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The proper timing of flowering, which is key to maximize reproductive success and yield, relies in many plant species on the coordination between environmental cues and endogenous developmental programs. The perception of changes in day length is one of the most reliable cues of seasonal change, and this involves the interplay between the sensing of light signals and the circadian clock. Here, we describe a Brachypodium distachyon mutant allele of the evening complex protein EARLY FLOWERING 3 (ELF3). We show that the elf3 mutant flowers more rapidly than wild type plants in short days as well as under longer photoperiods but, in very long (20 h) days, flowering is equally rapid in elf3 and wild type. Furthermore, flowering in the elf3 mutant is still sensitive to vernalization, but not to ambient temperature changes. Molecular analyses revealed that the expression of a short-day marker gene is suppressed in elf3 grown in short days, and the expression patterns of clock genes and flowering time regulators are altered. We also explored the mechanisms of photoperiodic perception in temperate grasses by exposing B. distachyon plants grown under a 12 h photoperiod to a daily night break consisting of a mixture of red and far-red light. We showed that 2 h breaks are sufficient to accelerate flowering in B. distachyon under non-inductive photoperiods and that this acceleration of flowering is mediated by red light. Finally, we discuss advances and perspectives for research on the perception of photoperiod in temperate grasses.more » « less
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Summary The timing of reproduction is a critical developmental decision in the life cycle of many plant species.
Fine mapping of a rapid‐flowering mutant was done using whole‐genome sequence data from bulked DNA from a segregating F2 mapping populations. The causative mutation maps to a gene orthologous with the third subunit of DNA polymerase δ (POLD3), a previously uncharacterized gene in plants. Expression analyses of POLD3 were conducted via real time qPCR to determine when and in what tissues the gene is expressed.
To better understand the molecular basis of the rapid‐flowering phenotype, transcriptomic analyses were conducted in the mutant vs wild‐type. Consistent with the rapid‐flowering mutant phenotype, a range of genes involved in floral induction and flower development are upregulated in the mutant.
Our results provide the first characterization of the developmental and gene expression phenotypes that result from a lesion in
POLD3 in plants. -
Summary Many plants require prolonged exposure to cold to acquire the competence to flower. The process by which cold exposure results in competence is known as vernalization. In
Arabidopsis thaliana , vernalization leads to the stable repression of the floral repressor via chromatin modification, including an increase of trimethylation on lysine 27 of histone H3 (H3K27me3) by Polycomb Repressive Complex 2 (FLOWERING LOCUS CPRC 2). Vernalization in pooids is associated with the stable induction of a floral promoter, (VERNALIZATION 1VRN1 ). From a screen for mutants with a reduced vernalization requirement in the model grassBrachypodium distachyon , we identified two recessive alleles of (ENHANCER OF ZESTE ‐LIKE 1 ).EZL 1 is orthologous toEZL 1A. thaliana , a gene that encodes the catalytic subunit ofCURLY LEAF 1PRC 2.B. distachyon ezl1 mutants flower rapidly without vernalization in long‐day (LD ) photoperiods; thus, is required for the proper maintenance of the vegetative state prior to vernalization. Transcriptomic studies inEZL 1ezl1 revealed mis‐regulation of thousands of genes, including ectopic expression of several floral homeotic genes in leaves. Loss of results in the global reduction of H3K27me3 and H3K27me2, consistent with this gene making a major contribution toEZL 1PRC 2 activity inB. distachyon . Furthermore, inezl1 mutants, the flowering genes andVRN 1 (AGAMOUS ) are ectopically expressed and have reduced H3K27me3. Artificial microAG RNA knock‐down of either orVRN 1 inAG ezl1‐1 mutants partially restores wild‐type flowering behavior in non‐vernalized plants, suggesting that ectopic expression inezl1 mutants may contribute to the rapid‐flowering phenotype.