Cryptochromes are blue, ultraviolet-A photoreceptors. They were first characterized for Arabidopsis and are also found in ferns and algae; they appear to be ubiquitous in the plant kingdom. They are flavoproteins similar in sequence to photolyases, their presumptive evolutionary ancestors. Cryptochromes mediate a variety of light responses, including entrainment of circadian rhythms in Arabidopsis, Drosophila, and mammals. Sequence comparison indicates that the plant and animal cryptochrome families have distinct evolutionary histories, with the plant cryptochromes being of ancient evolutionary origin and the animal cryptochromes having evolved relatively recently. This process of repeated evolution may have coincided with the origin in animals of a modified circadian clock based on the PERIOD, TIMELESS, CLOCK, and CYCLE proteins.
Flowering of Arabidopsis is induced by long summer days (LDs). The transcriptional regulator CONSTANS (CO) promotes flowering, and its transcription is increased under LDs. We systematically misexpressed transcription factors in companion cells and identified several DOF proteins that delay flowering by repressing CO transcription. Combining mutations in four of these, including CYCLING DOF FACTOR 2 (CDF2), caused photoperiod-insensitive early flowering by increasing CO mRNA levels. CO transcription is promoted to differing extents by GIGANTEA (GI) and the F-box protein FKF1. We show that GI stabilizes FKF1, thereby reducing CDF2 abundance and allowing transcription of CO. Despite the crucial function of GI in wild-type plants, introducing mutations in the four DOF-encoding genes into gi mutants restored the diurnal rhythm and light inducibility of CO. Thus, antagonism between GI and DOF transcription factors contributes to photoperiodic flowering by modulating an underlying diurnal rhythm in CO transcript levels.
In photosynthetic cells, chloroplasts migrate towards illuminated sites to optimize photosynthesis and move away from excessively illuminated areas to protect the photosynthetic machinery. Although this movement of chloroplasts in response to light has been known for over a century, the photoreceptor mediating this process has not been identified. The Arabidopsis gene NPL1 (ref. 2) is a paralogue of the NPH1 gene, which encodes phototropin, a photoreceptor for phototropic bending. Here we show that NPL1 is required for chloroplast relocation induced by blue light. A loss-of-function npl1 mutant showed no chloroplast avoidance response in strong blue light, whereas the accumulation of chloroplasts in weak light was normal. These results indicate that NPL1 may function as a photoreceptor mediating chloroplast relocation.
The initiation of flowering in plants is controlled by environmental and endogenous signals 1,2 . Molecular analysis of this process in Arabidopsis thaliana indicates that environmental control is exerted through the photoperiod and vernalization pathways, whereas endogenous signals regulate the autonomous and gibberellin pathways. The vernalization and autonomous pathways converge on the negative regulation of FLC 3,4 , a gene encoding a MADS-box protein that inhibits flowering 3,4 . We cloned FVE, a component of the autonomous pathway that encodes AtMSI4, a putative retinoblastomaassociated protein. FVE interacted with retinoblastoma protein in immunoprecipitation assays, and FLC chromatin was enriched in acetylated histones in fve mutants. We conclude that FVE participates in a protein complex repressing FLC transcription through a histone deacetylation mechanism. Our data provide genetic evidence of a new developmental function of these conserved proteins and identify a new genetic mechanism in the regulation of flowering. shown in the upper part, capital letters correspond to the wild-type or mutated nucleotides. In the protein schematic, gray boxes represent WD repeats, the narrow black box represents a putative nuclear localization signal and the asterisk indicates a putative retinoblastoma-binding motif.
The Arabidopsis thaliana early in short days6 (esd6) mutant was isolated in a screen for mutations that accelerate flowering time. Among other developmental alterations, esd6 displays early flowering in both long-and short-day conditions. Fine mapping of the mutation showed that the esd6 phenotype is caused by a lesion in the HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENES1 (HOS1) locus, which encodes a RING finger-containing E3 ubiquitin ligase. The esd6/hos1 mutation causes decreased FLOWERING LOCUS C expression and requires CONSTANS (CO) protein for its early flowering phenotype under long days. Moreover, CO and HOS1 physically interact in vitro and in planta, and HOS1 regulates CO abundance, particularly during the daylight period. Accordingly, hos1 causes a shift in the regular long-day pattern of expression of FLOWERING LOCUS T (FT ) transcript, starting to rise 4 h after dawn in the mutant. In addition, HOS1 interacts synergistically with CONSTITUTIVE PHOTOMORPHOGENIC1, another regulator of CO protein stability, in the regulation of flowering time. Taken together, these results indicate that HOS1 is involved in the control of CO abundance, ensuring that CO activation of FT occurs only when the light period reaches a certain length and preventing precocious flowering in Arabidopsis.
Anthocyanins, which accumulate in leaves and stems in response to low temperature and changes in light intensity, are synthesized through the phenylpropanoid pathway that is controlled by key enzymes that include phenylalanine ammonia-lyase (PAL) and chalcone synthase (CHS). In this work we demonstrate that PAL and CHS mRNAs accumulate in leaves of Arabidopsis thaliana (1.) Heynh. upon exposure to low temperature in a light-dependent manner. The regulation of the PALl gene expression by low temperature and light was examined by analyzing the expression of the P-glucuronidase (uidA) reporter gene in transgenic Arabidopsis plants containing the uidA gene of Escherichia coli under the control of the PALl promoter. The results indicate that the accumulation of PAL 7 mRNA is transcriptionally regulated. Histochemical staining for P-glucuronidase activity showed that the PAL7 promoter i s preferentially activated in photosynthetically active cells, paralleling anthocyanin accumulation. Moreover, we show that light may also be implicated in the regulation of the CHS gene in response to bacterial infiltration. Finally, using two fransparent testa Arabidopsis mutants that are unable to accumulate anthocyanins, we demonstrate that these pigments are not required for successful development of freezing tolerance in this species.
Plants have at least two major photosensory receptors: phytochrome (absorbing primarily red/far-red light) and cryptochrome (absorbing blue/UV-A light); considerable physiological and genetic evidence suggests some form of communication or functional dependence between the receptors. Here, we demonstrate in vitro, using purified recombinant photoreceptors, that Arabidopsis CRY1 and CRY2 (cryptochrome) are substrates for phosphorylation by a phytochrome A-associated kinase activity. Several mutations within the CRY1 C terminus lead to reduced phosphorylation by phytochrome preparations in vitro. Yeast two-hybrid interaction studies using expressed C-terminal fragments of CRY1 and phytochrome A from Arabidopsis confirm a direct physical interaction between both photoreceptors. In vivo labeling studies and specific mutant alleles of CRY1, which interfere with the function of phytochrome, suggest the possible relevance of these findings in vivo.
We have characterized Arabidopsis esd1 mutations, which cause early flowering independently of photoperiod, moderate increase of hypocotyl length, shortened inflorescence internodes, and altered leaf and flower development. Phenotypic analyses of double mutants with mutations at different loci of the flowering inductive pathways suggest that esd1 abolishes the FLC-mediated late flowering phenotype of plants carrying active alleles of FRI and of mutants of the autonomous pathway. We found that ESD1 is required for the expression of the FLC repressor to levels that inhibit flowering. However, the effect of esd1 in a flc-3 null genetic background and the downregulation of other members of the FLC-like/MAF gene family in esd1 mutants suggest that flowering inhibition mediated by ESD1 occurs through both FLC-and FLC-like gene-dependent pathways. The ESD1 locus was identified through a map-based cloning approach. ESD1 encodes ARP6, a homolog of the actin-related protein family that shares moderate sequence homology with conventional actins. Using chromatin immunoprecipitation (ChIP) experiments, we have determined that ARP6 is required for both histone acetylation and methylation of the FLC chromatin in Arabidopsis. Development 133, 1241Development 133, -1252Development 133, (2006 DEVELOPMENT 1242 and the trimethylation of lysine 4 of H3 (H3-K4), which are hallmarks of active genes (He et al., 2003; Ausin et al., 2004; He et al., 2004). Late-flowering autonomous pathway mutants also have increased levels of H3-K4 trimethylation and histone acetylation compared with the rapid-flowering parental line (He et al., 2003; Ausin et al., 2004; He et al., 2004;Kim et al., 2005). Many early flowering mutations suppressing the late flowering phenotype of FRI-containing lines have identified components that are required to maintain high levels of FLC expression. This is the case of mutants such as early flowering in short days (efs), photoperiod independent early flowering 1 (pie1), early flowering 5 (elf5), vernalization independence3 (vip3) and frigida-like1 (frl-1), and mutants in genes encoding components of the PAF1 complex (ELF7, VIP4, VIP5 and VIP6/ELF8) (Zhang and Van Nocker, 2002;Noh and Amasino, 2003;Zhang et al., 2003;Noh et al., 2004; He et al., 2004;Michaels et al., 2004;Oh et al., 2004;Kim et al., 2005). Most of these mutations also appear to affect flowering in an FLC-independent manner. KEY WORDS: Flowering time, Floral repression, Chromatin remodelling, ArabidopsisAfter exposure to an extended winter and the completion of vernalization, the level of modifications associated with 'active' chromatin is reduced, and the histone tails of FLC chromatin are deacetylated and become enriched in methylation of lysine 9 (K9) and 27 (K27) of H3 (Bastow et al., 2004;Sung and Amasino, 2004), which are hallmarks of repressed genes (Orlando, 2003). Mutants that are unable to reduce FLC transcript levels by vernalization or to maintain the vernalised state have permitted the identification of some of the proteins particip...
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