Plant cells store genetic information in the genomes of three organelles: the nucleus, plastid, and mitochondrion. The nucleus controls most aspects of organelle gene expression, development, and function. In return, organelles send signals to the nucleus to control nuclear gene expression, a process called retrograde signaling. This review summarizes our current understanding of plastid-to-nucleus retrograde signaling, which involves multiple, partially redundant signaling pathways. The best studied is a pathway that is triggered by buildup of Mg-ProtoporphyrinIX, the first intermediate in the chlorophyll branch of the tetrapyrrole biosynthetic pathway. In addition, there is evidence for a plastid gene expression-dependent pathway, as well as a third pathway that is dependent on the redox state of photosynthetic electron transport components. Although genetic studies have identified several players involved in signal generation, very little is known of the signaling components or transcription factors that regulate the expression of hundreds of nuclear genes.
RGA and GAI are homologous genes that encode putative transcriptional regulators that repress gibberellin (GA) signaling in Arabidopsis. Previously we showed that the green fluorescent protein (GFP)-RGA fusion protein is localized to the nucleus in transgenic Arabidopsis, and expression of this fusion protein rescues the rga null mutation. The GA signal seems to derepress the GA response pathway by degrading the repressor protein RGA. The GA-insensitive, semidominant, semidwarf gai-1 mutant encodes a mutant protein with a 17-amino acid deletion within the DELLA domain of GAI. It was hypothesized that this mutation turns the gai protein into a constitutive repressor of GA signaling. Because the sequences missing in gai-1 are identical between GAI and RGA, we tested whether an identical mutation (rga-⌬17) in the RGA gene would confer a phenotype similar to gai-1. We demonstrated that expression of rga-⌬17 or GFP-(rga-⌬17) under the control of the RGA promoter caused a GA-unresponsive severe dwarf phenotype in transgenic Arabidopsis. Analysis of the mRNA levels of a GA biosynthetic gene, GA4, showed that the feedback control of GA biosynthesis in these transgenic plants was less responsive to GA than that in wild type. Immunoblot and confocal microscopy analyses indicated that rga-⌬17 and GFP-(rga-⌬17) proteins were resistant to degradation after GA application. Our results illustrate that the DELLA domain in RGA plays a regulatory role in GAinduced degradation of RGA. Deletion of this region stabilizes the rga-⌬17 mutant protein, and regardless of the endogenous GA status rga-⌬17 becomes a constitutively active repressor of GA signaling.
The PsbS protein of photosystem II functions in the regulation of photosynthetic light harvesting. Along with a low thylakoid lumen pH and the presence of de-epoxidized xanthophylls, PsbS is necessary for photoprotective thermal dissipation (qE) of excess absorbed light energy in plants, measured as non-photochemical quenching of chlorophyll fluorescence. What is known about PsbS in relation to the hypothesis that this protein is the site of qE is reviewed here.
RGA (for repressor of ga1-3 ) and SPINDLY ( SPY ) are likely repressors of gibberellin (GA) signaling in Arabidopsis because the recessive rga and spy mutations partially suppressed the phenotype of the GA-deficient mutant ga1-3 . We found that neither rga nor spy altered the GA levels in the wild-type or the ga1-3 background. However, expression of the GA biosynthetic gene GA4 was reduced 26% by the rga mutation, suggesting that partial derepression of the GA response pathway by rga resulted in the feedback inhibition of GA4 expression. The green fluorescent protein (GFP)-RGA fusion protein was localized to nuclei in transgenic Arabidopsis. This result supports the predicted function of RGA as a transcriptional regulator based on sequence analysis. Confocal microscopy and immunoblot analyses demonstrated that the levels of both the GFP-RGA fusion protein and endogenous RGA were reduced rapidly by GA treatment. Therefore, the GA signal appears to derepress the GA signaling pathway by degrading the repressor protein RGA. The effect of rga on GA4 gene expression and the effect of GA on RGA protein level allow us to identify part of the mechanism by which GA homeostasis is achieved. INTRODUCTIONGibberellins (GAs) are members of a large family of diterpenoid compounds, some of which are plant growth regulators that control such diverse processes as seed germination, stem growth, and flower development. Although the GA biosynthetic pathway has been elucidated (reviewed in Lange, 1998;Hedden and Proebsting, 1999;Hedden and Phillips, 2000;Yamaguchi and Kamiya, 2000), much less is known about its signal transduction pathway in plants. Recent molecular and pharmacological studies in cereal aleurone showed that Ca 2 ϩ , calmodulin, cyclic GMP, heterotrimeric G proteins, GAMYB, and protein kinases may play a role in GA signaling (reviewed in Bethke and Jones, 1998;Lovegrove and Hooley, 2000). Isolation of GA response mutants and molecular cloning of corresponding genes in Arabidopsis also have identified several novel components of the GA signal transduction pathway (reviewed in Thornton et al., 1999;Sun, 2000). The putative repressors include SPINDLY ( SPY ;Jacobsen et al., 1996), RGA (for repressor of ga1-3 ; Silverstone et al., 1998), GAI (for GA insensitive; Peng et al., 1997), and SHORT INTERNODES ( SHI ;Fridborg et al., 1999), and the potential activators are SLEEPY ( SLY ;Steber et al., 1998) and PICKLE ( PKL ; Ogas et al., 1999).SPY was identified originally because spy mutations allowed the seed to germinate in the presence of the GA biosynthesis inhibitor paclobutrazol (PAC; Jacobsen and Olszewski, 1993). The defect in the SPY function also was able to partially suppress the phenotype of the GA biosynthetic mutant ga1-3 , which is a nongerminating, male-sterile, extreme dwarf (Silverstone et al., 1997). Sequence analysis of SPY and in vitro enzyme assays using the recombinant SPY protein suggest that SPY probably is a Ser/Thr O -linked N -acetylglucosamine transferase (OGT; Thornton et al., 1999).We identified RG...
Feedback deexcitation is a photosynthetic regulatory mechanism that can protect plants from high light stress by harmlessly dissipating excess absorbed light energy as heat. To understand the genetic basis for intraspecies differences in thermal dissipation capacity, we investigated natural variation in Arabidopsis (Arabidopsis thaliana). We determined the variation in the amount of thermal dissipation by measuring nonphotochemical quenching (NPQ) of chlorophyll fluorescence in Arabidopsis accessions of diverse origins. Ll-1 and Sf-2 were selected as high NPQ Arabidopsis accessions, and Columbia-0 (Col-0) and Wassilewskija-2 were selected as relatively low NPQ accessions. In spite of significant differences in NPQ, previously identified NPQ factors were indistinguishable between the high and the low NPQ accessions. Intermediate levels of NPQ in Ll-1 3 Col-0 F1 and Sf-2 3 Col-0 F1 compared to NPQ levels in their parental lines and continuous distribution of NPQ in F2 indicated that the variation in NPQ is under the control of multiple nuclear factors. To identify genetic factors responsible for the NPQ variation, we developed a polymorphic molecular marker set for Sf-2 3 Col-0 at approximately 10-centimorgan intervals. From quantitative trait locus (QTL) mapping with undistorted genotype data and NPQ measurements in an F2 mapping population, we identified two high NPQ QTLs, HQE1 (high qE 1, for high energy-dependent quenching 1) and HQE2, on chromosomes 1 and 2, and the phenotype of HQE2 was validated by analysis of near isogenic lines. Neither QTL maps to a gene that had been identified previously in extensive forward genetics screens using induced mutants, suggesting that quantitative genetics can be used to find new genes affecting thermal dissipation.
RGA (for repressor of ga1-3) and SPINDLY (SPY) are likely repressors of gibberellin (GA) signaling in Arabidopsis because the recessive rga and spy mutations partially suppressed the phenotype of the GA-deficient mutant ga1-3. We found that neither rga nor spy altered the GA levels in the wild-type or the ga1-3 background. However, expression of the GA biosynthetic gene GA4 was reduced 26% by the rga mutation, suggesting that partial derepression of the GA response pathway by rga resulted in the feedback inhibition of GA4 expression. The green fluorescent protein (GFP)-RGA fusion protein was localized to nuclei in transgenic Arabidopsis. This result supports the predicted function of RGA as a transcriptional regulator based on sequence analysis. Confocal microscopy and immunoblot analyses demonstrated that the levels of both the GFP-RGA fusion protein and endogenous RGA were reduced rapidly by GA treatment. Therefore, the GA signal appears to derepress the GA signaling pathway by degrading the repressor protein RGA. The effect of rga on GA4 gene expression and the effect of GA on RGA protein level allow us to identify part of the mechanism by which GA homeostasis is achieved.
We have identified a new locus that regulates vegetative phase change and flowering time in Arabidopsis. An early-flowering mutant, eaf1 (early flowering 1) was isolated and characterized. eaf1 plants flowered earlier than the wild type under either short-day or long-day conditions, and showed a reduction in the juvenile and adult vegetative phases. When grown under short-day conditions, eaf1 plants were slightly pale green and had elongated petioles, phenotypes that are observed in mutants altered in either phytochrome or the gibberellin (GA) response. eaf1 seed showed increased resistance to the GA biosynthesis inhibitor paclobutrazol, suggesting that GA metabolism and/or response had been altered. Comparison of eaf1 to other early-flowering mutants revealed that eaf1 shifts to the adult phase early and flowers early, similarly to the phyB (phytochrome B) and spy (spindly) mutants. eaf1 maps to chromosome 2, but defines a locus distinct from phyB, clf (curly leaf), and elf3 (early-flowering 3). These results demonstrate that eaf1 defines a new locus involved in an autonomous pathway and may affect GA regulation of flowering.
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