[Show abstract][Hide abstract] ABSTRACT: Circadian clocks generate endogenous rhythms in most organisms from cyanobacteria to humans and facilitate entrainment to environmental diurnal cycles, thus conferring a fitness advantage. Both transcriptional and posttranslational mechanisms are prominent in the basic network architecture of circadian systems. Posttranscriptional regulation, including mRNA processing, is emerging as a critical step for clock function. However, little is known about the molecular mechanisms linking RNA metabolism to the circadian clock network. Here, we report that a conserved SNW/Ski-interacting protein (SKIP) domain protein, SKIP, a splicing factor and component of the spliceosome, is involved in posttranscriptional regulation of circadian clock genes in Arabidopsis thaliana. Mutation in SKIP lengthens the circadian period in a temperature-sensitive manner and affects light input and the sensitivity of the clock to light resetting. SKIP physically interacts with the spliceosomal splicing factor Ser/Arg-rich protein45 and associates with the pre-mRNA of clock genes, such as PSEUDORESPONSE REGULATOR7 (PRR7) and PRR9, and is necessary for the regulation of their alternative splicing and mRNA maturation. Genome-wide investigations reveal that SKIP functions in regulating alternative splicing of many genes, presumably through modulating recognition or cleavage of 5' and 3' splice donor and acceptor sites. Our study addresses a fundamental question on how the mRNA splicing machinery contributes to circadian clock function at a posttranscriptional level.
Hongchun Yang · Zhifu Han · Ying Cao · Di Fan · Hong Li · Huixian Mo · Yi Feng · Lei Liu · Zheng Wang · Yanling Yue · Sujuan Cui · She Chen · Jijie Chai · Ligeng Ma
[Show abstract][Hide abstract] ABSTRACT: JMJ18 induced TSF expression. qRT-PCR analysis of TSF mRNA expression in the transgenic plants. The expression level was normalized to that of ACTIN. Error bars indicate the standard deviation of three independent biological replicates. Asterisks indicate the significant difference between wild-type and transgenic plants analyzed by Student's t test (P<0.05).
[Show abstract][Hide abstract] ABSTRACT: Author Summary
Flowering is an important developmental transition during plant life cycle and the key process for production of the next generation. Flowering time is controlled by both intrinsic developmental and environmental signals. FLC and its target FT work as repressor and activator, respectively, to regulate flowering time in Arabidopsis; thus the regulation of FLC and FT expression is the key for the control of floral transition. Epigenetic modifications are critical for transcription regulation. Here, we show that a novel JmjC domain-containing histone H3K4 demethylase, JMJ18, is a key regulator for the expression of FLC and FT in companion cells and flowering time. JMJ18 is dominantly expressed in vascular tissue; its temporal expression pattern was developmentally regulated, and negatively and positively correlated with FLC and FT, respectively. JMJ18 mutation leads to weak late-flowering, while JMJ18 overexpressor exhibited an obvious early-flowering phenotype. JMJ18 binds to chromatin of FLC, represses its expression, and releases expression of FT in companion cells. Our results suggest that JMJ18 is a developmentally regulated companion cell–dominantly expressed signal to control flowering time by binding to FLC—reducing level of H3K4 methylation in FLC and repressing expression of FLC—thereby promoting expression of FT in companion cells during vegetative development in Arabidopsis.
[Show abstract][Hide abstract] ABSTRACT: Flowering time relies on the integration of intrinsic developmental cues and environmental signals. FLC and its downstream
target FT are key players in the floral transition in Arabidopsis. Here, we characterized the expression pattern and function of
JMJ18, a novel JmjC domain-containing histone H3K4 demethylase gene in Arabidopsis. JMJ18 was dominantly expressed in
companion cells; its temporal expression pattern was negatively and positively correlated with that of FLC and FT,
respectively, during vegetative development. Mutations in JMJ18 resulted in a weak late-flowering phenotype, while JMJ18
overexpressors exhibited an obvious early-flowering phenotype. JMJ18 displayed demethylase activity toward H3K4me3
and H3K4me2, and bound FLC chromatin directly. The levels of H3K4me3 and H3K4me2 in chromatins of FLC clade genes
and the expression of FLC clade genes were reduced, whereas FT expression was induced and the protein expression of FT
increased in JMJ18 overexpressor lines. The early-flowering phenotype caused by the overexpression of JMJ18 was mainly
dependent on the functional FT. Our findings suggest that the companion cell–dominant and developmentally regulated
JMJ18 binds directly to the FLC locus, reducing the level of H3K4 methylation in FLC chromatin and repressing the
expression of FLC, thereby promoting the expression of FT in companion cells to stimulate flowering.
[Show abstract][Hide abstract] ABSTRACT: Our study provided experimental evidence that GCR2 is a membrane-associated abscisic acid receptor that interacts with the
G protein α subunit GPA1 in Arabidopsis. Although we cannot rule out GCR2 as a lanthionine synthetase homolog, our data indicate that it may define a new type of
nonclassical G protein–coupled receptor.
[Show abstract][Hide abstract] ABSTRACT: The plant hormone abscisic acid (ABA) regulates many physiological and developmental processes in plants. The mechanism of
ABA perception at the cell surface is not understood. Here, we report that a G protein–coupled receptor genetically and physically
interacts with the G protein α subunit GPA1 to mediate all known ABA responses in Arabidopsis. Overexpressing this receptor results in an ABA-hypersensitive phenotype. This receptor binds ABA with high affinity at physiological
concentration with expected kinetics and stereospecificity. The binding of ABA to the receptor leads to the dissociation of
the receptor-GPA1 complex in yeast. Our results demonstrate that this G protein–coupled receptor is a plasma membrane ABA