway at a magnitude that is proportional to the signal-strength input from the phyA photoreceptor. An amplification of phytochrome responsiveness also appears to occur in the high pigment (hp) mutants in tomato (
Regulation of phyA Signaling by SPA1
In an alternative scenario (Figure 10B), SPA1 could downregulate the activity or expression of a positive regulator of phyA signal transduction. FHY1 and FHY3 are potential candidates for an SPA1 target. fhy1 and fhy3 mutations cause a reduction in responsiveness specifically to FRc and are therefore also potential phyA-specific signal transduction intermediates ( There are several possible purposes for SPA1-mediated inhibition of phyA signal transduction. It is possible that the evolution of a negative regulatory factor, such as SPA1, in addition to positively acting factors may have allowed fine-tuning of plant responses to ambient light and environmental conditions. For example, SPA1-mediated inhibition of phyA signaling may be a mechanism permitting negative feedback control of phyA signal transduction by downstream phyA action. It is also possible that SPA1 mediates cross-talk from other signaling cascades that sense, for example, other environmental stimuli that lead to modulation of phyA signaling. Alternatively, SPA1 may function as a constitutive repressor of phyA signaling. In this scenario, SPA1 evolution may have been advantageous in the adaptation to a possibly changed environment.
SPA1 Plays an Important Role in Determining Photosensory Specificity of phyA In conclusion, we have genetically identified a new locus, SPA1, that is likely to encode a negative regulator of phyA-specific signal transduction. Genetic epistasis analysis of the spa1 mutations with fhy1 and fhy3 will help to place SPA1 within the phyA signaling network. Cloning and molecular characterization of SPA1 will shed light on the mechanisms involved in phyA signaling that are as yet not understood. Moreover, further analysis of the Rc responsiveness of phyA in the spa1 mutant background should enhance our knowledge of phyA function.
Alleles of Photomorphogenic Mutants Used
Seedling Growth and Screen for Mutants For mutagenesis, ~50,000 seeds homozygous for phyA-105 were exposed to 0.25% ethyl methanesulfonate for 16 hr and subsequently sown on soil in pots. M2 seeds were harvested in bulk for each of the 205 pots and considered independent families. M2 seeds (800 to 1000 per family) were treated and plated on growth medium supplemented with 2% sucrose, as described above, and screened in FRc (13 µmol m-2 sec-1) for seedlings with open cotyledons and/or short hypocotyls. Selected individuals were transferred to fresh plates and kept in the dark at 21°C for 3 days (FR rescue). Seedlings were then exposed to continuous white light (Wc) for several days and subsequently transferred to soil to produce M3 seeds. M3 seeds were rescreened in FRc (13 µmol m-2 sec-1) and in darkness. To distinguish between intragenic and extragenic suppressors, we determined linkage of the suppressor mutations to the phyA-105 gene: duplicate crosses between homozygous suppressor lines and wild type (RLD) were conducted, and three F1 plants per cross were grown to produce F2 seed. At least 200 F2 seeds obtained from each F1 plant were plated and grown in FRc (13 µmol m-2 sec-1) for 3 days. Lines that segregated tall seedlings were considered extragenic suppressors.
DNA Sequencing of phyA-105 Suppressors
Construction of spa1 Single Mutants and spa1 phyA-101 Double Mutants To construct spa1 phyA-101 double mutants, homozygous spa1 phyA-105 plants were crossed to phyA-101. In the F2 generation, 50 seedlings were randomly chosen and assayed for their genotype at the PHYA locus by using the PCR-based polymorphism of phyA-105 described above. F2 plants thus identified as homozygous mutant for phyA-101 were then testcrossed to the progenitor suppressor line to determine the genotype at the SPA1 locus. Hence, all F1 seeds produced were heterozygous at the PHYA locus carrying one allele each of phyA-105 and phyA-101. In contrast, F1 seeds segregated at the SPA1 locus. To detect segregation at the SPA1 locus, F1 seeds were plated and grown in FRc (7.5 µmol m-2 sec-1) for 3 days. Because spa1 mutations suppress the phenotype of homozygous mutant phyA-105, it was expected that spa1 mutations also cause a phenotype in a phyA-105/phyA-101 heterozygous background, which should produce half as much phyA-105 protein as a phyA-105 homozygote. Indeed, this was observed. When grown in FRc, F1 progenies of the testcrosses fell into three groups: those that segregated 100% seedlings with fully opened cotyledons and hypocotyls shorter than phyA-105, those that segregated 100% tall seedlings with almost fully closed cotyledons, and those that segregated these two phenotypes at a ratio of ~1:1. Hence, progeny in which all or no F1 seedlings displayed open cotyledons and hypocotyls shorter than phyA-105 were considered to be derived from a plant that was homozygous mutant or homozygous wild type, respectively, at the SPA1 locus.
Mapping of the spa1 Mutation In contrast, the F2 generation derived from the cross of spa1-2 phyA-105 to phyA-211 segregated seedlings displaying phenotypes ranging from full to intermediate suppression at ratios that were consistent with 3:16 (short plus intermediate to tall). PCR analysis showed that F2 seedlings were either homozygous for phyA-105 or heterozygous phyA-105/phyA-211. No F2 seedling selected for the suppressor phenotype was found to be homozygous phyA-211.
To confirm that selected F2 plants in both mapping populations were indeed homozygous mutant for spa1, F3 seed was rescored for the suppressor phenotype. Only those F3 seeds that showed 100% short seedlings in FRc were used for mapping of spa1. Hence, F3 seeds of the spa1-2 phyA-105 x phyA-211 mapping population that segregated tall seedlings because of phyA-105/phyA-211 heterozygosity were not used. Genomic DNA was isolated from populations of F3 seedlings derived from 50 selected F2 plants per mapping population, according to the method of
FRc-Preconditioned Block of Greening Experiments and Chlorophyll Determinations
Anthocyanin Accumulation
Immunoblot Analysis of phyA
1 Current address: Qiagen, 28159 Stanford Avenue, Valencia, CA 91355.
We thank Sharon Moran for outstanding technical assistance throughout the project, Yurah Kang for excellent help with the mapping of spa1, and David Hantz and his greenhouse staff for expert care of our plants. This research was supported by Grant No. GM4745 from the National Institutes of Health and U.S. Department of Agriculture Current Research Information Service Grant No. 5335-21000-006-00D. Received September 15, 1997; accepted November 13, 1997.
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