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Sonia Gazzarrini - One of the best experts on this subject based on the ideXlab platform.
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spatiotemporal restriction of fusca3 expression by class i bpcs promotes ovule development and coordinates embryo and endosperm growth
The Plant Cell, 2020Co-Authors: Jian Wu, Deka Mohamed, Sebastian Dowhanik, Rosanna Petrella, Veronica Gregis, Jingru Li, Lin Wu, Sonia GazzarriniAbstract:Spatiotemporal regulation of gene expression is critical for proper developmental timing in plants and animals. The transcription factor FUSCA3 (Fus3) regulates developmental phase transitions by acting as a link between hormonal pathways in Arabidopsis thaliana. However, the mechanisms governing its spatiotemporal expression pattern are poorly understood. Here, we show that Fus3 is repressed in the ovule integuments and seed endosperm. Fus3 repression requires class I BASIC PENTACYSTEINE (BPC) proteins, which directly bind GA/CT cis-elements in Fus3 and restrict its expression pattern. During vegetative and reproductive development, Fus3 derepression in bpc1-1 bpc2 (bpc½) double mutant or misexpression in ProML1:Fus3 lines causes dwarf plants carrying defective flowers and aborted ovules. Postfertilization, ectopic Fus3 expression in bpc½ endosperm or ProML1:Fus3 endosperm and endothelium increases endosperm nuclei proliferation and seed size, causing delayed or arrested embryo development. These phenotypes are rescued in bpc½ Fus3-3. Lastly, class I BPCs interact with FIS-PRC2 (FERTILIZATION-INDEPENDENT SEED-Polycomb Repressive Complex2), which represses Fus3 in the endosperm during early seed development. We propose that BPC1 and 2 promote the transition from reproductive to seed development by repressing Fus3 in ovule integuments. After fertilization, BPC1 and 2 and FIS-PRC2 repress Fus3 in the endosperm to coordinate early endosperm and embryo growth.
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spatiotemporal restriction of fusca3 expression by class i bpc promotes ovule development and coordinates embryo and endosperm growth
bioRxiv, 2019Co-Authors: Sonia Gazzarrini, Jian Wu, Rosanna Petrella, Veronica Gregis, Sebastian DowhanikAbstract:ABSTRACT Spatiotemporal regulation of gene expression plays an important role in developmental timing in plants and animals. FUSCA3 regulates the transition between different phases of development by acting as a link between different hormonal pathways in Arabidopsis. However, the mechanisms governing its spatiotemporal expression patterns are poorly understood. Here, we show that Fus3 is expressed in the chalaza and funiculus of the mature ovule and seed, but is repressed in the embryo sac, integuments and endosperm. Fus3 repression requires class I BASIC PENTACYSTEINE (BPC) proteins, which directly bind to the Fus3 locus and restrict its expression pattern. During vegetative and reproductive development, derepression of Fus3 in bpc1/2 or pML1:Fus3 misexpression lines results in dwarf plants carrying defective flowers and aborted ovules. Post-fertilization, ectopic Fus3 expression in the endosperm increases endosperm nuclei proliferation and seed size and delays or arrests embryo development. These phenotypes are rescued in bpc1/2 Fus3-3. Lastly, class I BPCs interact with FIS-PRC2 (FERTILIZATION-INDEPENDENT SEED-Polycomb Repressive Complex 2), which represses Fus3 in the endosperm. We propose that BPC1/2 promotes the transition from reproductive to seed development by repressing Fus3 in ovule integuments. After fertilization, BPC1/2 and FIS-PRC2 repress Fus3 in the endosperm to coordinate endosperm and embryo growth.
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Corrigendum: SnRK1 phosphorylation of FUSCA3 positively regulates embryogenesis, seed yield, and plant growth at high temperature in Arabidopsis.
Journal of experimental botany, 2017Co-Authors: Aaron T. Chan, Allen Yi-lun Tsai, Carina Steliana Carianopol, Kresanth Varatharajah, Rex Shun Chiu, Sonia GazzarriniAbstract:The transcription factor FUSCA3 (Fus3) acts as a major regulator of seed maturation in Arabidopsis. Fus3 is phosphorylated by the SnRK1 catalytic subunit AKIN10/SnRK1α1, which belongs to a conserved eukaryotic kinase complex involved in energy homeostasis. Here we show that AKIN10 and Fus3 share overlapping expression patterns during embryogenesis, and that Fus3 is phosphorylated by AKIN10 in embryo cell extracts. To understand the role of Fus3 phosphorylation, we generated Fus3-3 plants carrying Fus3 phosphorylation-null (Fus3S>A) and phosphorylation-mimic (Fus3S>D) variants. While Fus3S>A and Fus3S>D rescued all the Fus3-3 seed maturation defects, Fus3S>A showed reduced transcriptional activity and enhanced Fus3-3 previously uncharacterized phenotypes. Fus3S>A embryos displayed increased seed abortion due to maternal Fus3S>A and delayed embryo development, which correlated with a strong decrease in seed yield (~50%). Accordingly, the akin10 and akin11 mutants displayed a frequency of seed abortion similar to Fus3-3. When plants were grown at elevated temperature, most phenotypes were exaggerated in Fus3S>A plants, and progeny seedlings overall grew poorly, suggesting that phosphorylation of Fus3 plays an important role during early embryogenesis and under heat stress. Collectively, these results suggest that Fus3 phosphorylation and SnRK1 are required for embryogenesis and integration of environmental cues to ensure the survival of the progeny.
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the e3 ligase abi3 interacting protein2 negatively regulates fusca3 and plays a role in cotyledon development in arabidopsis thaliana
Journal of Experimental Botany, 2017Co-Authors: Simon Duong, Eliana Vonapartis, Cheukyan Li, Sajedabanu Patel, Sonia GazzarriniAbstract:FUSCA3 (Fus3) is a short-lived B3-domain transcription factor that regulates seed development and phase transitions in Arabidopsis thaliana. The mechanisms controlling Fus3 levels are currently poorly understood. Here we show that Fus3 interacts with the RING E3 ligase ABI3-INTERACTING PROTEIN2 (AIP2). AIP2–green fluorescent protein (GFP) is preferentially expressed in the protoderm during early embryogenesis, similarly to Fus3, suggesting that their interaction is biologically relevant. Fus3 degradation is delayed in the aip2-1 mutant and Fus3–GFP fluorescence is increased in aip2-1, but only during mid-embryogenesis, suggesting that Fus3 is negatively regulated by AIP2 at a specific time during embryogenesis. aip2-1 shows delayed flowering and therefore also functions post-embryonically to regulate developmental phase transitions. Plants overexpressing Fus3 post-embryonically in the L1 layer (ML1p:Fus3) show late flowering and other developmental phenotypes that can be rescued by ML1p:AIP2, further supporting a negative role for AIP2 in Fus3 accumulation. However, additional factors regulate Fus3 levels during embryogenesis, as ML1:AIP2 seeds do not resemble Fus3-3. Lastly, targeted expression of a RING-inactive AIP2 variant to the protoderm/L1 layer causes Fus3 and ABI3 overexpression phenotypes and defects in cotyledon development. Taken together, these results indicate that AIP2 targets Fus3 for degradation and plays a role in cotyledon development and flowering time in Arabidopsis.
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Inhibition of FUSCA3 degradation at high temperature is dependent on ABA signaling and is regulated by the ABA/GA ratio.
Plant signaling & behavior, 2016Co-Authors: Rex Shun Chiu, Yazan Saleh, Sonia GazzarriniAbstract:ABSTRACTDuring seed imbibition at supra-optimal temperature, an increase in the abscisic acid (ABA)/gibberellin (GA) ratio imposes secondary dormancy to prevent germination (thermoinhibition). FUSCA3 (Fus3), a positive regulator of seed dormancy, accumulates in seeds imbibed at high temperature and increases ABA levels to inhibit germination. Recently, we showed that ABA inhibits Fus3 degradation at high temperature, and that ABA and high temperature also inhibit the ubiquitin-proteasome system, by dampening both proteasome activity and protein polyubiquitination. Here, we investigated the role of ABA signaling components and the ABA antagonizing hormone, GA, in the regulation of Fus3 levels. We show that the ABA receptor mutant, pyl1-1, is less sensitive to ABA and thermoinhibition. In this mutant background, Fus3 degradation in vitro is faster. Similarly, GA alleviates thermoinhibition and also increases Fus3 degradation. These results indicate that inhibition of Fus3 degradation at high temperature is ...
Elaine A. Elion - One of the best experts on this subject based on the ideXlab platform.
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Counteractive Control of Polarized Morphogenesis during Mating by Mitogen-activated Protein Kinase Fus3 and G1 Cyclin-dependent Kinase
Molecular biology of the cell, 2008Co-Authors: Mark A. Sheff, Elaine A. ElionAbstract:Cell polarization in response to external cues is critical to many eukaryotic cells. During pheromone-induced mating in Saccharomyces cerevisiae, the mitogen-activated protein kinase (MAPK) Fus3 induces polarization of the actin cytoskeleton toward a landmark generated by the pheromone receptor. Here, we analyze the role of Fus3 activation and cell cycle arrest in mating morphogenesis. The MAPK scaffold Ste5 is initially recruited to the plasma membrane in random patches that polarize before shmoo emergence. Polarized localization of Ste5 is important for shmooing. In Fus3 mutants, Ste5 is recruited to significantly more of the plasma membrane, whereas recruitment of Bni1 formin, Cdc24 guanine exchange factor, and Ste20 p21-activated protein kinase are inhibited. In contrast, polarized recruitment still occurs in a far1 mutant that is also defective in G1 arrest. Remarkably, loss of Cln2 or Cdc28 cyclin-dependent kinase restores polarized localization of Bni1, Ste5, and Ste20 to a Fus3 mutant. These and other findings suggest Fus3 induces polarized growth in G1 phase cells by down-regulating Ste5 recruitment and by inhibiting Cln/Cdc28 kinase, which prevents basal recruitment of Ste5, Cdc42-mediated asymmetry, and mating morphogenesis.
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differential input by ste5 scaffold and msg5 phosphatase route a mapk cascade to multiple outcomes
The EMBO Journal, 2004Co-Authors: Jessica Andersson, David Simpson, Maosong Qi, Yunmei Wang, Elaine A. ElionAbstract:Pathway specificity is poorly understood for mitogen-activated protein kinase (MAPK) cascades that control different outputs in response to different stimuli. In yeast, it is not known how the same MAPK cascade activates Kss1 MAPK to promote invasive growth (IG) and proliferation, and both Fus3 and Kss1 MAPKs to promote mating. Previous work has suggested that the Kss1 MAPK cascade is activated independently of the mating G protein (Ste4)–scaffold (Ste5) system during IG. Here we demonstrate that Ste4 and Ste5 activate Kss1 during IG and in response to multiple stimuli including butanol. Ste5 activates Kss1 by generating a pool of active MAPKKK (Ste11), whereas additional scaffolding is needed to activate Fus3. Scaffold-independent activation of Kss1 can occur at multiple steps in the pathway, whereas Fus3 is strictly dependent on the scaffold. Pathway specificity is linked to Kss1 immunity to a MAPK phosphatase that constitutively inhibits basal activation of Fus3 and blocks activation of the mating pathway. These findings reveal the versatility of scaffolds and how a single MAPK cascade mediates different outputs.
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far4, far5, and far6 define three genes required for efficient activation of MAPKs Fus3 and Kss1 and accumulation of glycogen
Current Genetics, 2001Co-Authors: Vera Cherkasova, Elaine A. ElionAbstract:In Saccharomyces cerevisiae , mating pheromones induce G1 arrest through the activation of two MAP kinases, Fus3 and Kss1. Here we report the isolation of three mutants, far4 , far5 , and far6 , that have the novel phenotype of regulating both the activity of Fus3 and Kss1 and the accumulation of glycogen. A far4 mutation constitutively activates Fus3 and Kss1, reduces glycogen, and blocks G1 arrest in the presence of α factor. In contrast, far5 and far6 mutations increase glycogen and reduce activation of Fus3 and Kss1 by pheromone. far4 , far5 , and far6 are recessive and not allelic to FAR1 , FAR3 , or 14 genes known to regulate the pheromone response. Non-allelic non-complementation occurs between far6 and both far4 and far5 , suggesting that FAR6 functionally interacts with FAR4 and FAR5 . Additional observations suggest that FAR4 has functional overlap with FAR3 , which we also find to regulate glycogen accumulation. Our results suggest that the activation of the mating MAPK cascade and subsequent G1 arrest is influenced by a signal transduction pathway that regulates glycogen. In support of this possibility, we find that Fus3 is activated to a greater extent in a "wimp" strain with defective protein kinase A. Finally, BIM1 and BIK1 have been identified as CEN suppressors of far5 , suggesting that the microtubule apparatus may regulate the ability of the pheromone response pathway to promote G1 arrest.
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Characterization of Fus3 localization: active Fus3 localizes in complexes of varying size and specific activity.
Molecular biology of the cell, 1999Co-Authors: Kang Yell Choi, Janice E. Kranz, Sanjoy K. Mahanty, Ki-sook Park, Elaine A. ElionAbstract:The MAP kinase Fus3 regulates many different signal transduction outputs that govern the ability of Saccharomyces cerevisiae haploid cells to mate. Here we characterize Fus3 localization and association with other proteins. By indirect immunofluorescence, Fus3 localizes in punctate spots throughout the cytoplasm and nucleus, with slightly enhanced nuclear localization after pheromone stimulation. This broad distribution is consistent with the critical role Fus3 plays in mating and contrasts that of Kss1, which concentrates in the nucleus and is not required for mating. The majority of Fus3 is soluble and not bound to any one protein; however, a fraction is stably bound to two proteins of approximately 60 and approximately 70 kDa. Based on fractionation and gradient density centrifugation properties, Fus3 exists in a number of complexes, with its activity critically dependent upon association with other proteins. In the presence of alpha factor, nearly all of the active Fus3 localizes in complexes of varying size and specific activity, whereas monomeric Fus3 has little activity. Fus3 has highest specific activity within a 350- to 500-kDa complex previously shown to contain Ste5, Ste11, and Ste7. Ste5 is required for Fus3 to exist in this complex. Upon alpha factor withdrawal, a pool of Fus3 retains activity for more than one cell cycle. Collectively, these results support Ste5's role as a tether and suggest that association of Fus3 in complexes in the presence of pheromone may prevent inactivation in addition to enhancing activation.
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The osmoregulatory pathway represses mating pathway activity in Saccharomyces cerevisiae: isolation of a Fus3 mutant that is insensitive to the repression mechanism.
Molecular and cellular biology, 1996Co-Authors: J P Hall, Elaine A. Elion, V Cherkasova, M C Gustin, Edward WinterAbstract:Mitogen-activated protein (MAP) kinase cascades are conserved signal transduction pathways that are required for eukaryotic cells to respond to a variety of stimuli. Multiple MAP kinase pathways can function within a single cell type; therefore, mechanisms that insulate one MAP kinase pathway from adventitious activations by parallel pathways may exist. We have studied interactions between the mating pheromone response and the osmoregulatory (high-osmolarity glycerol response [HOG]) pathways in Saccharomyces cerevisiae which utilize the MAP kinases Fus3p and Hog1p, respectively. Inactivating mutations in HOG pathway kinases cause an increase in the phosphotyrosine content of Fus3p, greater expression of pheromone-responsive genes, and increased sensitivity to growth arrest by pheromone. Therefore, the HOG pathway represses mating pathway activity. In a HOG1+ strain, Fus3p phosphotyrosine increases modestly and transiently following an increase in the extracellular osmolarity; however, it increases to a greater extent and for a sustained duration in a hog1-delta strain. Thus, the HOG-mediated repression of mating pathway activity may insulate the mating pathway from activation by osmotic stress. A Fus3 allele whose gene product is resistant to the HOG-mediated repression of its phosphotyrosine content has been isolated. This mutant encodes an amino acid substitution in the highly conserved DPXDEP motif in subdomain XI. Other investigators have shown that the corresponding amino acid is also mutated in a gain-of-function allele of the MAP kinase encoded by the rolled locus in Drosophila melanogaster. These data suggest that the DPXDEP motif plays a role in the negative regulation of MAP kinases.
Francois Parcy - One of the best experts on this subject based on the ideXlab platform.
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a network of local and redundant gene regulation governs arabidopsis seed maturation
The Plant Cell, 2006Co-Authors: Alexandra To, Martine Devic, Christiane Valon, Gil Savino, Jocelyne Guilleminot, Jerome Giraudat, Francois ParcyAbstract:In Arabidopsis thaliana, four major regulators (ABSCISIC ACID INSENSITIVE3 [ABI3], FUSCA3 [Fus3], LEAFY COTYLEDON1 [LEC1], and LEC2) control most aspects of seed maturation, such as accumulation of storage compounds, cotyledon identity, acquisition of desiccation tolerance, and dormancy. The molecular basis for complex genetic interactions among these regulators is poorly understood. By analyzing ABI3 and Fus3 expression in various single, double, and triple maturation mutants, we have identified multiple regulatory links among all four genes. We found that one of the major roles of LEC2 was to upregulate Fus3 and ABI3. The lec2 mutation is responsible for a dramatic decrease in ABI3 and Fus3 expression, and most lec2 phenotypes can be rescued by ABI3 or Fus3 constitutive expression. In addition, ABI3 and Fus3 positively regulate themselves and each other, thereby forming feedback loops essential for their sustained and uniform expression in the embryo. Finally, LEC1 also positively regulates ABI3 and Fus3 in the cotyledons. Most of the genetic controls discovered were found to be local and redundant, explaining why they had previously been overlooked. This works establishes a genetic framework for seed maturation, organizing the key regulators of this process into a hierarchical network. In addition, it offers a molecular explanation for the puzzling variable features of lec2 mutant embryos.
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AtGA3ox2, a key gene responsible for bioactive gibberellin biosynthesis, is regulated during embryogenesis by LEAFY COTYLEDON2 and FUSCA3 in Arabidopsis.
Plant physiology, 2004Co-Authors: Julien Curaba, Francois Parcy, Thomas Moritz, Renaud Blervaque, Vered Raz, Michel Herzog, Gilles VachonAbstract:Embryonic regulators LEC2 (LEAFY COTYLEDON2) and Fus3 (FUSCA3) are involved in multiple aspects of Arabidopsis (Arabidopsis thaliana) seed development, including repression of leaf traits and premature germination and activation of seed storage protein genes. In this study, we show that gibberellin (GA) hormone biosynthesis is regulated by LEC2 and Fus3 pathways. The level of bioactive GAs is increased in immature seeds of lec2 and Fus3 mutants relative to wild-type level. In addition, we show that the formation of ectopic trichome cells on lec2 and Fus3 embryos is a GA-dependent process as in true leaves, suggesting that the GA pathway is misactivated in embryonic mutants. We next demonstrate that the GA-biosynthesis gene AtGA3ox2, which encodes the key enzyme AtGA3ox2 that catalyzes the conversion of inactive to bioactive GAs, is ectopically activated in embryos of the two mutants. Interestingly, both β-glucuronidase reporter gene expression and in situ hybridization indicate that Fus3 represses AtGA3ox2 expression mainly in epidermal cells of embryo axis, which is distinct from AtGA3ox2 pattern at germination. Finally, we show that the Fus3 protein physically interacts with two RY elements (CATGCATG) present in the AtGA3ox2 promoter. This work suggests that GA biosynthesis is directly controlled by embryonic regulators during Arabidopsis embryonic development.
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Regulation of storage protein gene expression in Arabidopsis.
Development (Cambridge England), 2003Co-Authors: Thomas Kroj, Christiane Valon, Gil Savino, Jerome Giraudat, Francois ParcyAbstract:The expression of seed storage proteins is under tight developmental regulation and represents a powerful model system to study the regulation of gene expression during plant development. In this study, we show that three homologous B3 type transcription factors regulate the model storage protein gene, At2S3, via two distinct mechanisms: FUSCA3 (Fus3) and LEAFY COTYLEDON2 (LEC2) activate the At2S3 promoter in yeast suggesting that they regulate At2S3 by directly binding its promoter; ABSCISIC ACID INSENSITIVE3 (ABI3), however, appears to act more indirectly on At2S3, possibly as a cofactor in an activation complex. In accordance with this, Fus3 and LEC2 were found to act in a partially redundant manner and differently from ABI3 in planta: At2S3 expression is reduced to variable and sometimes only moderate extent in Fus3 and lec2 single mutants but is completely abolished in the lec2 Fus3 double mutant. In addition, we found that Fus3 and LEC2 expression patterns, together with an unsuspected regulation of Fus3 by LEC2, enable us to explain the intriguing expression pattern of At2S3 in lec2 or Fus3 single mutants. Based on these results, we present a model of At2S3 regulation and discuss its implications for other aspects of seed maturation.
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the abscisic acid insensitive3 fusca3 and leafy cotyledon1 loci act in concert to control multiple aspects of arabidopsis seed development
The Plant Cell, 1997Co-Authors: Francois Parcy, Christiane Valon, Simon Miséra, Atuko Kohara, Jerome GiraudatAbstract:Previous studies have shown that recessive mutations at the Arabidopsis ABSCISIC ACID-INSENSITIVE3 (ABI3), FUSCA3 (Fus3), and LEAFY COTYLEDON1 (LEC1) loci lead to various abnormalities during mid-embryogenesis and late embryogenesis. In this study, we investigated whether these loci act in independent regulatory pathways or interact in controlling certain facets of seed development. Several developmental responses were quantified in abi3, Fus3, and lec1 single mutants as well as in double mutants combining either the weak abi3-1 or the severe abi3-4 mutations with either Fus3 or lec1 mutations. Our data indicate that ABI3 interacts genetically with both Fus3 and LEC1 in controlling each of the elementary processes analyzed, namely, accumulation of chlorophyll and anthocyanins, sensitivity to abscisic acid, and expression of individual members of the 12S storage protein gene family. In addition, both Fus3 and LEC1 regulate positively the abundance of the ABI3 protein in the seed. These results suggest that in contrast to previous models, the ABI3, Fus3, and LEC1 genes act synergistically to control multiple elementary processes during seed development.
Tsukaho Hattori - One of the best experts on this subject based on the ideXlab platform.
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Diverse roles and mechanisms of gene regulation by the Arabidopsis seed maturation master regulator Fus3 revealed by microarray analysis.
Plant & cell physiology, 2010Co-Authors: Akiko Yamamoto, Yasuaki Kagaya, Haruko Usui, Tokunori Hobo, Shin Takeda, Tsukaho HattoriAbstract:The FUSCA3 (Fus3) transcription factor is considered a master regulator of seed maturation because a wide range of seed maturation events are impaired in its defective mutant. To identify comprehensively genes under the control of Fus3, two types of microarray experiments were performed. First, transgenic plants in which Fus3 expression could be induced by the application of estrogen (ESTR) were used to identify any genes up-regulated in young seedlings of Arabidopsis in response to the ectopic expression of Fus3. Secondly, the transcriptomes of the Fus3 mutant and wild-type developing seeds were compared. The combined results of these experiments identified genes under the relatively immediate and robust control of Fus3 during seed development. The analysis has extended the range of identified gene types under the control of Fus3. The genes positively controlled by Fus3 are not confined to previously known seed maturation-related genes and include those involved in the production of secondary metabolites, such as glucosinolates, phenylpropanoids and flavonoids, and those involved in primary metabolism, such as photosynthesis and fatty acid biosynthesis. Furthermore, several different patterns were identified in the manner of ectopic activation by Fus3 with respect to the induction kinetics and ABA requirement of downstream gene induction depending on the nature of developmental regulation, suggesting mechanistic diversity of gene regulation by Fus3.
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Indirect ABA-dependent regulation of seed storage protein genes by FUSCA3 transcription factor in Arabidopsis.
Plant & cell physiology, 2005Co-Authors: Yasuaki Kagaya, Akiko Yamamoto, Haruko Usui, Rie Okuda, Atsushi Ban, Ryoko Toyoshima, Kumiko Tsutsumida, Tsukaho HattoriAbstract:The key transcription factors that control seed maturation, ABSCISIC ACID INSENSITIVE3 (ABI3) and FUSCA3 (Fus3), share homologous DNA-binding domains. Regulation of seed storage protein genes At2S3 and CRC by ABI3 and Fus3 was investigated using transgenic plants in which ABI3 and Fus3 could be ectopically induced by steroid hormones. Like ABI3, the presence of Fus3 led to expression of At2S3 and CRC in vegetative tissues. Fus3-mediated induction of CRC was completely dependent on exogenous abscisic acid (ABA), while At2S3 was weakly induced without ABA but strongly enhanced with ABA. This ABA dependency of Fus3-induced CRC and At2S3 expression was similar to that observed for ABI3. However, kinetic analysis revealed distinctions between the mechanisms of ABA-dependent CRC regulation by Fus3 or ABI3, and between target genes. While At2S3 activation by Fus3 was rapid, CRC induction by Fus3 in the presence of ABA, and by ABA followed by the presence of Fus3, took a significantly longer time (24-36 h). This suggested the involvement of an indirect mechanism requiring the ABA- and Fus3-dependent synthesis of intermediate regulatory factor(s). A chimeric protein composed of the Fus3 B3 domain, and a heterologous activation domain and nuclear localization signal exhibited a tight coupling with ABA regulation as observed for wild-type Fus3. Simultaneous induction of Fus3 and ABI3 did not result in the synergistic activation of CRC and At2S3. Based on these results, similarities and differences in the mechanisms of seed storage protein gene regulation by Fus3 and ABI3 are discussed.
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LEAFY COTYLEDON1 controls seed storage protein genes through its regulation of FUSCA3 and ABSCISIC ACID INSENSITIVE3.
Plant & cell physiology, 2005Co-Authors: Yasuaki Kagaya, Akiko Yamamoto, Haruko Usui, Rie Okuda, Ryoko Toyoshima, Tsukaho HattoriAbstract:Arabidopsis ABSCISIC ACID INSENSEITIVE3 (ABI3), FUSCA3 (Fus3) and LEAFY COTYLEDON1 (LEC1) encode key transcription factors that control seed maturation events, including seed storage protein (SSP) accumulation. Although lec1 mutations are known to down-regulate SSP gene expression as the Fus3 or abi3 mutation does, the mechanisms by which LEC1 regulates SSP gene expression are largely unknown compared with the mechanisms utilized by Fus3 or ABI3. We expressed LEC1 ectopically in transgenic plants using an artificial dexamethasone (Dex) induction system. The ectopic expression of LEC1 also resulted in the induction of Fus3 and ABI3 expression, which preceded the induction of SSP expression. The expression of Fus3 and ABI3 was found to be down-regulated in developing siliques of the lec1 mutant. Furthermore, the levels of ectopic SSP induction by LEC1 were greatly or moderately reduced in transgenic plants with an abi3 or Fus3 mutant background, respectively. LEC1-induced ectopic expression of the At1g62290 aspartic protease gene, which was identified to be regulated preferentially by Fus3, was more severely affected in the Fus3 mutant than in the abi3 mutant. From these data, we suggest that LEC1 controls the expression of the SSP genes in a hierarchical manner, which involves ABI3 and Fus3.
Yasuaki Kagaya - One of the best experts on this subject based on the ideXlab platform.
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Diverse roles and mechanisms of gene regulation by the Arabidopsis seed maturation master regulator Fus3 revealed by microarray analysis.
Plant & cell physiology, 2010Co-Authors: Akiko Yamamoto, Yasuaki Kagaya, Haruko Usui, Tokunori Hobo, Shin Takeda, Tsukaho HattoriAbstract:The FUSCA3 (Fus3) transcription factor is considered a master regulator of seed maturation because a wide range of seed maturation events are impaired in its defective mutant. To identify comprehensively genes under the control of Fus3, two types of microarray experiments were performed. First, transgenic plants in which Fus3 expression could be induced by the application of estrogen (ESTR) were used to identify any genes up-regulated in young seedlings of Arabidopsis in response to the ectopic expression of Fus3. Secondly, the transcriptomes of the Fus3 mutant and wild-type developing seeds were compared. The combined results of these experiments identified genes under the relatively immediate and robust control of Fus3 during seed development. The analysis has extended the range of identified gene types under the control of Fus3. The genes positively controlled by Fus3 are not confined to previously known seed maturation-related genes and include those involved in the production of secondary metabolites, such as glucosinolates, phenylpropanoids and flavonoids, and those involved in primary metabolism, such as photosynthesis and fatty acid biosynthesis. Furthermore, several different patterns were identified in the manner of ectopic activation by Fus3 with respect to the induction kinetics and ABA requirement of downstream gene induction depending on the nature of developmental regulation, suggesting mechanistic diversity of gene regulation by Fus3.
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Indirect ABA-dependent regulation of seed storage protein genes by FUSCA3 transcription factor in Arabidopsis.
Plant & cell physiology, 2005Co-Authors: Yasuaki Kagaya, Akiko Yamamoto, Haruko Usui, Rie Okuda, Atsushi Ban, Ryoko Toyoshima, Kumiko Tsutsumida, Tsukaho HattoriAbstract:The key transcription factors that control seed maturation, ABSCISIC ACID INSENSITIVE3 (ABI3) and FUSCA3 (Fus3), share homologous DNA-binding domains. Regulation of seed storage protein genes At2S3 and CRC by ABI3 and Fus3 was investigated using transgenic plants in which ABI3 and Fus3 could be ectopically induced by steroid hormones. Like ABI3, the presence of Fus3 led to expression of At2S3 and CRC in vegetative tissues. Fus3-mediated induction of CRC was completely dependent on exogenous abscisic acid (ABA), while At2S3 was weakly induced without ABA but strongly enhanced with ABA. This ABA dependency of Fus3-induced CRC and At2S3 expression was similar to that observed for ABI3. However, kinetic analysis revealed distinctions between the mechanisms of ABA-dependent CRC regulation by Fus3 or ABI3, and between target genes. While At2S3 activation by Fus3 was rapid, CRC induction by Fus3 in the presence of ABA, and by ABA followed by the presence of Fus3, took a significantly longer time (24-36 h). This suggested the involvement of an indirect mechanism requiring the ABA- and Fus3-dependent synthesis of intermediate regulatory factor(s). A chimeric protein composed of the Fus3 B3 domain, and a heterologous activation domain and nuclear localization signal exhibited a tight coupling with ABA regulation as observed for wild-type Fus3. Simultaneous induction of Fus3 and ABI3 did not result in the synergistic activation of CRC and At2S3. Based on these results, similarities and differences in the mechanisms of seed storage protein gene regulation by Fus3 and ABI3 are discussed.
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LEAFY COTYLEDON1 controls seed storage protein genes through its regulation of FUSCA3 and ABSCISIC ACID INSENSITIVE3.
Plant & cell physiology, 2005Co-Authors: Yasuaki Kagaya, Akiko Yamamoto, Haruko Usui, Rie Okuda, Ryoko Toyoshima, Tsukaho HattoriAbstract:Arabidopsis ABSCISIC ACID INSENSEITIVE3 (ABI3), FUSCA3 (Fus3) and LEAFY COTYLEDON1 (LEC1) encode key transcription factors that control seed maturation events, including seed storage protein (SSP) accumulation. Although lec1 mutations are known to down-regulate SSP gene expression as the Fus3 or abi3 mutation does, the mechanisms by which LEC1 regulates SSP gene expression are largely unknown compared with the mechanisms utilized by Fus3 or ABI3. We expressed LEC1 ectopically in transgenic plants using an artificial dexamethasone (Dex) induction system. The ectopic expression of LEC1 also resulted in the induction of Fus3 and ABI3 expression, which preceded the induction of SSP expression. The expression of Fus3 and ABI3 was found to be down-regulated in developing siliques of the lec1 mutant. Furthermore, the levels of ectopic SSP induction by LEC1 were greatly or moderately reduced in transgenic plants with an abi3 or Fus3 mutant background, respectively. LEC1-induced ectopic expression of the At1g62290 aspartic protease gene, which was identified to be regulated preferentially by Fus3, was more severely affected in the Fus3 mutant than in the abi3 mutant. From these data, we suggest that LEC1 controls the expression of the SSP genes in a hierarchical manner, which involves ABI3 and Fus3.
